Details of a Researcher

Personnel Information

写真a

FUNAYAMA RYO

Job title

Project Associate Professor

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Graduating School 【 display / non-display 】

Kanagawa University, Faculty of Science, 応用生物科学科, 1999.03, Graduated
Tokyo Institute of Technology, Graduate School, Division of Life Science and Engineering, 2007.03, Graduated

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Campus Career 【 display / non-display 】

2024.05

-

Now

Tokyo Medical and Dental University， TMDU Advanced Research Institute (TMDU-ARIS)，， -， Project Associate Professor

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External Career 【 display / non-display 】

2007.04

-

2007.09

京都大学大学院生命科学研究科, 博士研究員
2007.10

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2007.11

京都大学大学院生命科学研究科, 助教(特任)
2007.12

-

Now

東北大学大学院医学系研究科, 助教

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Research Areas 【 display / non-display 】

Molecular biology

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Research Theme 【 display / non-display 】

Elucidation of the signaling pathways that induce gene amplification, 2018.06 - 2020.03

Summary： When the time course of amplification after TGF-β stimulation was examined, cell proliferation had already stopped on the second day after the start of stimulation, but no gene amplification was observed, and amplification occurred on the 28th day.
To confirm that this is a universal phenomenon in NMuMG cells, we purchased new NMuMG cells and further cloned the cells by limitting dilution. After stimulation with TGF-β, all the clones stopped growing and then started growing again, avoiding the inhibition of growth by TGF-β, as previously reported. However, no amplification of myc was observed in these clones, suggesting that this is not a universal phenomenon in NMuMG cells.
Identification of novel microexon involved in the regulation of colorectal cancer, 2018.04 - 2021.03

Summary： Microexons are very small exons, whose alternative splicing is frequently deregulated in a neurological disease, autism spectrum disorder. However, little is known about the splicing pattern, regulatory mechanisms, and roles of microexon in cancer. We have examined the transcriptome-wide profile of microexon splicing in matched normal colon and colorectal cancer (CRC) tissue specimens. Out of 1,492 microexons with shorter than 15 nucleotides in length, seventeen (1%) were differentially spliced between normal colon and CRC tissues. Analyses of RNA sequence motifs, an RNA-binding protein database, and subsequent shRNA-mediated knockdown identified two splicing factors, RBFOX2 and PTBP1, as regulators of microexon splicing. Our data thus suggest that the altered expression of RBFOX2 and PTBP1 might affect cell adhesion and migration of CRC cells through the regulation of microexon splicing.
Identification of novel microexon involved in the regulation of colorectal cancer, 2018.04 - 2021.03

Summary： Microexons are very small exons, whose alternative splicing is frequently deregulated in a neurological disease, autism spectrum disorder. However, little is known about the splicing pattern, regulatory mechanisms, and roles of microexon in cancer. We have examined the transcriptome-wide profile of microexon splicing in matched normal colon and colorectal cancer (CRC) tissue specimens. Out of 1,492 microexons with shorter than 15 nucleotides in length, seventeen (1%) were differentially spliced between normal colon and CRC tissues. Analyses of RNA sequence motifs, an RNA-binding protein database, and subsequent shRNA-mediated knockdown identified two splicing factors, RBFOX2 and PTBP1, as regulators of microexon splicing. Our data thus suggest that the altered expression of RBFOX2 and PTBP1 might affect cell adhesion and migration of CRC cells through the regulation of microexon splicing.
Elucidation of the mechanism of transcription elongation rate control by histone code, 2017.04 - 2020.03

Summary： To measure the rate of transcription elongation, we used DRB treatment, an RNA polymerase inhibitor, and BrU labeling of the newly synthesized RNAs to recover the newly synthesized RNAs. We measured the elongation rate of model genes, such as the highly transcribed GAPDH gene. To determine how H3K27me3 modification affects the elongation rate of RNA polymerase in cells, cells were knocked down with SUZ12 and reduced H3K27me3 modification, resulting that H3K27me3 modification is negatively correlated with the elongation rate of transcription.
Now, to investigate the comprehensiveness of this phenomenon, we performed RNA seq of a newly synthesized RNA and ChIP seq of H3K27me3.
Elucidation of the mechanism of transcription elongation rate control by histone code, 2017.04 - 2020.03

Summary： To measure the rate of transcription elongation, we used DRB treatment, an RNA polymerase inhibitor, and BrU labeling of the newly synthesized RNAs to recover the newly synthesized RNAs. We measured the elongation rate of model genes, such as the highly transcribed GAPDH gene. To determine how H3K27me3 modification affects the elongation rate of RNA polymerase in cells, cells were knocked down with SUZ12 and reduced H3K27me3 modification, resulting that H3K27me3 modification is negatively correlated with the elongation rate of transcription.
Now, to investigate the comprehensiveness of this phenomenon, we performed RNA seq of a newly synthesized RNA and ChIP seq of H3K27me3.
PADI2 suppresses proliferation of colon cancer cells through protein citrullination, 2016.04 - 2019.03

Summary： PADI2 was expressed in normal colon epithelial cells and downregulated during colon carcinogenesis. Overexpression of PADI2 suppressed proliferation of colon cancer cells in vitro concomitant with increased protein citrullination. The growth defect was not caused by increased apoptosis but by suppression of cell cycle progression. Some citrullinated proteins were found in normal colon tissues. Our data thus suggest that PADI2 suppresses proliferation of colon epithelial cells through protein citrullination, and that downregulation of PADI2 expression might contribute to colon carcinogenesis.
PADI2 suppresses proliferation of colon cancer cells through protein citrullination, 2016.04 - 2019.03

Summary： PADI2 was expressed in normal colon epithelial cells and downregulated during colon carcinogenesis. Overexpression of PADI2 suppressed proliferation of colon cancer cells in vitro concomitant with increased protein citrullination. The growth defect was not caused by increased apoptosis but by suppression of cell cycle progression. Some citrullinated proteins were found in normal colon tissues. Our data thus suggest that PADI2 suppresses proliferation of colon epithelial cells through protein citrullination, and that downregulation of PADI2 expression might contribute to colon carcinogenesis.
Verification of genomic diversity required for tumorigenesis, 2016.04 - 2017.03

Summary： CRISPR/Cas9 library was introduced to NIH3T3 cells and MDA-MD-468 cells to generate cell library which are gene disrupted. Groups of cells which was disrupted a gene by CRISPR/Cas9 system were obtained. These cells were inoculated subcutaneously on the back of immunodeficient mice to grow tumors. Even NIH3T3 cells which were introduced library failed to stable tumorigenesis as well as wild type cells. These data suggested that NIH3T3 population containing different kinds of a single gene disrupted cells did not achieve capability of tumorigenesis. With MDA-MD-462 cells, we observed cells introduced CRISPR/Cas9 library gain function of tumorigenesis compared to wild-type cells.
Verification of genomic diversity required for tumorigenesis, 2016.04 - 2017.03

Summary： CRISPR/Cas9 library was introduced to NIH3T3 cells and MDA-MD-468 cells to generate cell library which are gene disrupted. Groups of cells which was disrupted a gene by CRISPR/Cas9 system were obtained. These cells were inoculated subcutaneously on the back of immunodeficient mice to grow tumors. Even NIH3T3 cells which were introduced library failed to stable tumorigenesis as well as wild type cells. These data suggested that NIH3T3 population containing different kinds of a single gene disrupted cells did not achieve capability of tumorigenesis. With MDA-MD-462 cells, we observed cells introduced CRISPR/Cas9 library gain function of tumorigenesis compared to wild-type cells.
Genome wide analysis of epigenetic regulation of enhancer activity via H3K27 modifications, 2015.04 - 2017.03

Summary： It is still unknown whether H3K27me3 histone modification has a repressive role toward enhancer activity. To address this issue, we performed series of genome wide analysis to map and quantify H3K27me3, H3K27ac, p300 and mRNA expression in H3K27me3-depleted K562 human leukemia cells. We observed that the decrease in H3K27me3 level in enhancer region led to massive accumulation of H3K27ac and p300 at the same enhancer region, whereas the decrease in H3K27me3 in gene body was associated with upregulation of transcription of the same gene. Our results thus provide insights into the causal relationship between H3K27 histone modifications in regulatory elements and gene expression.
Genome wide analysis of epigenetic regulation of enhancer activity via H3K27 modifications, 2015.04 - 2017.03

Summary： It is still unknown whether H3K27me3 histone modification has a repressive role toward enhancer activity. To address this issue, we performed series of genome wide analysis to map and quantify H3K27me3, H3K27ac, p300 and mRNA expression in H3K27me3-depleted K562 human leukemia cells. We observed that the decrease in H3K27me3 level in enhancer region led to massive accumulation of H3K27ac and p300 at the same enhancer region, whereas the decrease in H3K27me3 in gene body was associated with upregulation of transcription of the same gene. Our results thus provide insights into the causal relationship between H3K27 histone modifications in regulatory elements and gene expression.
Verification of genomic diversity required for tumorigenesis, 2015.04 - 2016.03

Summary： It has been demonstrated that solid tumors are composed of various genomic mutated cells by genomic sequencing and analysis of diversity. In this program, we tried to identify critical mutations to generate solid tumors by random mutagenesis using CRISPR/Cas9 library. We used library which randomly made deletions at promoter regions of almost all reported human genes. We infected CRISPR/Cas9 library to human cancer cell lines to generate randomly mutated cell pool. Diversity of library extracted cell line were reduced within several days culture after introduction of library compared to that of original library. This observation suggest that in introduction of library make some clones die or proliferate less, as these clones have disadvantage to survival in vitro compared to other clones.
Elucidation of transcriptional regulation by histone modification pattern, 2014.04 - 2017.03

Summary： TGF-β treatment to breast cancer cell lines induces epithelial-mesenchymal transition. We confirmed suppression of EZH2 expression by shRNA decreased modification levels of Histone H3K27me3. With this method, we analyzed the effect of suppression of H3K27me3 modification on transcript. Contrary to expectations, suppression of H3K27me3 did not cause a major effect.
Next to breast cancer cell lines, we analyzed EZH2 deficient B lymphocytes. As we expected, modification of H3K27me3 in these downregulated and we obtained list of transcriptional activated genes. We also analyzed the modification level of H3K4me1 as a marker of enhancer activity. We identified the region where H3K4me1 increased after EZH2 deletion. However, we could not recognize which genes were regulated by corresponding enhancers.
Elucidation of transcriptional regulation by histone modification pattern, 2014.04 - 2017.03

Summary： TGF-β treatment to breast cancer cell lines induces epithelial-mesenchymal transition. We confirmed suppression of EZH2 expression by shRNA decreased modification levels of Histone H3K27me3. With this method, we analyzed the effect of suppression of H3K27me3 modification on transcript. Contrary to expectations, suppression of H3K27me3 did not cause a major effect.
Next to breast cancer cell lines, we analyzed EZH2 deficient B lymphocytes. As we expected, modification of H3K27me3 in these downregulated and we obtained list of transcriptional activated genes. We also analyzed the modification level of H3K4me1 as a marker of enhancer activity. We identified the region where H3K4me1 increased after EZH2 deletion. However, we could not recognize which genes were regulated by corresponding enhancers.
Molecular mechanism of oncogenic RAS-induced gene silencing, 2014.04 - 2016.03

Summary： Cancer is caused by DNA mutations. Some mutations cause alterations in gene expression, which result in abnormal growth and viability in cancer cells. We uncovered the molecular mechanism of transcriptional repression induced by an oncogenic RAS mutation, one of the most recurrent mutation in cancer. Phosphorylation activity of protein kinase Erk2 is required for RAS-induced transcriptional repression. Moreover, transcriptional repression triggers alteration of chromatin environment including histone modification.
Molecular mechanism of oncogenic RAS-induced gene silencing, 2014.04 - 2016.03

Summary： Cancer is caused by DNA mutations. Some mutations cause alterations in gene expression, which result in abnormal growth and viability in cancer cells. We uncovered the molecular mechanism of transcriptional repression induced by an oncogenic RAS mutation, one of the most recurrent mutation in cancer. Phosphorylation activity of protein kinase Erk2 is required for RAS-induced transcriptional repression. Moreover, transcriptional repression triggers alteration of chromatin environment including histone modification.
Comprehensive screening of histone modifying enzyme, 2014.04 - 2015.03

Summary： In the nucleus, core histones, which genomic DNA wrap around, create an environment of genome DNA. Post-translational modifications of histone are thought to regulate the shape of existence and function of genomic DNA. This means the significance to elucidate the regulatory mechanisms of post-translational modifications of histone.
In this project, the final goal was set as the generation of cell group which is consist of cells with mutation of various enzymes of modification, and the examination of change of constituent cells after long-term culture or induction of differentiation. Effective protocol of introduction of mutation was determined for several cell lines.
Comprehensive screening of histone modifying enzyme, 2014.04 - 2015.03

Summary： In the nucleus, core histones, which genomic DNA wrap around, create an environment of genome DNA. Post-translational modifications of histone are thought to regulate the shape of existence and function of genomic DNA. This means the significance to elucidate the regulatory mechanisms of post-translational modifications of histone.
In this project, the final goal was set as the generation of cell group which is consist of cells with mutation of various enzymes of modification, and the examination of change of constituent cells after long-term culture or induction of differentiation. Effective protocol of introduction of mutation was determined for several cell lines.
Regulation of celullar differentiation by degradation of core promoter recognition complex, 2013.08 - 2015.03

Summary： Cell differentiation accompanies global gene expression change. Previous studies revealed that genes to be expressed are determined by transcription factors, but emerging evidences indicate that the general transcription machinery is also involved in gene expression change.
The general transcription machinery comprises several complexes, among which the promoter recognition complex TFIID plays a pivotal role in the selection of expressed genes. During the differentiation of myoblastic cell line and the epithelial-to-mesenchymal transition (EMT) of mammary epithelial cell line, several components of TFIID were found to be degraded by the ubiquitin-proteasome system. Induction of EMT caused the increase in an ubiquitin ligase which promoted the degradation of the TFIID component, leading to the reduction of translation-related gene expression. These results revealed a novel mechanism of regulation of the general transcription machinery by protein degradation during cell differentiation.
A novel role of oncogenic RAS in gene silencing, 2012.04 - 2014.03

Summary： RAS-MAPK signaling regulates cell growth and survival. It is abnormally activated in cancer cells and represses transcription of tumor-suppressive genes to enhance tumorigenesis of the cells. In this study, I investigated the molecular mechanism of RAS-mediated transcriptional repression. RAS-MAPK signaling increases the amount of a histone modification in transcriptionally repressed genes. The alteration of the histone modification occurs after alteration of transcription, suggesting that the histone modification functions to maintain transcriptionally repressed state. Furthermore, I identified three chromatin proteins, which are required for transcriptional repression.
A novel role of oncogenic RAS in gene silencing, 2012.04 - 2014.03

Summary： RAS-MAPK signaling regulates cell growth and survival. It is abnormally activated in cancer cells and represses transcription of tumor-suppressive genes to enhance tumorigenesis of the cells. In this study, I investigated the molecular mechanism of RAS-mediated transcriptional repression. RAS-MAPK signaling increases the amount of a histone modification in transcriptionally repressed genes. The alteration of the histone modification occurs after alteration of transcription, suggesting that the histone modification functions to maintain transcriptionally repressed state. Furthermore, I identified three chromatin proteins, which are required for transcriptional repression.
Analysis of M phase-regulation by GdX, 2008 - 2010

Summary： We found that cyclin F was covalently conjugated with GdX (GdXylation). Our data suggested that GdXylation of cyclin F regulated its protein stability and cell cycle progression. Although we identified 11 GdX- and 23 RNF (candidate of GdXligase)-binding proteins by biochemical techniques, identification of E1, E2 and E3 enzymes for GdXylation could not be achieved.It was suggested that RNF is functional as a ubiquitinligase in mouse spermatogenesis by analysis of RNF-deficient mice. So we will develop the functional analysis of RNF in future.
Molecular and temporal-spatial regulation of ubiquitin ligase , F-box protein, 2008 - 2010

Summary： F-box protein functions as a ubiquitin ligase constructing SCF protein complex. In this preject, I focused my interest on typical F-box proteins, Fbxw7 and β-TrCP. I analyzed their gene targeting mice to elucidate the biological function of these proteins. Although Fbxw7 suppressed tumorigenesis in T lymphocytes and hematopoietic stem cell, it facilitated cell proliferation in primary embryonic fibroblasts and keratinocytes. b-TrCP promoted cell proliferation.
Analysis of M phase-regulation by GdX, 2008 - 2010

Summary： We found that cyclin F was covalently conjugated with GdX (GdXylation). Our data suggested that GdXylation of cyclin F regulated its protein stability and cell cycle progression. Although we identified 11 GdX- and 23 RNF (candidate of GdXligase)-binding proteins by biochemical techniques, identification of E1, E2 and E3 enzymes for GdXylation could not be achieved.It was suggested that RNF is functional as a ubiquitinligase in mouse spermatogenesis by analysis of RNF-deficient mice. So we will develop the functional analysis of RNF in future.
Molecular and temporal-spatial regulation of ubiquitin ligase , F-box protein, 2008 - 2010

Summary： F-box protein functions as a ubiquitin ligase constructing SCF protein complex. In this preject, I focused my interest on typical F-box proteins, Fbxw7 and β-TrCP. I analyzed their gene targeting mice to elucidate the biological function of these proteins. Although Fbxw7 suppressed tumorigenesis in T lymphocytes and hematopoietic stem cell, it facilitated cell proliferation in primary embryonic fibroblasts and keratinocytes. b-TrCP promoted cell proliferation.
The turning point from cell proliferation to cell differentiation, 2007 - 2011

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Published Papers & Misc 【 display / non-display 】

Nishizawa, H; Matsumoto, M; Yamanaka, M; Irikura, R; Nakajima, K; Tada, K; Nakayama, Y; Konishi, M; Itoh, N; Funayama, R; Nakayama, K; Igarashi, K. BACH1 inhibits senescence, obesity, and short lifespan by ferroptotic FGF21 secretion CELL REPORTS. 2024.07; 43 (7): 114403. ( PubMed, DOI )
Sato Yukihiro, Kobayashi Minoru, Ohira Masahiro, Funayama Ryo, Maekawa Masamitsu, Karasawa Hideaki, Kashiwagi Ryosuke, Aoyama Yayoi, Mano Nariyasu, Ohnuma Shinobu, Unno Michiaki, Nakayama Keiko. Downregulation of ABCC3 activates MAPK signaling through accumulation of deoxycholic acid in colorectal cancer cells(タイトル和訳中) Cancer Science. 2024.06; 115 (6): 1778-1790. ( ichushi )
Sato, Y; Kobayashi, M; Ohira, M; Funayama, R; Maekawa, M; Karasawa, H; Kashiwagi, R; Aoyama, Y; Mano, N; Ohnuma, S; Unno, M; Nakayama, K. Downregulation of ABCC3 activates MAPK signaling through accumulation of deoxycholic acid in colorectal cancer cells CANCER SCIENCE. 2024.06; 115 (6): 1778-1790. ( PubMed, DOI )
Ochiai, K; Shima, H; Tamahara, T; Sugie, N; Funayama, R; Nakayama, K; Kurosaki, T; Igarashi, K. Accelerated plasma-cell differentiation in Bach2-deficient mouse B cells is caused by altered IRF4 functions EMBO JOURNAL. 2024.05; 43 (10): 1947-1964. ( PubMed, DOI )
Izumi, R; Ikeda, K; Niihori, T; Suzuki, N; Shirota, M; Funayama, R; Nakayama, K; Warita, H; Tateyama, M; Aoki, Y; Aoki, M. Nuclear pore pathology underlying multisystem proteinopathy type 3-related inclusion body myopathy ANNALS OF CLINICAL AND TRANSLATIONAL NEUROLOGY. 2024.03; 11 (3): 577-592. ( PubMed, DOI )
Kashiwagi, R; Funayama, R; Aoki, S; Matsui, A; Klein, S; Sato, Y; Suzuki, T; Murakami, K; Inoue, K; Iseki, M; Masuda, K; Mizuma, M; Naito, H; Duda, DG; Unno, M; Nakayama, K. Collagen XVII regulates tumor growth in pancreatic cancer through interaction with the tumor microenvironment CANCER SCIENCE. 2023.11; 114 (11): 4286-4298. ( PubMed, DOI )
Kashiwagi Ryosuke, Funayama Ryo, Aoki Shuichi, Matsui Aya, Klein Sebastian, Sato Yukihiro, Suzuki Tsubasa, Murakami Keigo, Inoue Koetsu, Iseki Masahiro, Masuda Kunihiro, Mizuma Masamichi, Naito Hisamichi, Duda Dan G., Unno Michiaki, Nakayama Keiko. XVII型コラーゲンは腫瘍微小環境との相互作用を通じて膵癌の腫瘍成長を調節する(Collagen XVII regulates tumor growth in pancreatic cancer through interaction with the tumor microenvironment) Cancer Science. 2023.11; 114 (11): 4286-4298. ( ichushi )
Okubo, Y; Shibuya, M; Nakamura, H; Kawashima, A; Kodama, K; Endo, W; Inui, T; Togashi, N; Aihara, Y; Shirota, M; Funayama, R; Niihori, T; Fujita, A; Nakayama, K; Aoki, Y; Matsumoto, N; Kure, S; Kikuchi, A; Haginoya, K. Neonatal developmental and epileptic encephalopathy with movement disorders and arthrogryposis: A case report with a novel missense variant of SCN1A BRAIN & DEVELOPMENT. 2023.10; 45 (9): 505-511. ( PubMed, DOI )
Okubo Yukimune, Shibuya Moriei, Nakamura Haruhiko, Kawashima Aritomo, Kodama Kaori, Endo Wakaba, Inui Takehiko, Togashi Noriko, Aihara Yu, Shirota Matsuyuki, Funayama Ryo, Niihori Tetsuya, Fujita Atsushi, Nakayama Keiko, Aoki Yoko, Matsumoto Naomichi, Kure Shigeo, Kikuchi Atsuo, Haginoya Kazuhiro. 運動障害と関節拘縮を伴う新生児発達てんかん性脳症　SCN1A新規ミスセンス変異陽性の症例報告(Neonatal developmental and epileptic encephalopathy with movement disorders and arthrogryposis: A case report with a novel missense variant of SCN1A) Brain & Development. 2023.10; 45 (9): 505-511. ( ichushi )
Yu, ZQ; Ueno, K; Funayama, R; Sakai, M; Nariai, N; Kojima, K; Kikuchi, Y; Li, X; Ono, CK; Kanatani, J; Ono, J; Iwamoto, K; Hashimoto, K; Kinoshita, K; Nakayama, K; Nagasaki, M; Tomita, H. Sex-Specific Differences in the Transcriptome of the Human Dorsolateral Prefrontal Cortex in Schizophrenia MOLECULAR NEUROBIOLOGY. 2023.02; 60 (2): 1083-1098. ( PubMed, DOI )
Aihara, Y; Shirota, M; Kikuchi, A; Katata, Y; Abe, Y; Niihori, T; Funayama, R; Nakayama, K; Aoki, Y; Kure, S. A novel variant in the transmembrane 4 domain of ANO3 identified in a two-year-old girl with developmental delay and tremor JOURNAL OF HUMAN GENETICS. 2023.01; 68 (1): 51-54. ( PubMed, DOI )
Aihara Yu, Shirota Matsuyuki, Kikuchi Atsuo, Katata Yu, Abe Yu, Niihori Tetsuya, Funayama Ryo, Nakayama Keiko, Aoki Yoko, Kure Shigeo. 発達遅滞と振戦を伴う2歳女児に同定されたANO3遺伝子のtransmembrane 4 domainでの新規バリアント(A novel variant in the transmembrane 4 domain of ANO3 identified in a two-year-old girl with developmental delay and tremor) Journal of Human Genetics. 2023.01; 68 (1): 51-54. ( ichushi )
Nakano, T; Sasahara, Y; Kikuchi, A; Moriya, K; Niizuma, H; Niihori, T; Shirota, M; Funayama, R; Nakayama, K; Aoki, Y; Kure, S. Novel POLE mutations identified in patients with IMAGE-I syndrome cause aberrant subcellular localisation and protein degradation in the nucleus JOURNAL OF MEDICAL GENETICS. 2022.11; 59 (11): 1116-1122. ( PubMed, DOI )
Niihori, T; Tanoshima, R; Sasahara, Y; Sato, A; Irie, M; Saito-Nanjo, Y; Funayama, R; Shirota, M; Abe, T; Okuyama, Y; Ishii, N; Nakayama, K; Kure, S; Imaizumi, M; Aoki, Y. Phenotypic heterogeneity in individuals with MECOM variants in 2 families BLOOD ADVANCES. 2022.09; 6 (18): 5257-5261. ( PubMed, DOI )
Iemura, K; Anzawa, H; Funayama, R; Iwakami, R; Nakayama, K; Kinoshita, K; Tanaka, K. High levels of chromosomal instability facilitate the tumor growth and sphere formation CANCER SCIENCE. 2022.08; 113 (8): 2727-2737. ( PubMed, DOI )
Iemura Kenji, Anzawa Hayato, Funayama Ryo, Iwakami Runa, Nakayama Keiko, Kinoshita Kengo, Tanaka Kozo. 高いレベルの染色体不安定性は腫瘍増殖とスフィア形成を促進する(High levels of chromosomal instability facilitate the tumor growth and sphere formation) Cancer Science. 2022.08; 113 (8): 2727-2737. ( ichushi )
Kanno Miyako, Suzuki Mitsuyoshi, Tanikawa Ken, Numakura Chikahiko, Matsuzawa Shu-ichi, Niihori Tetsuya, Aoki Yoko, Matsubara Yoichi, Makino Satoshi, Tamiya Gen, Nakano Satoshi, Funayama Ryo, Shirota Matsuyuki, Nakayama Keiko, Mitsui Tetsuo, Hayasaka Kiyoshi. calcyclin-binding protein/Siah1-interacting protein(CACYBP/SIP)遺伝子のヘテロ接合病的バリアントは、肝内胆管減少症の優性遺伝(顕性遺伝)家系と連関する(Heterozygous calcyclin-binding protein/Siah1-interacting protein(CACYBP/SIP) gene pathogenic variant linked to a dominant family with paucity of interlobular bile duct) Journal of Human Genetics. 2022.07; 67 (7): 393-397. ( ichushi )
Kanno, M; Suzuki, M; Tanikawa, K; Numakura, C; Matsuzawa, S; Niihori, T; Aoki, Y; Matsubara, Y; Makino, S; Tamiya, G; Nakano, S; Funayama, R; Shirota, M; Nakayama, K; Mitsui, T; Hayasaka, K. Heterozygous calcyclin-binding protein/Siah1-interacting protein (CACYBP/SIP) gene pathogenic variant linked to a dominant family with paucity of interlobular bile duct JOURNAL OF HUMAN GENETICS. 2022.07; 67 (7): 393-397. ( PubMed, DOI )
Mochizuki, Y; Funayama, R; Shirota, M; Kikukawa, Y; Ohira, M; Karasawa, H; Kobayashi, M; Ohnuma, S; Unno, M; Nakayama, K. Alternative microexon splicing by RBFOX2 and PTBP1 is associated with metastasis in colorectal cancer INTERNATIONAL JOURNAL OF CANCER. 2021.11; 149 (10): 1787-1800. ( PubMed, DOI )
Kato, H; Long, NC; Ishii, Y; Matsumoto, M; Rhee, C; Saigusa, D; Funayama, R; Okae, H; Fujiwara, T; Muto, A; Harigae, H; Scadden, DT; Igarashi, K. Inhibition of S-Adenosylmethionine Synthesis Promotes Erythropoiesis Via Epigenetic Modifications BLOOD. 2021.11; 138 1991-+. ( DOI )
Inoue-Shibui, A; Niihori, T; Kobayashi, M; Suzuki, N; Izumi, R; Warita, H; Hara, K; Shirota, M; Funayama, R; Nakayama, K; Nishino, I; Aoki, M; Aoki, Y. A novel deletion in the C-terminal region of HSPB8 in a family with rimmed vacuolar myopathy JOURNAL OF HUMAN GENETICS. 2021.10; 66 (10): 965-972. ( PubMed, DOI )
Inoue-Shibui Aya, Niihori Tetsuya, Kobayashi Michio, Suzuki Naoki, Izumi Rumiko, Warita Hitoshi, Hara Kenju, Shirota Matsuyuki, Funayama Ryo, Nakayama Keiko, Nishino Ichizo, Aoki Masashi, Aoki Yoko. 縁取り空胞性ミオパチーの家系でみられたHSPB8のC-末端領域の新規欠失(A novel deletion in the C-terminal region of HSPB8 in a family with rimmed vacuolar myopathy) Journal of Human Genetics. 2021.10; 66 (10): 965-972. ( ichushi )
Hirashima, T; Karasawa, H; Aizawa, T; Suzuki, T; Yamamura, A; Suzuki, H; Kajiwara, T; Musha, H; Funayama, R; Shirota, M; Ohnuma, S; Nakayama, K; Unno, M. Wnt5a in cancer-associated fibroblasts promotes colorectal cancer progression BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS. 2021.09; 568 37-42. ( PubMed, DOI )
幹細胞から赤血球への通り道メチオニン代謝によるエピゲノム調節をかいした赤血球造血制御(Methionine metabolism controls erythropoiesis by epigenetic regulation) 2021.09; 83回 PSY-4. ( ichushi )
Nakayama, K; Funayama, R; Mochizuki, Y; Kobayashi, M. What we learned from a colorectal cancer patient CANCER SCIENCE. 2021.02; 112 151.
Ochiai K, Yamaoka M, Swaminathan A, Shima H, Hiura H, Matsumoto M, Kurotaki D, Nakabayashi J, Funayama R, Nakayama K, Arima T, Ikawa T, Tamura T, Sciammas R, Bouvet P, Kundu TK, Igarashi K. Chromatin Protein PC4 Orchestrates B Cell Differentiation by Collaborating with IKAROS and IRF4. Cell reports. 2020.12; 33 (12): 108517. ( PubMed, DOI )
がん研究における女性研究者(WSCR) 大腸がん患者から学んだこと 2020.10; 79回 SS2-6. ( ichushi )
Wada Y, Kikuchi A, Arai-Ichinoi N, Sakamoto O, Takezawa Y, Iwasawa S, Niihori T, Nyuzuki H, Nakajima Y, Ogawa E, Ishige M, Hirai H, Sasai H, Fujiki R, Shirota M, Funayama R, Yamamoto M, Ito T, Ohara O, Nakayama K, Aoki Y, Koshiba S, Fukao T, Kure S. Correction: Biallelic GALM pathogenic variants cause a novel type of galactosemia. Genetics in medicine : official journal of the American College of Medical Genetics. 2020.07; 22 (7): 1281. ( PubMed, DOI )
Niitsuma, S; Kudo, H; Kikuchi, A; Hayashi, T; Kumakura, S; Kobayashi, S; Okuyama, Y; Kumagai, N; Niihori, T; Aoki, Y; So, T; Funayama, R; Nakayama, K; Shirota, M; Kondo, S; Kagami, S; Tsukaguchi, H; Iijima, K; Kure, S; Ishii, N. Biallelic variants/mutations of IL1RAP in patients with steroid-sensitive nephrotic syndrome INTERNATIONAL IMMUNOLOGY. 2020.04; 32 (4): 283-292. ( PubMed, DOI )
Nakagawa, T; Hattori, S; Nobuta, R; Kimura, R; Nakagawa, M; Matsumoto, M; Nagasawa, Y; Funayama, R; Miyakawa, T; Inada, T; Osumi, N; Nakayama, KI; Nakayama, K. The Autism-Related Protein SETD5 Controls Neural Cell Proliferation through Epigenetic Regulation of rDNA Expression ISCIENCE. 2020.04; 23 (4): 101030. ( PubMed, DOI )
Niitsuma Sou, Kudo Hiroki, Kikuchi Atsuo, Hayashi Takaya, Kumakura Satoshi, Kobayashi Shuhei, Okuyama Yuko, Kumagai Naonori, Niihori Tetsuya, Aoki Yoko, So Takanori, Funayama Ryo, Nakayama Keiko, Shirota Matsuyuki, Kondo Shuji, Kagami Shoji, Tsukaguchi Hiroyasu, Iijima Kazumoto, Kure Shigeo, Ishii Naoto. ステロイド感受性ネフローゼ症候群の患者におけるIL1RAPの両アレル多型/変異(Biallelic variants/mutations of IL1RAP in patients with steroid-sensitive nephrotic syndrome) International Immunology. 2020.04; 32 (4): 283-292. ( ichushi )
Sato, M; Matsumoto, M; Saiki, Y; Alam, M; Nishizawa, H; Rokugo, M; Brydun, A; Yamada, S; Kaneko, MK; Funayama, R; Ito, M; Kato, Y; Nakayama, K; Unno, M; Igarashi, K. BACH1 Promotes Pancreatic Cancer Metastasis by Repressing Epithelial Genes and Enhancing Epithelial-Mesenchymal Transition CANCER RESEARCH. 2020.03; 80 (6): 1279-1292. ( PubMed, DOI )
Wada, Y; Kikuchi, A; Kaga, A; Shimizu, N; Ito, J; Onuma, R; Fujishima, F; Totsune, E; Sato, R; Niihori, T; Shirota, M; Funayama, R; Sato, K; Nakazawa, T; Nakayama, K; Aoki, Y; Aiba, S; Nakagawa, K; Kure, S. Metabolic and pathologic profiles of human LSS deficiency recapitulated in mice PLOS GENETICS. 2020.02; 16 (2): e1008628. ( PubMed, DOI )
Masamune A, Kotani H, Sörgel FL, Chen JM, Hamada S, Sakaguchi R, Masson E, Nakano E, Kakuta Y, Niihori T, Funayama R, Shirota M, Hirano T, Kawamoto T, Hosokoshi A, Kume K, Unger L, Ewers M, Laumen H, Bugert P, Mori MX, Tsvilovskyy V, Weißgerber P, Kriebs U, Fecher-Trost C, Freichel M, Diakopoulos KN, Berninger A, Lesina M, Ishii K, Itoi T, Ikeura T, Okazaki K, Kaune T, Rosendahl J, Nagasaki M, Uezono Y, Algül H, Nakayama K, Matsubara Y, Aoki Y, Férec C, Mori Y, Witt H, Shimosegawa T. Variants That Affect Function of Calcium Channel TRPV6 Are Associated With Early-Onset Chronic Pancreatitis. Gastroenterology. 2020.01; 158 (6): 1626-1641.e8. ( PubMed, DOI )
Ozeki, M; Aoki, Y; Nozawa, A; Yasue, S; Endo, S; Hori, Y; Matsuoka, K; Niihori, T; Funayama, R; Shirota, M; Nakayama, K; Fukao, T. Detection of NRAS mutation in cell-free DNA biological fluids from patients with kaposiform lymphangiomatosis ORPHANET JOURNAL OF RARE DISEASES. 2019.09; 14 (1): 215. ( PubMed, DOI )
Akiyama, T; Suzuki, N; Ishikawa, M; Fujimori, K; Sone, T; Kawada, J; Funayama, R; Fujishima, F; Mitsuzawa, S; Ikeda, K; Ono, H; Shijo, T; Osana, S; Shirota, M; Nakagawa, T; Kitajima, Y; Nishiyama, A; Izumi, R; Morimoto, S; Okada, Y; Kamei, T; Nishida, M; Nogami, M; Kaneda, S; Ikeuchi, Y; Mitsuhashi, H; Nakayama, K; Fujii, T; Warita, H; Okano, H; Aoki, M. Aberrant axon branching via Fos-B dysregulation in FUS-ALS motor neurons EBIOMEDICINE. 2019.07; 45 362-378. ( PubMed, DOI )
Wada, Y; Kikuchi, A; Arai-Ichinoi, N; Sakamoto, O; Takezawa, Y; Iwasawa, S; Niihori, T; Nyuzuki, H; Nakajima, Y; Ogawa, E; Ishige, M; Hirai, H; Sasai, H; Fujiki, R; Shirota, M; Funayama, R; Yamamoto, M; Ito, T; Ohara, O; Nakayama, K; Aoki, Y; Koshiba, S; Fukao, T; Kure, S. Biallelic GALM pathogenic variants cause a novel type of galactosemia GENETICS IN MEDICINE. 2019.06; 21 (6): 1286-1294. ( PubMed, DOI )
Niihori, T; Nagai, K; Fujita, A; Ohashi, H; Okamoto, N; Okada, S; Harada, A; Kihara, H; Arbogast, T; Funayama, R; Shirota, M; Nakayama, K; Abe, T; Inoue, S; Tsai, IC; Matsumoto, N; Davis, EE; Katsanis, N; Aoki, Y. Germline-Activating RRAS2 Mutations Cause Noonan Syndrome AMERICAN JOURNAL OF HUMAN GENETICS. 2019.06; 104 (6): 1233-1240. ( PubMed, DOI )
Iwasawa, S; Yanagi, K; Kikuchi, A; Kobayashi, Y; Haginoya, K; Matsumoto, H; Kurosawa, K; Ochiai, M; Sakai, Y; Fujita, A; Miyake, N; Niihori, T; Shirota, M; Funayama, R; Nonoyama, S; Ohga, S; Kawame, H; Nakayama, K; Aoki, Y; Matsumoto, N; Kaname, T; Matsubara, Y; Shoji, W; Kure, S. Recurrent de novo MAPK8IP3 variants cause neurological phenotypes ANNALS OF NEUROLOGY. 2019.06; 85 (6): 927-933. ( PubMed, DOI )
Takezawa Yusuke, Fujie Hiromi, Kikuchi Atsuo, Niihori Tetsuya, Funayama Ryo, Shirota Matsuyuki, Nakayama Keiko, Aoki Yoko, Sasaki Masayuki, Kure Shigeo. CAGSSS、Leigh、West症候群の日本人同胞における新規IARS2変異(Novel IARS2 mutations in Japanese siblings with CAGSSS, Leigh, and West syndrome) Brain & Development. 2018.11; 40 (10): 934-938. ( ichushi )
Takezawa, Y; Fujie, H; Kikuchi, A; Niihori, T; Funayama, R; Shirota, M; Nakayama, K; Aoki, Y; Sasaki, M; Kure, S. Novel IARS2 mutations in Japanese siblings with CAGSSS, Leigh, and West syndrome BRAIN & DEVELOPMENT. 2018.11; 40 (10): 934-938. ( PubMed, DOI )
Kayaba, A; Itoh-Nakadai, A; Niibe, K; Shirota, M; Funayama, R; Sugahara-Tobinai, A; Wong, YL; Inui, M; Nakayama, K; Takai, T. Bone marrow PDGFRα+Sca-1+-enriched mesenchymal stem cells support survival of and antibody production by plasma cells in vitro through IL-6 INTERNATIONAL IMMUNOLOGY. 2018.06; 30 (6): 241-253. ( PubMed, DOI )
Kayaba Atsuko, Itoh-Nakadai Ari, Niibe Kunimichi, Shirota Matsuyuki, Funayama Ryo, Sugahara-Tobinai Akiko, Wong Yi Li, Inui Masanori, Nakayama Keiko, Takai Toshiyuki. 骨髄PDGFRα+Sca-1+エンリッチ間葉系幹細胞はIL-6を通してin vitroで形質細胞の生存と抗体産生を支援する(Bone marrow PDGFRα+Sca-1+-enriched mesenchymal stem cells support survival of and antibody production by plasma cells in vitro through IL-6) International Immunology. 2018.06; 30 (6): 241-253. ( ichushi )
Takezawa, Y; Kikuchi, A; Haginoya, K; Niihori, T; Numata-Uematsu, Y; Inui, T; Yamamura-Suzuki, S; Miyabayashi, T; Anzai, M; Suzuki-Muromoto, S; Okubo, Y; Endo, W; Togashi, N; Kobayashi, Y; Onuma, A; Funayama, R; Shirota, M; Nakayama, K; Aoki, Y; Kure, S. Genomic analysis identifies masqueraders of full-term cerebral palsy ANNALS OF CLINICAL AND TRANSLATIONAL NEUROLOGY. 2018.05; 5 (5): 538-551. ( PubMed, DOI )
Nakamura Haruhiko, Uematsu Mitsugu, Numata-Uematsu Yurika, Abe Yu, Endo Wakaba, Kikuchi Atsuo, Takezawa Yusuke, Funayama Ryo, Shirota Matsuyuki, Nakayama Keiko, Niihori Tetsuya, Aoki Yoko, Haginoya Kazuhiro, Kure Shigeo. HECW2変異を有する日本人患者のRett様特徴と皮質視覚障害(Rett-like features and cortical visual impairment in a Japanese patient with HECW2 mutation) Brain & Development. 2018.05; 40 (5): 410-414. ( ichushi )
Ashraf, S; Kudo, H; Rao, J; Kikuchi, A; Widmeier, E; Lawson, JA; Tan, WZ; Hermle, T; Warejko, JK; Shril, S; Airik, M; Jobst-Schwan, T; Lovric, S; Braun, DA; Gee, HY; Schapiro, D; Majmundar, AJ; Sadowski, CE; Pabst, WL; Daga, A; van der Ven, AT; Schmidt, JM; Low, BC; Gupta, AB; Tripathi, BK; Wong, J; Campbell, K; Metcalfe, K; Schanze, D; Niihori, T; Kaito, H; Nozu, K; Tsukaguchi, H; Tanaka, R; Hamahira, K; Kobayashi, Y; Takizawa, T; Funayama, R; Nakayama, K; Aoki, Y; Kumagai, N; Iijima, K; Fehrenbach, H; Kari, JA; El Desoky, S; Jalalah, S; Bogdanovic, R; Stajic, N; Zappel, H; Rakhmetova, A; Wassmer, SR; Jungraithmayr, T; Strehlau, J; Kumar, AS; Bagga, A; Soliman, NA; Mane, SM; Kaufman, L; Lowy, DR; Jairajpuri, MA; Lifton, RP; Pei, Y; Zenker, M; Kure, S; Hildebrandt, F. Mutations in six nephrosis genes delineate a pathogenic pathway amenable to treatment NATURE COMMUNICATIONS. 2018.05; 9 (1): 1960. ( PubMed, DOI )
Nakamura, H; Uematsu, M; Numata-Uematsu, Y; Abe, Y; Endo, W; Kikuchi, A; Takezawa, Y; Funayama, R; Shirota, M; Nakayama, K; Niihori, T; Aoki, Y; Haginoya, K; Kure, S. Rett-like features and cortical visual impairment in a Japanese patient with HECW2 mutation BRAIN & DEVELOPMENT. 2018.05; 40 (5): 410-414. ( PubMed, DOI )
Miura, Y; Morooka, M; Sax, N; Roychoudhuri, R; Itoh-Nakadai, A; Brydun, A; Funayama, R; Nakayama, K; Satomi, S; Matsumoto, M; Igarashi, K; Muto, A. Bach2 Promotes B Cell Receptor-Induced Proliferation of B Lymphocytes and Represses Cyclin-Dependent Kinase Inhibitors JOURNAL OF IMMUNOLOGY. 2018.04; 200 (8): 2882-2893. ( PubMed, DOI )
Nakagawa, T; Hosogane, M; Nakagawa, M; Morohoshi, A; Funayama, R; Nakayama, K. Transforming Growth Factor β-Induced Proliferative Arrest Mediated by TRIM26-Dependent TAF7 Degradation and Its Antagonism by MYC MOLECULAR AND CELLULAR BIOLOGY. 2018.03; 38 (5): ( PubMed, DOI )
Tamate, S; Iwasaki, WM; Krysko, KL; Camposano, BJ; Mori, H; Funayama, R; Nakayama, K; Makino, T; Kawata, M. Inferring evolutionary responses of Anolis carolinensis introduced into the Ogasawara archipelago using whole genome sequence data SCIENTIFIC REPORTS. 2017.12; 7 (1): 18008. ( PubMed, DOI )
Ebina-Shibuya, R; Matsumoto, M; Kuwahara, M; Jang, KJ; Sugai, M; Ito, Y; Funayama, R; Nakayama, K; Sato, Y; Ishii, N; Okamura, Y; Kinoshita, K; Kometani, K; Kurosaki, T; Muto, A; Ichinose, M; Yamashita, M; Igarashi, K. Inflammatory responses induce an identity crisis of alveolar macrophages, leading to pulmonary alveolar proteinosis JOURNAL OF BIOLOGICAL CHEMISTRY. 2017.11; 292 (44): 18098-18112. ( PubMed, DOI )
Sato, Y; Katoh, Y; Matsumoto, M; Sato, M; Ebina, M; Itoh-Nakadai, A; Funayama, R; Nakayama, K; Unno, M; Igarashi, K. Regulatory signatures of liver regeneration distilled by integrative analysis of mRNA, histone methylation, and proteomics JOURNAL OF BIOLOGICAL CHEMISTRY. 2017.05; 292 (19): 8019-8037. ( PubMed, DOI )
Hino-Fukuyo Naomi, Kikuchi Atsuo, Iwasaki Masaki, Sato Yuko, Kubota Yuki, Kobayashi Tomoko, Nakayama Tojo, Haginoya Kazuhiro, Arai-Ichinoi Natsuko, Niihori Tetsuya, Sato Ryo, Suzuki Tasuku, Kudo Hiroki, Funayama Ryo, Nakayama Keiko, Aoki Yoko, Kure Shigeo. de novo COL4A1突然変異を有するてんかん性脳症患者の機能的半球摘出術後の劇的な反応(Dramatic response after functional hemispherectomy in a patient with epileptic encephalopathy carrying a de novo COL4A1 mutation) Brain & Development. 2017.04; 39 (4): 337-340. ( ichushi )
Hino-Fukuyo, N; Kikuchi, A; Iwasaki, M; Sato, Y; Kubota, Y; Kobayashi, T; Nakayama, T; Haginoya, K; Arai-Ichinoi, N; Niihori, T; Sato, R; Suzuki, T; Kudo, H; Funayama, R; Nakayama, K; Aoki, Y; Kure, S. Dramatic response after functional hemispherectomy in a patient with epileptic encephalopathy carrying a de novo COL4A1 mutation BRAIN & DEVELOPMENT. 2017.04; 39 (4): 337-340. ( PubMed, DOI )
Funayama, R; Taniguchi, H; Mizuma, M; Fujishima, F; Kobayashi, M; Ohnuma, S; Unno, M; Nakayama, K. Protein-arginine deiminase 2 suppresses proliferation of colon cancer cells through protein citrullination CANCER SCIENCE. 2017.04; 108 (4): 713-718. ( PubMed, DOI )
Itoh-Nakadai, A; Matsumoto, M; Kato, H; Sasaki, J; Uehara, Y; Sato, Y; Ebina-Shibuya, R; Morooka, M; Funayama, R; Nakayama, K; Ochiai, K; Muto, A; Igarashi, K. A Bach2-Cebp Gene Regulatory Network for the Commitment of Multipotent Hematopoietic Progenitors CELL REPORTS. 2017.03; 18 (10): 2401-2414. ( PubMed, DOI )
Matsumoto, M; Matsuzaki, F; Oshikawa, K; Goshima, N; Mori, M; Kawamura, Y; Ogawa, K; Fukuda, E; Nakatsumi, H; Natsume, T; Fukui, K; Horimoto, K; Nagashima, T; Funayama, R; Nakayama, K; Nakayama, KI. A large-scale targeted proteomics assay resource based on an in vitro human proteome NATURE METHODS. 2017.03; 14 (3): 251-+. ( PubMed, DOI )
Baird, L; Tsujita, T; Kobayashi, EH; Funayama, R; Nagashima, T; Nakayama, K; Yamamoto, M. A Homeostatic Shift Facilitates Endoplasmic Reticulum Proteostasis through Transcriptional Integration of Proteostatic Stress Response Pathways MOLECULAR AND CELLULAR BIOLOGY. 2017.02; 37 (4): E00651-U199. ( DOI )
Baird L, Tsujita T, Kobayashi EH, Funayama R, Nagashima T, Nakayama K, Yamamoto M. A Homeostatic Shift Facilitates Endoplasmic Reticulum Proteostasis through Transcriptional Integration of Proteostatic Stress Response Pathways. Molecular and cellular biology. 2017.02; 37 (4): ( PubMed, DOI )
Hidaka, T; Ogawa, E; Kobayashi, EH; Suzuki, T; Funayama, R; Nagashima, T; Fujimura, T; Aiba, S; Nakayama, K; Okuyama, R; Yamamoto, M. The aryl hydrocarbon receptor AhR links atopic dermatitis and air pollution via induction of the neurotrophic factor artemin NATURE IMMUNOLOGY. 2017.01; 18 (1): 64-73. ( PubMed, DOI )
Ebina-Shibuya R, Watanabe-Matsui M, Matsumoto M, Itoh-Nakadai A, Funayama R, Nakayama K, Muto A, Igarashi K. The double knockout of Bach1 and Bach2 in mice reveals shared compensatory mechanisms in regulating alveolar macrophage function and lung surfactant homeostasis. Journal of biochemistry. 2016.12; 160 (6): 333-344. ( PubMed, DOI )
Kobayashi Minoru, Funayama Ryo, Ohnuma Shinobu, Unno Michiaki, Nakayama Keiko. Wnt-β-カテニンシグナル伝達は大腸癌におけるABCC3(MRP3)トランスポーターの発現を制御する(Wnt-β-catenin signaling regulates ABCC3(MRP3) transporter expression in colorectal cancer) Cancer Science. 2016.12; 107 (12): 1776-1784. ( ichushi )
Kobayashi M, Funayama R, Ohnuma S, Unno M, Nakayama K. Wnt-β-catenin signaling regulates ABCC3 (MRP3) transporter expression in colorectal cancer. Cancer science. 2016.12; 107 (12): 1776-1784. ( PubMed, DOI )
井泉瑠美子, 割田仁, 新堀哲也, 高橋俊明, 竪山真規, 鈴木直輝, 西山亜由美, 城田松之, 舟山亮, 中山啓子, 三橋里美, 西野一三, 青木洋子, 青木正志. 多系統プロテイノパチー連鎖性hnRNPA1変異に起因する孤立性封入体ミオパチー(Isolated inclusion body myopathy caused by a multisystem proteinopathy-linked hnRNPA1 mutation) 臨床神経学. 2016.12; 56 (Suppl.): S280. ( ichushi )
Ebina-Shibuya Risa, Watanabe-Matsui Miki, Matsumoto Mitsuyo, Itoh-Nakadai Ari, Funayama Ryo, Nakayama Keiko, Muto Akihiko, Igarashi Kazuhiko. 肺胞マクロファージの肺恒常性維持におけるBach1とBach2の相補的機能の解明(The double knockout of Bach1 and Bach2 in mice reveals shared compensatory mechanisms in regulating alveolar macrophage function and lung surfactant homeostasis) The Journal of Biochemistry. 2016.12; 160 (6): 333-344. ( ichushi )
井泉瑠美子, 割田仁, 新堀哲也, 高橋俊明, 竪山真規, 鈴木直輝, 西山亜由美, 城田松之, 舟山亮, 中山啓子, 三橋里美, 西野一三, 青木洋子, 青木正志. 多系統プロテイノパチー連鎖性hnRNPA1変異に起因する孤立性封入体ミオパチー(Isolated inclusion body myopathy caused by a multisystem proteinopathy-linked hnRNPA1 mutation) 臨床神経学. 2016.12; 56 (Suppl.): S280. ( ichushi )
大腸癌で発現が抑制されるPeptidylarginine deiminase 2の機能解析 2016.10; 75回 P-1267. ( ichushi )
Takahashi Y, Suyama Y, Matsuki Y, Funayama R, Nakayama K, Kawata M. Lack of genetic variation prevents adaptation at the geographic range margin in a damselfly. Molecular ecology. 2016.09; 25 (18): 4450-4460. ( PubMed, DOI )
MUTATIONS IN MECOM, ENCODING ONCOPROTEIN EVI1, CAUSE AMEGAKARYOCYTIC THROMBOCYTOPENIA WITH RADIOULNAR SYNOSTOSIS, AN INHERITED BONE MARROW FAILURE SYNDROME 2016.09; 44 (9): S44-S45. ( DOI )
MUTATIONS IN MECOM, ENCODING ONCOPROTEIN EVI1, CAUSE AMEGAKARYOCYTIC THROMBOCYTOPENIA WITH RADIOULNAR SYNOSTOSIS, AN INHERITED BONE MARROW FAILURE SYNDROME 2016.09; 44 (9): S44-S45. ( DOI )
Hosogane M, Funayama R, Shirota M, Nakayama K. Lack of Transcription Triggers H3K27me3 Accumulation in the Gene Body. Cell reports. 2016.07; 16 (3): 696-706. ( PubMed, DOI )
Matsumoto M, Kondo K, Shiraki T, Brydun A, Funayama R, Nakayama K, Yaegashi N, Katagiri H, Igarashi K. Genomewide approaches for BACH1 target genes in mouse embryonic fibroblasts showed BACH1-Pparg pathway in adipogenesis. Genes to cells : devoted to molecular & cellular mechanisms. 2016.06; 21 (6): 553-567. ( PubMed, DOI )
Higasa K, Miyake N, Yoshimura J, Okamura K, Niihori T, Saitsu H, Doi K, Shimizu M, Nakabayashi K, Aoki Y, Tsurusaki Y, Morishita S, Kawaguchi T, Migita O, Nakayama K, Nakashima M, Mitsui J, Narahara M, Hayashi K, Funayama R, Yamaguchi D, Ishiura H, Ko WY, Hata K, Nagashima T, Yamada R, Matsubara Y, Umezawa A, Tsuji S, Matsumoto N, Matsuda F. Human genetic variation database, a reference database of genetic variations in the Japanese population. Journal of human genetics. 2016.06; 61 (6): 547-53. ( PubMed, DOI )
Higasa Koichiro, Miyake Noriko, Yoshimura Jun, Okamura Kohji, Niihori Tetsuya, Saitsu Hirotomo, Doi Koichiro, Shimizu Masakazu, Nakabayashi Kazuhiko, Aoki Yoko, Tsurusaki Yoshinori, Morishita Shinichi, Kawaguchi Takahisa, Migita Osuke, Nakayama Keiko, Nakashima Mitsuko, Mitsui Jun, Narahara Maiko, Hayashi Keiko, Funayama Ryo, Yamaguchi Daisuke, Ishiura Hiroyuki, Ko Wen-Ya, Hata Kenichiro, Nagashima Takeshi, Yamada Ryo, Matsubara Yoichi, Umezawa Akihiro, Tsuji Shoji, Matsumoto Naomichi, Matsuda Fumihiko. 日本人集団での遺伝的変異の参照データベースであるヒト遺伝的変異データベース(Human genetic variation database, a reference database of genetic variations in the Japanese population) Journal of Human Genetics. 2016.06; 61 (6): 547-553. ( ichushi )
Kobayashi EH, Suzuki T, Funayama R, Nagashima T, Hayashi M, Sekine H, Tanaka N, Moriguchi T, Motohashi H, Nakayama K, Yamamoto M. Nrf2 suppresses macrophage inflammatory response by blocking proinflammatory cytokine transcription. Nature communications. 2016.05; 7 11624. ( PubMed, DOI )
Ninomiya M, Kondo Y, Kimura O, Funayama R, Nagashima T, Kogure T, Morosawa T, Tanaka Y, Nakayama K, Shimosegawa T. The Expression of miR-125b-5p is Increased in the Serum of Patients with Chronic Hepatitis B Infection and Inhibits the Detection of Hepatitis B Virus Surface Antigen J Viral Hepat. 2016 May;23(5):330-9. doi: 10.1111/jvh.12522.. 2016; 23 (5): 330-9. ( PubMed, DOI )
Niihori T, Ouchi-Uchiyama M, Sasahara Y, Kaneko T, Hashii Y, Irie M, Sato A, Saito-Nanjo Y, Funayama R, Nagashima T, Inoue S, Nakayama K, Ozono K, Kure S, Matsubara Y, Imaizumi M, Aoki Y. Mutations in MECOM, Encoding Oncoprotein EVI1, Cause Radioulnar Synostosis with Amegakaryocytic Thrombocytopenia. American journal of human genetics. 2015.12; 97 (6): 848-54. ( PubMed, DOI )
Wong WF, Kohu K, Nagashima T, Funayama R, Matsumoto M, Movahed E, Tan GM, Yeow TC, Looi CY, Kurokawa M, Osato M, Igarashi K, Nakayama K, Satake M. The artificial loss of Runx1 reduces the expression of quiescence-associated transcription factors in CD4(+) T lymphocytes. Molecular immunology. 2015.12; 68 (2): 223-233. ( PubMed, DOI )
Izumi R, Warita H, Niihori T, Takahashi T, Tateyama M, Suzuki N, Nishiyama A, Shirota M, Funayama R, Nakayama K, Mitsuhashi S, Nishino I, Aoki Y, Aoki M. Isolated inclusion body myopathy caused by a multisystem proteinopathy-linked hnRNPA1 mutation. Neurology. Genetics. 2015.10; 1 (3): e23. ( PubMed, DOI )
Hino-Fukuyo N, Kikuchi A, Arai-Ichinoi N, Niihori T, Sato R, Suzuki T, Kudo H, Sato Y, Nakayama T, Kakisaka Y, Kubota Y, Kobayashi T, Funayama R, Nakayama K, Uematsu M, Aoki Y, Haginoya K, Kure S. Genomic analysis identifies candidate pathogenic variants in 9 of 18 patients with unexplained West syndrome. Human genetics. 2015.06; 134 (6): 649-58. ( PubMed, DOI )
Fujiwara I, Murakami Y, Niihori T, Kanno J, Hakoda A, Sakamoto O, Okamoto N, Funayama R, Nagashima T, Nakayama K, Kinoshita T, Kure S, Matsubara Y, Aoki Y. Mutations in PIGL in a patient with Mabry syndrome. American journal of medical genetics. Part A. 2015.04; 167A (4): 777-85. ( PubMed, DOI )
Izumi R, Niihori T, Suzuki N, Sasahara Y, Rikiishi T, Nishiyama A, Nishiyama S, Endo K, Kato M, Warita H, Konno H, Takahashi T, Tateyama M, Nagashima T, Funayama R, Nakayama K, Kure S, Matsubara Y, Aoki Y, Aoki M. GNE myopathy associated with congenital thrombocytopenia: a report of two siblings. Neuromuscular disorders : NMD. 2014.12; 24 (12): 1068-72. ( PubMed, DOI )
Fujiwara T, Fukuhara N, Funayama R, Nariai N, Kamata M, Nagashima T, Kojima K, Onishi Y, Sasahara Y, Ishizawa K, Nagasaki M, Nakayama K, Harigae H. Identification of acquired mutations by whole-genome sequencing in GATA-2 deficiency evolving into myelodysplasia and acute leukemia. Annals of hematology. 2014.09; 93 (9): 1515-1522. ( PubMed, DOI )
Kondo Y, Ninomiya M, Kimura O, Machida K, Funayama R, Nagashima T, Kobayashi K, Kakazu E, Kato T, Nakayama K, Lai MM, Shimosegawa T. HCV infection enhances Th17 commitment, which could affect the pathogenesis of autoimmune diseases. PloS one. 2014.06; 9 (6): e98521. ( PubMed, DOI )
RNA sequencing-based identification of aberrant imprinting in cloned mice 2014.02; 23 (4): 992-1001. ( DOI )
Ogata T, Niihori T, Tanaka N, Kawai M, Nagashima T, Funayama R, Nakayama K, Nakashima S, Kato F, Fukami M, Aoki Y, Matsubara Y. TBX1 mutation identified by exome sequencing in a Japanese family with 22q11.2 deletion syndrome-like craniofacial features and hypocalcemia. PloS one. 2014; 9 (3): e91598. ( PubMed, DOI )
Hosogane M, Funayama R, Nishida Y, Nagashima T, Nakayama K. Ras-induced changes in H3K27me3 occur after those in transcriptional activity. PLoS genetics. 2013.08; 9 (8): e1003698. ( PubMed, DOI )
Nakanome A, Brydun A, Matsumoto M, Ota K, Funayama R, Nakayama K, Ono M, Shiga K, Kobayashi T, Igarashi K. Bach1 is critical for the transformation of mouse embryonic fibroblasts by Ras(V12) and maintains ERK signaling. Oncogene. 2013.07; 32 (27): 3231-3245. ( PubMed, DOI )
Aoki Y, Niihori T, Banjo T, Okamoto N, Mizuno S, Kurosawa K, Ogata T, Takada F, Yano M, Ando T, Hoshika T, Barnett C, Ohashi H, Kawame H, Hasegawa T, Okutani T, Nagashima T, Hasegawa S, Funayama R, Nagashima T, Nakayama K, Inoue S, Watanabe Y, Ogura T, Matsubara Y. Gain-of-function mutations in RIT1 cause Noonan syndrome, a RAS/MAPK pathway syndrome. American journal of human genetics. 2013.07; 93 (1): 173-80. ( PubMed, DOI )
Ninomiya M, Kondo Y, Funayama R, Nagashima T, Kogure T, Kakazu E, Kimura O, Ueno Y, Nakayama K, Shimosegawa T. Distinct microRNAs expression profile in primary biliary cirrhosis and evaluation of miR 505-3p and miR197-3p as novel biomarkers. PloS one. 2013.06; 8 (6): e66086. ( PubMed, DOI )
Sun SL, Horino S, Itoh-Nakadai A, Kawabe T, Asao A, Takahashi T, So T, Funayama R, Kondo M, Saitsu H, Matsumoto N, Nakayama K, Ishii N. Y chromosome-linked B and NK cell deficiency in mice. Journal of immunology (Baltimore, Md. : 1950). 2013.06; 190 (12): 6209-6220. ( PubMed, DOI )
Izumi R, Niihori T, Aoki Y, Suzuki N, Kato M, Warita H, Takahashi T, Tateyama M, Nagashima T, Funayama R, Abe K, Nakayama K, Aoki M, Matsubara Y. Exome sequencing identifies a novel TTN mutation in a family with hereditary myopathy with early respiratory failure. Journal of human genetics. 2013.05; 58 (5): 259-66. ( PubMed, DOI )
Izumi Rumiko, Niihori Tetsuya, Aoki Yoko, Suzuki Naoki, Kato Masaaki, Warita Hitoshi, Takahashi Toshiaki, Tateyama Maki, Nagashima Takeshi, Funayama Ryo, Abe Koji, Nakayama Keiko, Aoki Masashi, Matsubara Yoichi. エクソーム配列分析によって同定された早期呼吸不全を示す遺伝的ミオパシーの一家族での新規TTN変異(Exome sequencing identifies a novel TTN mutation in a family with hereditary myopathy with early respiratory failure) Journal of Human Genetics. 2013.05; 58 (5): 259-266. ( ichushi )
Nrf2-MafG heterodimers contribute globally to antioxidant and metabolic networks 2012.11; 40 (20): 10228-10239. ( DOI )
Characterization of circulating microRNAs in patients with primary biliary cirrhosis by Illumina deep sequencing 2012.10; 56 1132A.
Circulating microRNAs in some patients with viral hepatitis by deep sequencing showed characteristic expression 2012.10; 56 437A.
Characterization of circulating microRNAs in patients with primary biliary cirrhosis by Illumina deep sequencing 2012.10; 56 1132A.
Circulating microRNAs in some patients with viral hepatitis by deep sequencing showed characteristic expression 2012.10; 56 437A.
Wong WF, Kohu K, Nakamura A, Ebina M, Kikuchi T, Tazawa R, Tanaka K, Kon S, Funaki T, Sugahara-Tobinai A, Looi CY, Endo S, Funayama R, Kurokawa M, Habu S, Ishii N, Fukumoto M, Nakata K, Takai T, Satake M. Runx1 deficiency in CD4+ T cells causes fatal autoimmune inflammatory lung disease due to spontaneous hyperactivation of cells. Journal of immunology (Baltimore, Md. : 1950). 2012.06; 188 (11): 5408-5420. ( PubMed, DOI )
Ninomiya M, Ueno Y, Funayama R, Nagashima T, Nishida Y, Kondo Y, Inoue J, Kakazu E, Kimura O, Nakayama K, Shimosegawa T. Use of illumina deep sequencing technology to differentiate hepatitis C virus variants. Journal of clinical microbiology. 2012.03; 50 (3): 857-866. ( PubMed, DOI )
Okae H, Hiura H, Nishida Y, Funayama R, Tanaka S, Chiba H, Yaegashi N, Nakayama K, Sasaki H, Arima T. Re-investigation and RNA sequencing-based identification of genes with placenta-specific imprinted expression. Human molecular genetics. 2012.02; 21 (3): 548-558. ( PubMed, DOI )
Funayama R, Ishikawa F. Cellular senescence and chromatin structure. Chromosoma. 2007.10; 116 (5): 431-440. ( PubMed, DOI )
Funayama R, Ishikawa F. Cellular senescence and chromatin structure. Chromosoma. 2007.10; 116 (5): 431-440. ( PubMed, DOI )
Funayama R, Saito M, Tanobe H, Ishikawa F. Loss of linker histone H1 in cellular senescence. The Journal of cell biology. 2006.12; 175 (6): 869-880. ( PubMed, DOI )

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Conference Activities & Talks 【 display / non-display 】

Mitsuzawa Shio, Suzuki Naoki, Akiyama Tetsuya, Ishikawa Mitsuru, Kawada Jiro, Funayama Ryo, Mitsuhashi Hiroaki, Nishiyama Ayumi, Ikeda Kensuke, Shijo Tomomi, Nakamura Naoko, Ono Hiroya, Ono Risako, Izumi Rumiko, Ohno Akiyuki, Nakagawa Tadashi, Nakayama Keiko, Warita Hitoshi, Okano Hideyuki, Aoki Masashi. TARDBP変異を有するiPS由来運動神経細胞における軸索伸長障害(Axonal growth impairment in iPS-derived motor neurons with TARDBP mutations). 臨床神経学 2021.09.01
加藤浩貴, Long Nugyen, 石井悠翔, 松本光代, 三枝大輔, 舟山亮, 岡江寛明, 藤原亨, 武藤哲彦, 中山啓子, 有馬隆博, Scadden David, 五十嵐和彦, 張替秀郎. 幹細胞から赤血球への通り道　メチオニン代謝によるエピゲノム調節をかいした赤血球造血制御(Methionine metabolism controls erythropoiesis by epigenetic regulation). 日本血液学会学術集会 2021.09.01
Mitsuzawa Shio, Suzuki Naoki, Akiyama Tetsuya, Ishikawa Mitsuru, Kawada Jiro, Funayama Ryo, Mitsuhashi Hiroaki, Nishiyama Ayumi, Ikeda Kensuke, Shijo Tomomi, Nakamura Naoko, Ono Hiroya, Ono Risako, Izumi Rumiko, Ohno Akiyuki, Nakagawa Tadashi, Nakayama Keiko, Warita Hitoshi, Okano Hideyuki, Aoki Masashi. TARDBP変異を有するiPS由来運動神経細胞における軸索伸長障害(Axonal growth impairment in iPS-derived motor neurons with TARDBP mutations). 臨床神経学 2021.09.01
加藤浩貴, Long Nugyen, 石井悠翔, 松本光代, 三枝大輔, 舟山亮, 岡江寛明, 藤原亨, 武藤哲彦, 中山啓子, 有馬隆博, Scadden David, 五十嵐和彦, 張替秀郎. 幹細胞から赤血球への通り道　メチオニン代謝によるエピゲノム調節をかいした赤血球造血制御(Methionine metabolism controls erythropoiesis by epigenetic regulation). 日本血液学会学術集会 2021.09.01
Mitsuzawa Shio, Suzuki Naoki, Akiyama Tetsuya, Mitsuru Ishikawa, Sone Takefumi, Kawada Jiro, Funayama Ryo, Mitsuhashi Hiroaki, Nishiyama Ayumi, Ikeda Kensuke, Shijo Tomomi, Nakamura Naoko, Ono Hiroya, Ono Risako, Izumi Rumiko, Nakagawa Tadashi, Nakayama Keiko, Warita Hitoshi, Okano Hideyuki, Aoki Masashi. TARDBP遺伝子変異を伴う筋萎縮性側索硬化症における軸索の病理(Axonal pathology in amyotrophic lateral sclerosis with TARDBP mutations). 臨床神経学 2020.11.01
Mitsuzawa Shio, Suzuki Naoki, Akiyama Tetsuya, Mitsuru Ishikawa, Sone Takefumi, Kawada Jiro, Funayama Ryo, Mitsuhashi Hiroaki, Nishiyama Ayumi, Ikeda Kensuke, Shijo Tomomi, Nakamura Naoko, Ono Hiroya, Ono Risako, Izumi Rumiko, Nakagawa Tadashi, Nakayama Keiko, Warita Hitoshi, Okano Hideyuki, Aoki Masashi. TARDBP遺伝子変異を伴う筋萎縮性側索硬化症における軸索の病理(Axonal pathology in amyotrophic lateral sclerosis with TARDBP mutations). 臨床神経学 2020.11.01
中山啓子, 舟山亮, 望月保志, 小林実. がん研究における女性研究者(WSCR)　大腸がん患者から学んだこと. 日本癌学会総会記事 2020.10.01
中山啓子, 舟山亮, 望月保志, 小林実. がん研究における女性研究者(WSCR)　大腸がん患者から学んだこと. 日本癌学会総会記事 2020.10.01
Akiyama Tetsuya, Suzuki Naoki, Ishikawa Mitsuru, Kawada Jiro, Teruo Fujii, Fujishima Fumiyoshi, Funayama Ryo, Nakayama Keiko, Mitsuhashi Hiroaki, Warita Hitoshi, Okano Hideyuki, Aoki Masashi. FUS遺伝子変異によるALS運動ニューロンの軸索病態の解明(Elucidating axonal pathophysiology under fused in sarcoma(FUS)-mutant ALS motor neurons). 臨床神経学 2019.11.01
Akiyama Tetsuya, Suzuki Naoki, Ishikawa Mitsuru, Kawada Jiro, Teruo Fujii, Fujishima Fumiyoshi, Funayama Ryo, Nakayama Keiko, Mitsuhashi Hiroaki, Warita Hitoshi, Okano Hideyuki, Aoki Masashi. FUS遺伝子変異によるALS運動ニューロンの軸索病態の解明(Elucidating axonal pathophysiology under fused in sarcoma(FUS)-mutant ALS motor neurons). 臨床神経学 2019.11.01
Takezawa Yusuke, Fujie Hiromi, Kikuchi Atsuo, Niihori Tetsuya, Funayama Ryo, Shirota Matsuyuki, Nakayama Keiko, Aoki Yoko, Sasaki Masayuki, Kure Shigeo. 新規IARS2変異によるCAGSSS症候群、Leigh症候群とWest症候群を呈した日本人姉妹症例(Novel IARS2 mutations in Japanese siblings with CAGSSS, Leigh, and West syndrome). 脳と発達 2019.05.01
Takezawa Yusuke, Fujie Hiromi, Kikuchi Atsuo, Niihori Tetsuya, Funayama Ryo, Shirota Matsuyuki, Nakayama Keiko, Aoki Yoko, Sasaki Masayuki, Kure Shigeo. 新規IARS2変異によるCAGSSS症候群、Leigh症候群とWest症候群を呈した日本人姉妹症例(Novel IARS2 mutations in Japanese siblings with CAGSSS, Leigh, and West syndrome). 脳と発達 2019.05.01
Takezawa Yusuke, Kikuchi Atsuo, Haginoya Kazuhiro, Niihari Tetsuya, Numata-Uematsu Yurika, Inui Takehiko, Yamamura-Suzuki Saeko, Miyabayashi Takuya, Anzai Mai, Suzuki-Muromoto Sato, Okubo Yukimune, Endo Wakaba, Togashi Noriko, Kobayashi Yasuko, Onuma Akira, Funayama Ryo, Shirota Matsuyuki, Nakayama Keiko, Aoki Yoko, Kure Shigeo. 遺伝学的分析から特定された17患者中9名における病原性変異の候補(Genomic analysis identified candidate pathogenic variants in 9 of 17 patients). 日本小児科学会雑誌 2019.02.01
Niitsuma Sou, Kumagai Naonori, Kudo Hiroki, Kikuchi Atsuo, Kure Shigeo, Hayashi Takaya, So Takanori, Ishii Naoto, Niihori Tetsuya, Aoki Yoko, Funayama Ryo, Nakayama Keiko, Tsukaguchi Hiroyasu, Kondo Shuji, Kagami Shoji, Iijima Kazumoto. 家族性ステロイド感受性ネフローゼ症候群に関する原因候補遺伝子の機能的分析(Functional analysis of the causative candidate gene for familial steroid sensitive nephrotic syndrome). 日本小児腎臓病学会雑誌 2018.05.01
Niitsuma Sou, Kumagai Naonori, Kudo Hiroki, Kikuchi Atsuo, Kure Shigeo, Hayashi Takaya, So Takanori, Ishii Naoto, Niihori Tetsuya, Aoki Yoko, Funayama Ryo, Nakayama Keiko, Tsukaguchi Hiroyasu, Kondo Shuji, Kagami Shoji, Iijima Kazumoto. 家族性ステロイド感受性ネフローゼ症候群に関する原因候補遺伝子の機能的分析(Functional analysis of the causative candidate gene for familial steroid sensitive nephrotic syndrome). 日本小児腎臓病学会雑誌 2018.05.01
井泉瑠美子, 割田仁, 新堀哲也, 高橋俊明, 竪山真規, 鈴木直輝, 西山亜由美, 城田松之, 舟山亮, 中山啓子, 三橋里美, 西野一三, 青木洋子, 青木正志. 多系統プロテイノパチー連鎖性hnRNPA1変異に起因する孤立性封入体ミオパチー(Isolated inclusion body myopathy caused by a multisystem proteinopathy-linked hnRNPA1 mutation). 臨床神経学 2016.12.01
井泉瑠美子, 割田仁, 新堀哲也, 高橋俊明, 竪山真規, 鈴木直輝, 西山亜由美, 城田松之, 舟山亮, 中山啓子, 三橋里美, 西野一三, 青木洋子, 青木正志. 多系統プロテイノパチー連鎖性hnRNPA1変異に起因する孤立性封入体ミオパチー(Isolated inclusion body myopathy caused by a multisystem proteinopathy-linked hnRNPA1 mutation). 臨床神経学 2016.12.01
Imaizumi Masue, Niihori Tetsuya, Uchiyama Meri, Sasahara Yoji, Kaneko Takashi, Hashii Yoshiko, Irie Masahiro, Sato Atsushi, Nanjo Yuka, Funayama Ryo, Nagashima Takeshi, Inoue Shinichi, Nakayama Keiko, Ozono Keiichi, Kure Shigeo, Matsubara Yoichi, Aoki Yoko. 腫瘍タンパク質EVI1をエンコードするMECOM遺伝子変異は無巨核球性血小板減少症を伴う橈尺骨癒合症を引き起こす(Mutations in MECOM, encoding oncoprotein EVI1, cause radioulnar synostosis with amegakaryocytic thrombosytopenia). 日本小児血液・がん学会雑誌 2016.11.01
谷口肇, 舟山亮, 小林実, 高館達之, 阿部友哉, 水間正道, 藤島史喜, 大沼忍, 内藤剛, 海野倫明, 中山啓子. 大腸癌で発現が抑制されるPeptidylarginine deiminase 2の機能解析. 日本癌学会総会記事 2016.10.01
谷口肇, 舟山亮, 小林実, 高館達之, 阿部友哉, 水間正道, 藤島史喜, 大沼忍, 内藤剛, 海野倫明, 中山啓子. 大腸癌で発現が抑制されるPeptidylarginine deiminase 2の機能解析. 日本癌学会総会記事 2016.10.01
Kume Kiyoshi, Masamune Atsushi, Nakano Eriko, Niihori Tetsuya, Aoki Yoko, Funayama Ryo, Nakayama Keiko, Shimosegawa Tooru. 次世代シーケンシングは膵炎候補遺伝子を同定する新しい戦略となる(Next generation sequencing might become the new strategy to identify the candidate genes for pancreatitis). 膵臓 2016.07.01
Kume Kiyoshi, Masamune Atsushi, Nakano Eriko, Niihori Tetsuya, Aoki Yoko, Funayama Ryo, Nakayama Keiko, Shimosegawa Tooru. 次世代シーケンシングは膵炎候補遺伝子を同定する新しい戦略となる(Next generation sequencing might become the new strategy to identify the candidate genes for pancreatitis). 膵臓 2016.07.01
Fujiwara Tohru, Fukuhara Noriko, Funayama Ryo, Nariai Naoki, Kamata Mayumi, Nagashima Takeshi, Kojima Kaname, Onishi Yasushi, Sasahara Yoji, Ishizawa Kenichi, Nagasaki Masao, Nakayama Keiko, Harigae Hideo. MDS/AMLへと進行するMonoMAC症候群における後天性突然変異の全ゲノムシークエンシングによる特定(Whole genome sequencing to identify acquired mutations in MonoMAC syndrome evolving into MDS/AML). 臨床血液 2014.09.01
Fujiwara Tohru, Fukuhara Noriko, Funayama Ryo, Nariai Naoki, Kamata Mayumi, Nagashima Takeshi, Kojima Kaname, Onishi Yasushi, Sasahara Yoji, Ishizawa Kenichi, Nagasaki Masao, Nakayama Keiko, Harigae Hideo. MDS/AMLへと進行するMonoMAC症候群における後天性突然変異の全ゲノムシークエンシングによる特定(Whole genome sequencing to identify acquired mutations in MonoMAC syndrome evolving into MDS/AML). 臨床血液 2014.09.01
舟山亮, 石川冬木. 細胞老化におけるヒストンH1の消失(Cancer and Cellular Senescence　Loss of linker histone H1 in cellular senescence). 日本癌学会総会記事 2007.08.01

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Others 【 display / non-display 】

子宮頸がん細胞の全遺伝子発現解析，2011.10

子宮頸がん細胞の全遺伝子発現解析
次世代シークエンサーを用いた家族性腎炎の遺伝子解析，2011.06

次世代シークエンサーを用いた家族性腎炎の遺伝子解析
次世代シークエンサーを用いた疾患原因遺伝子の解析，2011.06

次世代シークエンサーを用いた疾患原因遺伝子の解析
次世代シークエンサーを駆使した希少遺伝性難病の原因解明と治療法開発の研究，2011.04

次世代シークエンサーを駆使した希少遺伝性難病の原因解明と治療法開発の研究
C型肝炎ウイルスのゲノム解析，2011.03

C型肝炎ウイルスのゲノム解析
次世代シークエンサーを用いたタイヌビエの遺伝子発現解析，2011.01

次世代シークエンサーを用いたタイヌビエの遺伝子発現解析
転写因子結合領域の網羅的解析，2011.01

転写因子結合領域の網羅的解析
アノールトカゲのゲノム解析，2010.11

アノールトカゲのゲノム解析
次世代シークエンサーを用いた転写因子結合領域の解析，2010.11

次世代シークエンサーを用いた転写因子結合領域の解析
次世代シークエンス解析による希少性遺伝子疾患の解析，2010.07

次世代シークエンス解析による希少性遺伝子疾患の解析
インプリント遺伝子の網羅的解析，2010.05

インプリント遺伝子の網羅的解析

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FUNAYAMA RYO

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