研究者基本情報

• 博士（薬学）, 北海道大学, 1997年09月

• https://researchmap.jp/read0002243

• https://jglobal.jst.go.jp/detail?JGLOBAL_ID=200901043922720613

• 200901043922720613

• DNA損傷
• 胃がん
• ヘリコバクター・ピロリ
• Molecular biology

• ライフサイエンス, 腫瘍生物学
• ライフサイエンス, 分子生物学
• ライフサイエンス, 細菌学

• 修士課程, 生命科学院
• 博士課程, 生命科学院

研究活動情報

• Cryptic redundancy between PAR1b and PAR1a, two members of the PAR1 kinase family, in the survival of PAR1b-knockout mice.
  Naoko Murata-Kamiya; Adriana Alejandra Del Valle Lazarte; Ippei Kikuchi; Masanori Hatakeyama
  Scientific reports, 16, 1, 2026年03月12日, ［国際誌］
  英語, 研究論文（学術雑誌）, The PAR1/MARK family of serine/threonine kinases (PAR1a-d) redundantly controls the cell polarity. PAR1b also mediates the phosphorylation of BRCA1, which promotes its nuclear translocation. In the nucleus, BRCA1 protects stalled replication forks and repairs double-strand DNA breaks via homologous recombination. Consequently, conventional BRCA1-knockout mice are embryonically lethal. In contrast, conventional PAR1b-knockout mice reach adulthood, suggesting a compensatory mechanism for PAR1b in regulating BRCA1 in these knockout mice. Here we find that, while PAR1b knockout in embryonic fibroblasts (MEFs) derived from wild-type mice elicits growth inhibition/death, MEFs lacking PAR1b can be readily established from conventional PAR1b-knockout mice. In PAR1b-null MEFs from PAR1b-knockout mice, PAR1a, but not PAR1c and PAR1d, becomes essential for survival and expansion. Thus, PAR1a-mediated cryptic redundancy, most likely due to BRCA1 phosphorylation by PAR1a, is unleashed only when functional PAR1b is absent from the earliest stages of embryogenesis, which induces significant epigenetic changes in gene regulation, including 53BP1 silencing. Reduced 53BP1 diminishes the role of BRCA1 in genome protection, thereby contributing to the survival of conventional PAR1b-knockout mice, in which PAR1a only partially compensates for the function of PAR1b in BRCA1 regulation. This study presents the first evidence of epigenetic modification-driven cryptic redundancy during early embryogenesis.
• Helicobacter pylori-induced DNA double-strand break in the development of gastric cancer.
  Naoko Murata-Kamiya; Masanori Hatakeyama
  Cancer science, 2022年03月31日, ［査読有り］, ［筆頭著者］, ［国際誌］
  英語, 研究論文（学術雑誌）, Infection with cagA-positive Helicobacter pylori strains plays an etiological role in the development of gastric cancer. The CagA protein is injected into gastric epithelial cells through a bacterial Type IV secretion system. Inside the host cells, CagA promiscuously associates with multiple host cell proteins including the prooncogenic phosphatase SHP2 that is required for full activation of the RAS-ERK pathway. CagA-SHP2 interaction aberrantly activates SHP2 and thereby deregulates RAS-ERK signaling. Cancer is regarded as a disease of the genome, indicating that H. pylori-mediated gastric carcinogenesis is also associated with genomic alterations in the host cell. Indeed, accumulating evidence has indicated that H. pylori infection provokes DNA double-strand breaks (DSBs) by both CagA-dependent and -independent mechanisms. DSBs are repaired by either error-free homologous recombination (HR) or error-prone non-homologous end joining (NHEJ) or microhomology-mediated end joining (MMEJ). Infection with cagA-positive H. pylori inhibits RAD51 expression while dampening cytoplasmic-to-nuclear translocalization of BRCA1, causing replication fork instability and HR defects (known as "BRCAness"), which collectively provoke genomic hypermutation via non-HR-mediated DSB repair. H. pylori also subverts multiple DNA damage responses including DNA repair systems. Infection with H. pylori additionally inhibits the function of the p53 tumor suppressor, thereby dampening DNA damage-induced apoptosis while promoting proliferation of CagA-delivered cells. Thus, H. pylori cagA-positive strains promote abnormal expansion of cells with BRCAness, which dramatically increases the chance of generating driver gene mutations in the host cells. Once such driver mutations are acquired, H. pylori CagA is no longer required for subsequent gastric carcinogenesis (Hit-and-Run carcinogenesis).
• Mouse Gastric Epithelial Cells Resist CagA Delivery by the Helicobacter pylori Type IV Secretion System.
  Rejina Shrestha; Naoko Murata-Kamiya; Satoshi Imai; Masami Yamamoto; Tetsuya Tsukamoto; Sachiyo Nomura; Masanori Hatakeyama
  International journal of molecular sciences, 23, 5, 2022年02月24日, ［査読有り］, ［国際誌］
  英語, 研究論文（学術雑誌）, The initial step in bacterial infection is adherence of the bacterium to the target cell surface. Helicobacter pylori exploits the interaction of bacterial adhesin protein HopQ with human epithelial CEACAMs (CEACAM1, 5, and 6) to stably adhere to gastric epithelial cells, which is necessary for delivery of the H. pylori CagA oncoprotein into the epithelial cells via a type IV secretion system. In contrast to human CEACAMs, however, HopQ does not interact with Ceacam1 (mouse CEACAM1) in vitro or in CHO cells ectopically expressing Ceacam1. Since the mouse genome lacks Ceacam5 and Ceacam6, no significant HopQ-Ceacam interaction may occur in mouse gastric epithelial cells. Here, we found that the mouse stomach has a much lower expression level of Ceacam1 than the expression level of CEACAM1 in the human stomach. Consistently, mouse gastric epithelial cells resist CagA delivery by cagA-positive H. pylori, and the delivery is restored by ectopic expression of human CEACAM1 or CEACAM5 in mouse gastric epithelial cells. Thus, despite the fact that mice are routinely used for H. pylori infection studies, a low expression level of Ceacam1 in the mouse stomach together with the loss or greatly reduced interaction of HopQ with Ceacams make the mouse an inappropriate model for studying the role of H. pylori-delivered CagA in gastric pathogenesis, including the development of gastric cancer.
• The H. pylori CagA Oncoprotein Induces DNA Double Strand Breaks through Fanconi Anemia Pathway Downregulation and Replication Fork Collapse.
  Arun Mouli Kolinjivadi; Haresh Sankar; Ramveer Choudhary; Lavina Sierra Tay; Tuan Zea Tan; Naoko Murata-Kamiya; Dominic Chih-Cheng Voon; Dennis Kappei; Masanori Hatakeyama; Vaidehi Krishnan; Yoshiaki Ito
  International journal of molecular sciences, 23, 3, 2022年01月31日, ［査読有り］, ［国際誌］
  英語, 研究論文（学術雑誌）, The proteins from the Fanconi Anemia (FA) pathway of DNA repair maintain DNA replication fork integrity by preventing the unscheduled degradation of nascent DNA at regions of stalled replication forks. Here, we ask if the bacterial pathogen H. pylori exploits the fork stabilisation machinery to generate double stand breaks (DSBs) and genomic instability. Specifically, we study if the H. pylori virulence factor CagA generates host genomic DSBs through replication fork destabilisation and collapse. An inducible gastric cancer model was used to examine global CagA-dependent transcriptomic and proteomic alterations, using RNA sequencing and SILAC-based mass spectrometry, respectively. The transcriptional alterations were confirmed in gastric cancer cell lines infected with H. pylori. Functional analysis was performed using chromatin fractionation, pulsed-field gel electrophoresis (PFGE), and single molecule DNA replication/repair fiber assays. We found a core set of 31 DNA repair factors including the FA genes FANCI, FANCD2, BRCA1, and BRCA2 that were downregulated following CagA expression. H. pylori infection of gastric cancer cell lines showed downregulation of the aforementioned FA genes in a CagA-dependent manner. Consistent with FA pathway downregulation, chromatin purification studies revealed impaired levels of Rad51 but higher recruitment of the nuclease MRE11 on the chromatin of CagA-expressing cells, suggesting impaired fork protection. In line with the above data, fibre assays revealed higher fork degradation, lower fork speed, daughter strands gap accumulation, and impaired re-start of replication forks in the presence of CagA, indicating compromised genome stability. By downregulating the expression of key DNA repair genes such as FANCI, FANCD2, BRCA1, and BRCA2, H. pylori CagA compromises host replication fork stability and induces DNA DSBs through fork collapse. These data unveil an intriguing example of a bacterial virulence factor that induces genomic instability by interfering with the host replication fork stabilisation machinery.
• Helicobacter pylori CagA elicits BRCAness to induce genome instability that may underlie bacterial gastric carcinogenesis.
  Satoshi Imai; Takuya Ooki; Naoko Murata-Kamiya; Daisuke Komura; Kamrunnesa Tahmina; Weida Wu; Atsushi Takahashi-Kanemitsu; Christopher Takaya Knight; Akiko Kunita; Nobumi Suzuki; Adriana A Del Valle; Mayo Tsuboi; Masahiro Hata; Yoku Hayakawa; Naomi Ohnishi; Koji Ueda; Masashi Fukayama; Tetsuo Ushiku; Shumpei Ishikawa; Masanori Hatakeyama
  Cell host & microbe, 29, 6, 941, 958, 2021年06月09日, ［査読有り］, ［責任著者］, ［国際誌］
  英語, 研究論文（学術雑誌）, Infection with CagA-producing Helicobacter pylori plays a causative role in the development of gastric cancer. Upon delivery into gastric epithelial cells, CagA deregulates prooncogenic phosphatase SHP2 while inhibiting polarity-regulating kinase PAR1b through complex formation. Here, we show that CagA/PAR1b interaction subverts nuclear translocation of BRCA1 by inhibiting PAR1b-mediated BRCA1 phosphorylation. It hereby induces BRCAness that promotes DNA double-strand breaks (DSBs) while disabling error-free homologous recombination-mediated DNA repair. The CagA/PAR1b interaction also stimulates Hippo signaling that circumvents apoptosis of DNA-damaged cells, giving cells time to repair DSBs through error-prone mechanisms. The DSB-activated p53-p21Cip1 axis inhibits proliferation of CagA-delivered cells, but the inhibition can be overcome by p53 inactivation. Indeed, sequential pulses of CagA in TP53-mutant cells drove somatic mutation with BRCAness-associated genetic signatures. Expansion of CagA-delivered cells with BRCAness-mediated genome instability, from which CagA-independent cancer-predisposing cells arise, provides a plausible "hit-and-run mechanism" of H. pylori CagA for gastric carcinogenesis.
• Helicobacter pylori CagA oncoprotein interacts with SHIP2 to increase its delivery into gastric epithelial cells.
  Yumiko Fujii; Naoko Murata-Kamiya; Masanori Hatakeyama
  Cancer science, 111, 5, 1596, 1606, 2020年05月, ［査読有り］, ［国際誌］
  英語, 研究論文（学術雑誌）, Chronic infection with Helicobacter pylori cagA-positive strains is causally associated with the development of gastric diseases, most notably gastric cancer. The cagA-encoded CagA protein, which is injected into gastric epithelial cells by bacterial type IV secretion, undergoes tyrosine phosphorylation at the Glu-Pro-Ile-Tyr-Ala (EPIYA) segments (EPIYA-A, EPIYA-B, EPIYA-C, and EPIYA-D), which are present in various numbers and combinations in its C-terminal polymorphic region, thereby enabling CagA to promiscuously interact with SH2 domain-containing host cell proteins, including the prooncogenic SH2 domain-containing protein tyrosine phosphatase 2 (SHP2). Perturbation of host protein functions by aberrant complex formation with CagA has been considered to contribute to the development of gastric cancer. Here we show that SHIP2, an SH2 domain-containing phosphatidylinositol 5'-phosphatase, is a hitherto undiscovered CagA-binding host protein. Similar to SHP2, SHIP2 binds to the Western CagA-specific EPIYA-C segment or East Asian CagA-specific EPIYA-D segment through the SH2 domain in a tyrosine phosphorylation-dependent manner. In contrast to the case of SHP2, however, SHIP2 binds more strongly to EPIYA-C than to EPIYA-D. Interaction with CagA tethers SHIP2 to the plasma membrane, where it mediates production of phosphatidylinositol 3,4-diphosphate [PI(3,4)P2 ]. The CagA-SHIP2 interaction also potentiates the morphogenetic activity of CagA, which is caused by CagA-deregulated SHP2. This study indicates that initially delivered CagA interacts with SHIP2 and thereby strengthens H. pylori-host cell attachment by altering membrane phosphatidylinositol compositions, which potentiates subsequent delivery of CagA that binds to and thereby deregulates the prooncogenic phosphatase SHP2.
• High-molecular-weight hyaluronan is a Hippo pathway ligand directing cell density-dependent growth inhibition via PAR1b
  Ooki T; Murata-Kamiya N; Takahashi-Kanemitsu A; Wu W; Hatakeyama M
  Developmental Cell, 49, 4, 1, 15, Elsevier BV, 2019年05月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Enhanced expression of the M2 isoform of pyruvate kinase is involved in gastric cancer development by regulating cancer-specific metabolism
  Takeharu Shiroki; Misa Yokoyama; Nobuhiro Tanuma; Ryuhei Maejima; Keiichi Tamai; Kazunori Yamaguchi; Tomoyuki Oikawa; Tetsuya Noguchi; Koh Miura; Tsuneaki Fujiya; Hiroshi Shima; Ikuro Sato; Naoko Murata-Kamiya; Masanori Hatakeyama; Katsunori Iijima; Tooru Shimosegawa; Kennichi Satoh
  Cancer Science, 108, 5, 931, 940, Blackwell Publishing Ltd, 2017年05月01日, ［査読有り］
  英語, 研究論文（学術雑誌）
• CEACAM6 is upregulated by Helicobacter pylori CagA and is a biomarker for early gastric cancer
  Rony K. Roy; Michal M. Hoppe; Supriya Srivastava; Animesh Samanta; Neel Sharma; Kar Tong Tan; Henry Yang; Dominic C. Voon; Brendan Pang; Ming Teh; Naoko Murata-Kamiya; Masanori Hatakeyama; Young-Tae Chang; Wei Peng Yong; Yoshiaki Ito; Khek Yu Ho; Patrick Tan; Richie Soong; Phillip H. Koeffler; Khay Guan Yeoh; Anand D. Jeyasekharan
  ONCOTARGET, 7, 34, 55290, 55301, 2016年08月, ［査読有り］
  英語, 研究論文（学術雑誌）
• C-terminal Src kinase-mediated EPIYA phosphorylation of Pragmin creates a feed-forward C-terminal Src kinase activation loop that promotes cell motility
  Yoshie Senda; Naoko Murata-Kamiya; Masanori Hatakeyama
  CANCER SCIENCE, 107, 7, 972, 980, 2016年07月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Host SHP1 phosphatase antagonizes Helicobacter pylori CagA and can be downregulated by Epstein-Barr virus
  Priya Saju; Naoko Murata-Kamiya; Takeru Hayashi; Yoshie Senda; Lisa Nagase; Saori Noda; Keisuke Matsusaka; Sayaka Funata; Akiko Kunita; Masayuki Urabe; Yasuyuki Seto; Masashi Fukayama; Atsushi Kaneda; Masanori Hatakeyama
  NATURE MICROBIOLOGY, 1, 4, 16026, 2016年04月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Exosomes as nanocarriers for systemic delivery of the Helicobacter pylori virulence factor CagA
  Asako Shimoda; Koji Ueda; Shin Nishiumi; Naoko Murata-Kamiya; Sada-atsu Mukai; Shin-ichi Sawada; Takeshi Azuma; Masanori Hatakeyama; Kazunari Akiyoshi
  SCIENTIFIC REPORTS, 6, 18346, 2016年01月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Helicobacter pylori induces IL-1β protein through the inflammasome activation in differentiated macrophagic cells.
  Kameoka S; Kameyama T; Hayashi T; Sato S; Ohnishi N; Hayashi T; Murata-Kamiya N; Higashi H; Hatakeyama M; Takaoka A
  Biomedical Research (Tokyo, Japan), 37, 1, 21, 27, 2016年, ［査読有り］
  英語, 研究論文（学術雑誌）
• Mutual reinforcement of inflammation and carcinogenesis by the Helicobacter pylori CagA oncoprotein
  Nobumi Suzuki; Naoko Murata-Kamiya; Kohei Yanagiya; Wataru Suda; Masahira Hattori; Hiroaki Kanda; Atsuhiro Bingo; Yumiko Fujii; Shin Maeda; Kazuhiko Koike; Masanori Hatakeyama
  SCIENTIFIC REPORTS, 5, 10024, 2015年05月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Natural variant of the Helicobacter pylori CagA oncoprotein that lost the ability to interact with PAR1
  Kana Hashi; Naoko Murata-Kamiya; Christine Varon; Francis Megraud; Maria Gloria Dominguez-Bello; Masanori Hatakeyama
  CANCER SCIENCE, 105, 3, 245, 251, 2014年03月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Helicobacter pylori stimulates epithelial cell migration via CagA-mediated perturbation of host cell signaling
  Kenji Kikuchi; Naoko Murata-Kamiya; Satoshi Kondo; Masanori Hatakeyama
  MICROBES AND INFECTION, 14, 5, 470, 476, 2012年05月, ［査読有り］
  英語, 研究論文（学術雑誌）
• ¹H, ¹³C and ¹⁵N NMR assignments of the Escherichia coli Orf135 protein.
  Kawasaki K; Yoneyama M; Murata-Kamiya N; Harashima H; Kojima C; Ito Y; Kamiya H; Mishima M
  Biomolecular NMR Assignments, 6, 1, 1, 4, 2012年04月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Insights into substrate recognition by the Escherichia coli Orf135 protein through its solution structure
  Kumiko Kawasaki; Teppei Kanaba; Momoko Yoneyama; Naoko Murata-Kamiya; Chojiro Kojima; Yutaka Ito; Hiroyuki Kamiya; Masaki Mishima
  BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 420, 2, 263, 268, 2012年04月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Helicobacter pylori CagA triggers expression of the bactericidal lectin REG3γ via gastric STAT3 activation.
  Lee KS; Kalantzis A; Jackson CB; O'Connor L; Murata-Kamiya N; Hatakeyama M; Judd LM; Giraud AS; Menheniott TR
  PLoS One, 7, 2, e30786, 2012年02月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Polarity-regulating Kinase Partitioning-defective 1b (PAR1b) Phosphorylates Guanine Nucleotide Exchange Factor H1 (GEF-H1) to Regulate RhoA-dependent Actin Cytoskeletal Reorganization
  Yukie Yamahashi; Yasuhiro Saito; Naoko Murata-Kamiya; Masanori Hatakeyama
  JOURNAL OF BIOLOGICAL CHEMISTRY, 286, 52, 44576, 44584, 2011年12月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Pathophysiological functions of the CagA oncoprotein during infection by Helicobacter pylori
  Naoko Murata-Kamiya
  MICROBES AND INFECTION, 13, 10, 799, 807, 2011年09月, ［査読有り］
  英語
• Potentiation of Helicobacter pylori CagA Protein Virulence through Homodimerization
  Lisa Nagase; Naoko Murata-Kamiya; Masanori Hatakeyama
  JOURNAL OF BIOLOGICAL CHEMISTRY, 286, 38, 33622, 33631, 2011年09月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Mammalian Pragmin regulates Src family kinases via the Glu-Pro-Ile-Tyr-Ala (EPIYA) motif that is exploited by bacterial effectors
  Fatemeh Safari; Naoko Murata-Kamiya; Yasuhiro Saito; Masanori Hatakeyama
  PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 108, 36, 14938, 14943, 2011年09月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Conversion of Helicobacter pylori CagA from senescence inducer to oncogenic driver through polarity-dependent regulation of p21
  Yasuhiro Saito; Naoko Murata-Kamiya; Toshiya Hirayama; Yusuke Ohba; Masanori Hatakeyama
  JOURNAL OF EXPERIMENTAL MEDICINE, 207, 10, 2157, 2174, 2010年09月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Helicobacter pylori Exploits Host Membrane Phosphatidylserine for Delivery, Localization, and Pathophysiological Action of the CagA Oncoprotein
  Naoko Murata-Kamiya; Kenji Kikuchi; Takeru Hayashi; Hideaki Higashi; Masanori Hatakeyama
  CELL HOST & MICROBE, 7, 5, 399, 411, 2010年05月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Helicobacter pylori CagA Causes Mitotic Impairment and Induces Chromosomal Instability
  Mayumi Umeda; Naoko Murata-Kamiya; Yasuhiro Saito; Yusuke Ohba; Masayuki Takahashi; Masanori Hatakeyama
  JOURNAL OF BIOLOGICAL CHEMISTRY, 284, 33, 22166, 22172, 2009年08月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Role of Partitioning-defective 1/Microtubule Affinity-regulating Kinases in the Morphogenetic Activity of Helicobacter pylori CagA
  Huaisheng Lu; Naoko Murata-Kamiya; Yasuhiro Saito; Masanori Hatakeyama
  JOURNAL OF BIOLOGICAL CHEMISTRY, 284, 34, 23024, 23036, 2009年08月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Structural and functional diversity in the PAR1b/MARK2-binding region of Helicobacter pylori CagA
  Huai-Sheng Lu; Yasuhiro Saito; Mayumi Umeda; Naoko Murata-Kamiya; Hong-Mei Zhang; Hideaki Higashi; Masanori Hatakeyama
  CANCER SCIENCE, 99, 10, 2004, 2011, 2008年10月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Deregulation of beta-catenin signal by Helicobacter pylori CagA requires the CagA-multimerization sequence
  Yo Kurashima; Naoko Murata-Kamiya; Kenji Kikuchi; Hideaki Higashi; Takeshi Azuma; Satoshi Kondo; Masanori Hatakeyama
  INTERNATIONAL JOURNAL OF CANCER, 122, 4, 823, 831, 2008年02月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Helicobacter pylori CagA interacts with E-cadherin and deregulates the beta-catenin signal that promotes intestinal transdifferentiation in gastric epithelial cells
  N. Murata-Kamiya; Y. Kurashima; Y. Teishikata; Y. Yamahashi; Y. Saito; H. Higashi; H. Aburatani; T. Akiyama; R. M. Peek; T. Azuma; M. Hatakeyama
  ONCOGENE, 26, 32, 4617, 4626, 2007年07月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Helicobacter pylori CagA targets PAR1/MARK kinase to disrupt epithelial cell polarity
  Iraj Saadat; Hideaki Higashi; Chikashi Obuse; Mayumi Umeda; Naoko Murata-Kamiya; Yasuhiro Saito; Huaisheng Lu; Naomi Ohnishi; Takeshi Azuma; Atsushi Suzuki; Shigeo Ohno; Masanori Hatakeyama
  NATURE, 447, 7142, 330, U8, 2007年05月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Vascular endothelium-selective gene induction by tie2 promoter/enhancer in the brain and retina of a transgenic rat
  S Ohtsuki; N Kamiya; S Hori; T Terasaki
  PHARMACEUTICAL RESEARCH, 22, 6, 852, 857, 2005年06月, ［査読有り］
  英語, 研究論文（学術雑誌）
• EPIYA motif is a membrane-targeting signal of Helicobacter pylori virulence factor CagA in mammalian cells
  H Higashi; K Yokoyama; Y Fujii; S Ren; H Yuasa; Saadat, I; NM Kamiya; T Azuma; M Hatakeyama
  JOURNAL OF BIOLOGICAL CHEMISTRY, 280, 24, 23130, 23137, 2005年06月, ［査読有り］
  英語, 研究論文（学術雑誌）
• mRNA expression of the ATP-binding cassette transporter subfamily A (ABCA) in rat and human brain capillary endothelial cells
  S Ohtsuki; Y Watanabe; S Hori; H Suzuki; J Bhongsatiern; M Fujiyoshi; M Kamoi; N Kamiya; H Takanaga; T Terasaki
  BIOLOGICAL & PHARMACEUTICAL BULLETIN, 27, 9, 1437, 1440, 2004年09月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Suppression of spontaneous and hydrogen peroxide-induced mutations by a MutT-type nucleotide pool sanitization enzyme, the Escherichia coli Orf135 protein
  H Kamiya; E Iida; N Murata-Kamiya; Y Yamamoto; T Miki; H Harashima
  GENES TO CELLS, 8, 12, 941, 950, 2003年12月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Induction of T→G and T→A transversions by 5-formyluracil in mammalian cells.
  Kamiya H; Murata-Kamiya N; Karino N; Ueno Y; Matsuda A; Kasai H
  Mutation Research, 513, 1-2, 213, 222, 2002年01月, ［査読有り］
• Hydrolysis of oxidized nucleotides by the Escherichia coli Orf135 protein
  H Kamiya; N Murata-Kamiya; E Iida; H Harashima
  BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 288, 3, 499, 502, 2001年11月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Methylglyoxal, an endogenous, aldehyde, crosslinks DNA polymerase and the substrate DNA
  N Murata-Kamiya; H Kamiya
  NUCLEIC ACIDS RESEARCH, 29, 16, 3433, 3438, 2001年08月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Methylglyoxal induces G:C to C:G and G:C to T:A transversions in the supF gene on a shuttle vector plasmid replicated in mammalian cells.
  Murata-Kamiya N; Kamiya H; Kaji H; Kasai H
  Mutation Research, 468, 2, 173, 182, 2000年07月, ［査読有り］
• Formation of 5-formyl-2 '-deoxycytidine from 5-methyl-2 '-deoxycytidine in duplex DNA by Fenton-type reactions and gamma-irradiation
  N Murata-Kamiya; H Kamiya; N Karino; Y Ueno; H Kaji; A Matsuda; H Kasai
  NUCLEIC ACIDS RESEARCH, 27, 22, 4385, 4390, 1999年11月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Deficient nucleotide excision repair increases base-pair substitutions but decreases TGGC frameshifts induced by methylglyoxal in Escherichia coli.
  Murata-Kamiya N; Kaji H; Kasai H
  Mutation Research, 442, 1, 19, 28, 1999年06月, ［査読有り］
• Nucleotide excision repair proteins may be involved in the fixation of glyoxal-induced mutagenesis in Escherichia coli
  N Murata-Kamiya; H Kamiya; H Kaji; H Kasai
  BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 248, 2, 412, 417, 1998年07月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Induction of chromosomal gene mutations in Escherichia coli by direct incorporation of oxidatively damaged nucleotides - New evaluation method for mutagenesis by damaged DNA precursors in vivo
  M Inoue; H Kamiya; K Fujikawa; Y Ootsuyama; N Murata-Kamiya; T Osaki; K Yasumoto; H Kasai
  JOURNAL OF BIOLOGICAL CHEMISTRY, 273, 18, 11069, 11074, 1998年05月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Determination of carcinogenic potential of mineral fibers by 8-hydroxydeoxyguanosine as a marker of oxidative DNA damage in mammalian cells
  N MurataKamiya; T Tsutsui; A Fujino; H Kasai; H Kaji
  INTERNATIONAL ARCHIVES OF OCCUPATIONAL AND ENVIRONMENTAL HEALTH, 70, 5, 321, 326, 1997年11月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Mutational specificity of glyoxal, a product of DNA oxidation, in the lacI gene of wild-type Escherichia coli W3110
  N MurataKamiya; H Kamiya; H Kaji; H Kasai
  MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS, 377, 2, 255, 262, 1997年07月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Comparison of oxidation products from DNA components by gamma-irradiation and Fenton-type reactions
  N MurataKamiya; H Kamiya; M Muraoka; H Kaji; H Kasai
  JOURNAL OF RADIATION RESEARCH, 38, 2, 121, 131, 1997年06月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Types of mutations induced by glyoxal, a major oxidative DNA-damage product, in Salmonella typhimurium
  N MurataKamiya; H Kaji; H Kasai
  MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS, 377, 1, 13, 16, 1997年06月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Glyoxal, a major product of DNA oxidation, induces mutations at G:C sites on a shuttle vector plasmid replicated in mammalian cells
  N MurataKamiya; H Kamiya; H Kaji; H Kasai
  NUCLEIC ACIDS RESEARCH, 25, 10, 1897, 1902, 1997年05月, ［査読有り］
  英語, 研究論文（学術雑誌）
• FORMATION OF A MUTAGEN, GLYOXAL, FROM DNA TREATED WITH OXYGEN-FREE RADICALS
  N MURATAKAMIYA; H KAMIYA; N IWAMOTO; H KASAI
  CARCINOGENESIS, 16, 9, 2251, 2253, 1995年09月, ［査読有り］
  英語
• 8-HYDROXYADENINE (7,8-DIHYDRO-8-OXOADENINE) INDUCES MISINCORPORATION IN IN-VITRO DNA-SYNTHESIS AND MUTATIONS IN NIH 3T3 CELLS
  H KAMIYA; H MIURA; N MURATAKAMIYA; H ISHIKAWA; T SAKAGUCHI; H INOUE; T SASAKI; C MASUTANI; F HANAOKA; S NISHIMURA; E OHTSUKA
  NUCLEIC ACIDS RESEARCH, 23, 15, 2893, 2899, 1995年08月, ［査読有り］
  英語, 研究論文（学術雑誌）
• 8-HYDROXYGUANINE (7,8-DIHYDRO-8-OXOGUANINE) IN HOT-SPOTS OF THE C-HA-RAS GENE - EFFECTS OF SEQUENCE CONTEXTS ON MUTATION SPECTRA
  H KAMIYA; N MURATAKAMIYA; S KOIZUME; H INOUE; S NISHIMURA; E OHTSUKA
  CARCINOGENESIS, 16, 4, 883, 889, 1995年04月, ［査読有り］
  英語, 研究論文（学術雑誌）
• COMPARISON OF INCORPORATION AND EXTENSION OF NUCLEOTIDES IN-VITRO OPPOSITE 8-HYDROXYGUANINE (7,8-DIHYDRO-8-OXOGUANINE) IN HOT-SPOTS OF THE C-HA-RAS GENE
  H KAMIYA; N MURATAKAMIYA; M FUJIMURO; K KIDO; H INOUE; S NISHIMURA; C MASUTANI; F HANAOKA; E OHTSUKA
  JAPANESE JOURNAL OF CANCER RESEARCH, 86, 3, 270, 276, 1995年03月, ［査読有り］
  英語, 研究論文（学術雑誌）
• Nucleotide incorporation opposite degenerate bases by taq dna polymerase§
  Hiroyuki Kamiya; Hiroyuki Kamiya; Hiroyuki Kamiya; Naoko Murata-Kamiya; Naoko Murata-Kamiya; Naoko Murata-Kamiya; Eiko Ohtsuka; Hiroyuki Kamiya; Eiko Ohtsuka; Eiko Ohtsuka; Naoko Murata-Kamiya; Eiko Ohtsuka; Hiroyuki Kamiya; Naoko Murata-Kamiya; Eiko Ohtsuka; Paul Kong; Thoo Lin; Daniel M. Brown
  Nucleosides and Nucleotides, 13, 6-7, 1483, 1492, 1994年
  英語, 研究論文（学術雑誌）
• CYCLOBUTANE THYMINE DIMERS IN A RAS PROTOONCOGENE HOT-SPOT ACTIVATE THE GENE BY POINT MUTATION
  H KAMIYA; N MURATA; T MURATA; S IWAI; A MATSUKAGE; C MASUTANI; F HANAOKA; E OHTSUKA
  NUCLEIC ACIDS RESEARCH, 21, 10, 2355, 2361, 1993年05月, ［査読有り］
  英語, 研究論文（学術雑誌）
• INVITRO REPLICATION STUDY OF MODIFIED BASES IN RAS SEQUENCES
  H KAMIYA; T SAKAGUCHI; N MURATA; M FUJIMURO; H MIURA; H ISHIKAWA; M SHIMIZU; H INOUE; S NISHIMURA; A MATSUKAGE; C MASUTANI; F HANAOKA; E OHTSUKA
  CHEMICAL & PHARMACEUTICAL BULLETIN, 40, 10, 2792, 2795, 1992年10月, ［査読有り］
  英語, 研究論文（学術雑誌）
• AN ABASIC SITE ANALOG ACTIVATES A C-HA-RAS GENE BY A POINT MUTATION AT MODIFIED AND ADJACENT POSITIONS
  H KAMIYA; M SUZUKI; Y KOMATSU; H MIURA; K KIKUCHI; T SAKAGUCHI; N MURATA; C MASUTANI; F HANAOKA; E OHTSUKA
  NUCLEIC ACIDS RESEARCH, 20, 17, 4409, 4415, 1992年09月, ［査読有り］
  英語, 研究論文（学術雑誌）

• ピロリ菌CagAによる変異誘発性のDNA二本鎖切断修復の活性化
  紙谷尚子, 26, 2, 155, 159, 2025年01月
• Helicobacter pylori 傷害機序の新知見
  紙谷尚子, 26, 2, 24, 28, 2022年09月
• ピロリ菌CagAはゲノム不安定性を介して胃がん発症を促す
  紙谷尚子, 23, 2, 86, 91, 2022年01月
• 【胃癌-診断・治療の最新知見-】 胃癌発症における細菌とウイルスの連携
  紙谷 尚子; 畠山 昌則, 日本臨床, 76, 3, 362, 366, 2018年03月
  (株)日本臨床社, 日本語
• EBウイルスとヘリコバクター・ピロリ
  紙谷 尚子; 畠山 昌則, 臨床免疫・アレルギー科, 68, 3, 314, 320, 2017年09月
  (有)科学評論社, 日本語
• SHP1 is the Helicobacter pylori CagA-Specific phosphatase that is dampened by Epstein-Barr virus
  P. Saju; N. Murata-Kamiya; M. Hatakeyama, HELICOBACTER, 21, 71, 72, 2016年09月
  英語, 研究発表ペーパー・要旨（国際会議）
• 【慢性炎症とがん】 慢性炎症による発がん誘導 胃がん発症におけるヘリコバクター・ピロリの役割
  紙谷 尚子; 畠山 昌則, 別冊Bio Clinica: 慢性炎症と疾患, 5, 1, 19, 24, 2016年02月
  (株)北隆館, 日本語
• ピロリ菌の病原因子CagAはNLRP3inflammasomeを活性化し,IL-1βを産生する
  亀岡章一郎; 亀山武志; 佐藤精一; 林剛瑠; 大西なおみ; 紙谷尚子; 東秀明; 畠山昌則; 高岡晃教, 日本生化学会大会(Web), 88th, 2015年
• 【細菌感染が癌を引き起こす 胃癌とピロリ菌の関係から見えてきた発癌の新たなパラダイム】 胃癌発症におけるピロリ菌癌タンパク質CagAの役割
  紙谷 尚子; 畠山 昌則, 細胞工学, 29, 6, 554, 560, 2010年05月
  (株)学研メディカル秀潤社, 日本語
• 【シグナル伝達研究 2008'09 疾患発症の分子メカニズムと実現化する分子標的薬開発】 シグナル伝達研究 現象から因子へ ヘリコバクター・ピロリCagAによる細胞がん化メカニズム
  齊藤 康弘; 紙谷 尚子; 畠山 昌則, 実験医学, 26, 15, 2445, 2452, 2008年09月
  (株)羊土社, 日本語
• Helicobacter pylori CagA cytotoxin stimulates inappropriate STAT3 activation in gastric epithelial cells by a phosphorylation dependent mechanism
  Trevelyan Menheniott; Cameron Jackson; Naoko Murata-Kamiya; Masanori Hatakeyama; Andrew S. Giraud, GASTROENTEROLOGY, 134, 4, A387, A387, 2008年04月
  英語, 研究発表ペーパー・要旨（国際会議）
• 胃がん発症におけるHelicobacter pylori CagAの意義
  齊藤 康弘; 紙谷 尚子; 畠山 昌則, 血液・腫瘍科, 56, 2, 219, 225, 2008年02月
  (有)科学評論社, 日本語
• Activation of beta-catenin signal by Helicobacter pylori CagA
  M. Hatakeyama; N. Murata-Kamiya; Y. Kurashima; Y. Yamahashi; Y. Saito, HELICOBACTER, 11, 4, 330, 330, 2006年08月
  英語, 研究発表ペーパー・要旨（国際会議）
• 【ヘリコバクター・ピロリ感染症の研究と臨床の進歩】 ヘリコバクター・ピロリの分子細菌学
  紙谷 尚子; 畠山 昌則, 化学療法の領域, 21, 7, 935, 941, 2005年06月
  (株)医薬ジャーナル社, 日本語
• Tie2/GFP導入トランスジェニックラットにおける血液脳及び網膜関門選択的な遺伝子発現
  大槻 純男; 大倉 直人; 紙谷 尚子; 堀 里子; 寺崎 哲也, 日本薬学会年会要旨集, 125年会, 2, 113, 113, 2005年03月
  (公社)日本薬学会, 日本語
• ABCA subfamilyのラット及びヒト脳関門における発現解析
  紙谷 尚子; 渡辺 有紀; 大槻 純男; 鴨井 真由; 高長 ひとみ, 薬剤学: 生命とくすり, 62, Suppl., 247, 247, 2002年03月
  (公社)日本薬剤学会, 日本語
• 経口糖負荷試験にみられるoxyhyperglycemia(OHG)-胃切除者60名における検討
  加地 浩; 森田 恵美子; 池田 正人; 日野 義之; 筒井 隆夫; 紙谷 尚子, 糖尿病, 44, 10, 862, 862, 2001年10月
  (一社)日本糖尿病学会, 日本語
• 条件的不死化脳毛細血管内皮細胞株を用いたABCA transporterのmRNA解析
  渡邉 有紀; 高長 ひとみ; 紙谷 尚子; 堀 里子; 大槻 純男; 寺崎 哲也, 神経化学, 40, 2-3, 455, 455, 2001年09月
  日本神経化学会, 日本語
• Mutations induced by glyoxal and methylglyoxal in mammalian cells.
  Nucleic Acids Symp. Ser., 44, 3, 4, 2000年
• Mutagenicity of 5-formyluracil in mammalian cells.
  Nucleic Acids Symp. Ser., 44, 81, 82, 2000年
• ピリミジン２量体の変異作用.
  紙谷 浩之; 紙谷 尚子; 田; 大塚 栄子, 環境変異原研究, 20, 3, 213, 220, 1998年10月
  Ultraviolet(UV)light damages biologically important molecules including DNA, and the damage to DNA appears to be involved in the process of skin cancer through the mutagenic activation of proto-oncogenes and/or the inactivation of tumor suppressor genes. In this paper, we review the mutational properties of UV-induced DNA lesions, and in particular, those of photoproducts at thymine-thymine sites., 日本環境変異原学会, 日本語
• Mutagenesis by pyrimidine dimers.
  Environ. Mutagen Res., 20, 3, 213, 220, 1998年
• 酸素ラジカル及び一酸化窒素（NO）によって生ずるDNA損傷がNIH3T3細胞中で誘発する点変異．
  紙谷 浩之; 紙谷 尚子; 三浦 裕幸, 環境変異原研究, 16, 3, 385, 390, 1995年03月
  8-Hydroxyguanine (8-OHG),10,及び1の誘発する変異スペクトルを明らかにした。哺乳動物細胞中で活性酸素及びNOによって生ずる変異のうちの少なくとも一部は,これらのDNA損傷によって引き起こされると思われる, 日本環境変異原学会, 日本語
• 酸素ラジカル及び一酸化窒素(NO)によって生ずるDNA損傷がNIH3T3細胞中で誘発する点変異
  紙谷 浩之; 紙谷(村田) 尚子; 三浦 裕幸; 小井詰 史朗; 清水 美穂; 井上 英夫; 西村 〓; 大塚 栄子, 環境変異原研究, 16, 3, 385, 390, 1995年
  日本語
• Mutations induced by DNA lesions in hot spots of the c-Ha-ras gene.
  Nucleic Acids Symp. Ser., 27, 179, 180, 1992年

• 生物学Ⅰ, 2024年, 学士課程, 全学教育

• ピロリ菌感染胃癌の背景にあるBRCA1核移行制御機構の破綻
  科学研究費助成事業
  2022年04月01日 - 2025年03月31日
  紙谷 尚子
  日本学術振興会, 基盤研究(C), 北海道大学, 22K07068
• ピロリ菌CagAによる胃上皮細胞のDNA損傷誘発機構と発がんにおける役割の解明
  科学研究費助成事業
  2019年04月01日 - 2022年03月31日
  紙谷 尚子
  CagA蛋白質を産生するピロリ菌感染は胃癌発症の最大の危険因子である。CagAはヒト胃上皮細胞細胞内でPAR1bキナーゼに結合しキナーゼ活性を抑制する。本研究では、CagAが宿主ゲノムに重篤なDNA損傷であるDNA二本鎖切断(DSB)を誘発 することを見出した。その分子機序として、CagAはPAR1bを抑制することによってBRCA1のリン酸化を阻害した。BRCA1リン酸化は核移行に必須であり、CagAがBRCA1の核移行を阻害 する結果、DNA複製フォークが不安定化されDSBが誘導された。従って、CagAはPAR1b抑制を介して一過性BRCAnessを誘導することが示された。
  日本学術振興会, 基盤研究(C), 東京大学, 19K07535