WordNet

the 23rd letter of the Roman alphabet (同)w, double-u
(genetics) a segment of DNA that is involved in producing a polypeptide chain; it can include regions preceding and following the coding DNA as well as introns between the exons; it is considered a unit of heredity; "genes were formerly called factors" (同)cistron, factor
informal term for information; "give me the gen on your new line of computers"

PrepTutorEJDIC

Watt / West; Western
wolfram(=tungsten)の原子記号
遺伝子

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1. 原発性免疫不全症に対する遺伝子治療 gene therapy for primary immunodeficiency
2. 肥満の病因 pathogenesis of obesity
3. 大腸癌の分子遺伝学 molecular genetics of colorectal cancer
4. 拡張型心筋症の遺伝学 genetics of dilated cardiomyopathy
5. 急性骨髄性白血病の分子遺伝学 molecular genetics of acute myeloid leukemia

English Journal

Werner syndrome protein positively regulates XRCC4-like factor transcription.

Liu D1, Deng X2, Yuan C1, Chen L1, Cong Y2, Xu X1.Author information 1Beijing Key Laboratory of DNA Damage Response, College of Life Science, Capital Normal University, Beijing 100048, P.R. China.2Institute of Aging Research, Hangzhou Normal University School of Medicine, Hangzhou, Zhejiang 310036, P.R. China.AbstractXRCC4-like factor (XLF) is involved in non-homologous end joining-mediated repair of DNA double-strand breaks (DSBs). Mutations in the WRN gene results in the development of Werner syndrome (WS), a rare autosomal recessive disorder characterized by premature ageing and genome instability. In the present study, it was identified that XLF protein levels were lower in WRN-deficient fibroblasts, compared with normal fibroblasts. Depletion of WRN in HeLa cells led to a decrease of XLF mRNA and its promoter activity. Chromatin immunoprecipitation assays demonstrated that WRN was associated with the XLF promoter. Depletion of XLF in normal human fibroblasts increased the percentage of β-galactosidase (β-gal) staining-positive cells, indicating acceleration in cellular senescence. Taken together, the results suggest that XLF is a transcriptional target of WRN and may be involved in the regulation of cellular senescence.
Molecular medicine reports.Mol Med Rep.2014 May;9(5):1648-52. doi: 10.3892/mmr.2014.2030. Epub 2014 Mar 10.
XRCC4-like factor (XLF) is involved in non-homologous end joining-mediated repair of DNA double-strand breaks (DSBs). Mutations in the WRN gene results in the development of Werner syndrome (WS), a rare autosomal recessive disorder characterized by premature ageing and genome instability. In the pre
PMID 24626809

Polymorphisms in DNA Repair Genes and MDR1 and the Risk for Non-Hodgkin Lymphoma.

Kim HN1, Kim NY2, Yu L3, Kim YK4, Lee IK5, Yang DH6, Lee JJ7, Shin MH8, Park KS9, Choi JS10, Kim HJ11.Author information 1Center for Creative Biomedical Scientists, Chonnam National University, Gwangju 501-746, Korea. kimhnamx@paran.com.2Environmental Health Center for Childhood Leukemia and Cancer, Chonnam National University Hwasun Hospital, Jeollanamdo 519-763, Korea. sylvia-plath@hanmail.net.3Environmental Health Center for Childhood Leukemia and Cancer, Chonnam National University Hwasun Hospital, Jeollanamdo 519-763, Korea. cookie1018@nate.com.4Department of Hematology/Oncology, Chonnam National University Hwasun Hospital 160 Ilsim-ri, Hwasun-eup, Hwasun-gun, Jellanam-do 519-809, Korea. elysium1015@hanmail.net.5Environmental Health Center for Childhood Leukemia and Cancer, Chonnam National University Hwasun Hospital, Jeollanamdo 519-763, Korea. biospace@cnuh.com.6Department of Hematology/Oncology, Chonnam National University Hwasun Hospital 160 Ilsim-ri, Hwasun-eup, Hwasun-gun, Jellanam-do 519-809, Korea. drydh1685@hotmail.com.7Department of Hematology/Oncology, Chonnam National University Hwasun Hospital 160 Ilsim-ri, Hwasun-eup, Hwasun-gun, Jellanam-do 519-809, Korea. drjejung@chonnam.ac.kr.8Center for Creative Biomedical Scientists, Chonnam National University, Gwangju 501-746, Korea. jschoix@chonnam.ac.kr.9Department of Preventive Medicine, College of Medicine, Seonam University, Namwon 590-711, Korea. pys0903@hitel.net.10Department of Preventive Medicine, Chonnam National University Medical School, Gwangju 501-746, Korea. jschoix@chonnam.ac.kr.11Environmental Health Center for Childhood Leukemia and Cancer, Chonnam National University Hwasun Hospital, Jeollanamdo 519-763, Korea. hjoonk@chonnam.ac.kr.AbstractThe damage caused by oxidative stress and exposure to cigarette smoke and alcohol necessitate DNA damage repair and transport by multidrug resistance-1 (MDR1). To explore the association between polymorphisms in these genes and non-Hodgkin lymphoma risk, we analyzed 15 polymorphisms of 12 genes in a population-based study in Korea (694 cases and 1700 controls). Four genotypes of DNA repair pathway genes (XRCC1 399 GA, OGG1 326 GG, BRCA1 871 TT, and WRN 787 TT) were associated with a decreased risk for NHL [odds ratio (OR)XRCC1 GA = 0.80, p = 0.02; OROGG1 GG = 0.70, p = 0.008; ORBRCA1 TT = 0.71, p = 0.048; ORWRN TT = 0.68, p = 0.01]. Conversely, the MGMT 115 CT genotype was associated with an increased risk for NHL (OR = 1.25, p = 0.04). In the MDR1 gene, the 1236 CC genotype was associated with a decreased risk for NHL (OR = 0.74, p = 0.04), and the 3435 CT and TT genotypes were associated with an increased risk (OR3435CT = 1.50, p < 0.0001; OR3435TT = 1.43, p = 0.02). These results suggest that polymorphisms in the DNA repair genes XRCC1, OGG1, BRCA1, WRN1, and MGMT and in the MDR1 gene may affect the risk for NHL in Korean patients.
International journal of molecular sciences.Int J Mol Sci.2014 Apr 21;15(4):6703-16. doi: 10.3390/ijms15046703.
The damage caused by oxidative stress and exposure to cigarette smoke and alcohol necessitate DNA damage repair and transport by multidrug resistance-1 (MDR1). To explore the association between polymorphisms in these genes and non-Hodgkin lymphoma risk, we analyzed 15 polymorphisms of 12 genes in a
PMID 24756092

Downregulation of the Werner syndrome protein induces a metabolic shift that compromises redox homeostasis and limits proliferation of cancer cells.

Li B, Iglesias-Pedraz JM, Chen LY, Yin F, Cadenas E, Reddy S, Comai L.AbstractThe Werner syndrome protein (WRN) is a nuclear protein required for cell growth and proliferation. Loss-of-function mutations in the Werner syndrome gene are associated with the premature onset of age-related diseases. How loss of WRN limits cell proliferation and induces replicative senescence is poorly understood. Here, we show that WRN depletion leads to a striking metabolic shift that coordinately weakens the pathways that generate reducing equivalents for detoxification of reactive oxygen species and increases mitochondrial respiration. In cancer cells, this metabolic shift counteracts the Warburg effect, a defining characteristic of many malignant cells, resulting in altered redox balance and accumulation of oxidative DNA damage that inhibits cell proliferation and induces a senescence-like phenotype. Consistent with these findings, supplementation with antioxidant rescues at least in part cell proliferation and decreases senescence in WRN-knockdown cancer cells. These results demonstrate that WRN plays a critical role in cancer cell proliferation by contributing to the Warburg effect and preventing metabolic stress.
Aging cell.Aging Cell.2014 Apr;13(2):367-78.
The Werner syndrome protein (WRN) is a nuclear protein required for cell growth and proliferation. Loss-of-function mutations in the Werner syndrome gene are associated with the premature onset of age-related diseases. How loss of WRN limits cell proliferation and induces replicative senescence is p
PMID 24757718

Japanese Journal

Role of NBS1 in DNA damage response and its relationship with cancer development

Saito Yuichiro,Fujimoto Hiroko,Kobayashi Junya
Translational Cancer Research 2(3), 178-189, 2013-06
… NBS1, the product of the causative gene in NBS, contains several protein-interaction motifs in the N-terminus and C-terminus. … The N-terminal FHA/BRCT domains interact with MDC1, γ-H2AX, TopBP1, and WRN, and the C-terminal motifs are indispensable for binding MRE11, ataxia telangiectasia mutated (ATM), RAD18, and RNF20. … NBS1 also participates in the regulation of RAD18/Polη-dependent translesion DNA synthesis (TLS) through its interaction with RAD18 and WRN. …
NAID 120005300469

Werner syndrome: A changing pattern of clinical manifestations in Japan (1917~2008)

Goto Makoto,Ishikawa Yuichi,Sugimoto Masanobu,Furuichi Yasuhiro
BioScience Trends 7(1), 13-22, 2013
… Although WS has been characterized by a variety of clinical manifestations mimicking premature aging, the recent longevity and delayed age-associated manifestations observed both from Japanese WS and general population may suggest a common environmental effect on some gene(s) other than WRN and may give us a newer pathophysiological look at WS and also natural aging through the molecular dysfunction of WRN. …
NAID 130004572581

Single Nucleotide Polymorphism WRN Leu1074Phe Is Associated with Prostate Cancer Susceptibility in Chinese Subjects

Wang Lei,Kaku Haruki,Huang Peng,Xu Kexin,Yang Kai,Zhang Jiheng,Li Ming,Xie Liping,Wang Xiaofeng,Sakai Akiko,Watanabe Masami,Nasu Yasutomo,Shimizu Kenji,Kumon Hiromi,Na Yanqun
Acta Medica Okayama 65(5), 315-323, 2011-10
… Deficiencies in the human DNA repair gene WRN are the cause of Werner syndrome, a rare autosomal recessive disorder characterized by premature aging and a predisposition to cancer. … This study evaluated the association of WRN Leu1074Phe (rs1801195), a common missense single nucleotide polymorphism in WRN, with prostate cancer susceptibility in Chinese subjects. …
NAID 80022078062