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    KCI등재 SCOPUS SCIE

    Expression of Fanconi Anemia D2 Gene and Its Function in Hela and MCF10A Cells

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    https://www.riss.kr/link?id=A104428226

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    다국어 초록 (Multilingual Abstract) kakao i 다국어 번역

    Fanconi Anemia (FA) is a disease with autosomal recessive inheritance and characterized by
    developmental abnormalities, progressive bone marrow failure and cancer predisposition.
    Especially, the phenotypes of FA cells show the extreme sensitivity towards oxygen and DNA
    crosslinking agents such as diepoxybutane and mitomycin C (MMC). In the current study, I
    made the retroviruses which expressed FANCD2 gene for making the stable cell lines, Hela
    (cervical carcinoma) and MCF10A (breast). I could detect the expression of FANCD2 protein
    in the Hela and MCF10A stable cells after the puromycin selection. When I incubated the
    cells lines with crosslinking agents, MMC, the MCF10A cells which expressed the exogenous
    FANCD2 was resistant to the MMC, compared with the MCF10 parent cells. But the Hela
    cells which expressed the FANCD2 did not show the resistance to the MMC. Together, I
    conclude that FANCD2 protein is an important factor for resistance to the crosslinking agent,
    MMC in the MCF10A breast cell, but not the Hela cervical carcinoma cells.
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    Fanconi Anemia (FA) is a disease with autosomal recessive inheritance and characterized by developmental abnormalities, progressive bone marrow failure and cancer predisposition. Especially, the phenotypes of FA cells show the extreme sensitivity towa...

    Fanconi Anemia (FA) is a disease with autosomal recessive inheritance and characterized by
    developmental abnormalities, progressive bone marrow failure and cancer predisposition.
    Especially, the phenotypes of FA cells show the extreme sensitivity towards oxygen and DNA
    crosslinking agents such as diepoxybutane and mitomycin C (MMC). In the current study, I
    made the retroviruses which expressed FANCD2 gene for making the stable cell lines, Hela
    (cervical carcinoma) and MCF10A (breast). I could detect the expression of FANCD2 protein
    in the Hela and MCF10A stable cells after the puromycin selection. When I incubated the
    cells lines with crosslinking agents, MMC, the MCF10A cells which expressed the exogenous
    FANCD2 was resistant to the MMC, compared with the MCF10 parent cells. But the Hela
    cells which expressed the FANCD2 did not show the resistance to the MMC. Together, I
    conclude that FANCD2 protein is an important factor for resistance to the crosslinking agent,
    MMC in the MCF10A breast cell, but not the Hela cervical carcinoma cells.

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    참고문헌 (Reference)

    1 "Unusual response to bifunctional alkylating agents in a case of Fanconi anaemia" 384-387, 1983

    2 "The emerging genetic and molecular basis of Fanconi anaemia" 2: : 446-457, 2001

    3 "The Fanconi anaemia/BRCA pathway. Nat. Rev" 3 : 23-34, 2003

    4 "Pathways of DNA double-strand break repair and their impact on the prevention and formation of chromosomal aberrations" ge 104 (ge 104): 7-, 2004

    5 "Mutation in Brca2 stimulates eror-prone homology- directed repair of DNA double-strand breaks occurring between repeated sequences" 20: : 4704-20 4716, 2001

    6 "Molecular views of recombination proteinsand their control" 4: : 435-445, 2003

    7 "Interaction of the Fanconi anemia proteins and BRCA1 in a common pathway" 7 : 249-7 262, 2001

    8 "Genetic basis of Fanconi anemia" 10: : 68-76, 2003

    9 "Evidence for at least eight Fanconi anemia genes" 61 : 940-944, 1997

    10 "Direct interactions of the five known Fanconi anaemia proteins suggest a common functional pathway" 10: : 423-429, 2001

    1 "Unusual response to bifunctional alkylating agents in a case of Fanconi anaemia" 384-387, 1983

    2 "The emerging genetic and molecular basis of Fanconi anaemia" 2: : 446-457, 2001

    3 "The Fanconi anaemia/BRCA pathway. Nat. Rev" 3 : 23-34, 2003

    4 "Pathways of DNA double-strand break repair and their impact on the prevention and formation of chromosomal aberrations" ge 104 (ge 104): 7-, 2004

    5 "Mutation in Brca2 stimulates eror-prone homology- directed repair of DNA double-strand breaks occurring between repeated sequences" 20: : 4704-20 4716, 2001

    6 "Molecular views of recombination proteinsand their control" 4: : 435-445, 2003

    7 "Interaction of the Fanconi anemia proteins and BRCA1 in a common pathway" 7 : 249-7 262, 2001

    8 "Genetic basis of Fanconi anemia" 10: : 68-76, 2003

    9 "Evidence for at least eight Fanconi anemia genes" 61 : 940-944, 1997

    10 "Direct interactions of the five known Fanconi anaemia proteins suggest a common functional pathway" 10: : 423-429, 2001

    11 "Direct interaction of the Fanconi anaemia protein FANCG with BRCA2/FANCD1" 12 : 2503-2510, 2003

    12 "Direct interaction of FANCD2 with BRCA2 in DNA damage response pathways" 13 : 1241-1248, 2004

    13 "Deficient DNA end joining activity in extracts from fanconi anemia fibroblasts" 276 : 9543-9549, 2001

    14 "DNA double-strand break repair by homologousrecombination" 383 : 873-892, 2002

    15 "Convergence of the fanconi anemia and ataxia telangiectasia signaling pathways" 109 : 459-472, 2002

    16 "Brca1 controls homology-directed DNA repair." 4 : 511-518, 1999

    17 "Biallelic inactivation of BRCA2 in Fanconi anemia" 297 : 606- 609, 2002

    18 "BRCA2 is required for homology-directed repair of chromosomal breaks" 7: : 263-272, 2001

    19 "BRCA2 function in DNA bindingand recombination from a BRCA2-DSS1-ssDNAstructure" 297 : 1837--1848, 2002

    20 "Asociation of bialelic BRCA2/FANCD1 mutations with spontaneous chromosomal instability and solid tumors of childhood" 103 : 2554-2559, 2004

    21 "A novel ubiquitin ligase is deficient in Fanconi anemia" 35 : 165-170, 2003

    22 "A Rad50-dependent pathway of DNA repair is deficient in Fanconi anemia fibroblasts" 32: : 3248-3257, 2004

    23 "A DNA double strand break repair defect in Fanconi anemia fibroblasts" 277 : 46243-46247, 2002

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    학술지 이력

    학술지 이력
    연월일 이력구분 이력상세 등재구분
    2023 평가 해외DB학술지평가 신청대상 (해외등재 학술지 평가)
    2020-01-01 등재 등재학술지 유지 (해외등재 학술지 평가) KCI등재
    2015-01-01 등재 등재학술지 유지 (등재유지) KCI등재
    2012-05-07 학술지명변경 한글명 : 한국유전학회지 -> Genes & Genomics KCI등재
    2011-01-01 등재 등재학술지 유지 (등재유지) KCI등재
    2009-01-01 등재 등재학술지 유지 (등재유지) KCI등재
    2008-04-14 학술지명변경 외국어명 : Korean Journal of Genetics -> Genes and Genomics KCI등재
    2007-01-01 등재 등재학술지 유지 (등재유지) KCI등재
    2004-01-01 등재 등재학술지 선정 (등재후보2차) KCI등재
    2003-01-01 등재 등재후보 1차 PASS (등재후보1차) KCI등재후보
    2002-01-01 등재 등재후보학술지 유지 (등재후보1차) KCI등재후보
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    학술지 인용정보

    학술지 인용정보
    기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
    2016 0.51 0.12 0.38
    KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
    0.32 0.27 0.258 0.02
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