Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2 (Q28236543)

Breast cancer 2, early onset

GOA release 2020-03-11

1 reference

GOA release 2020-03-11

author name string

S K Sharan

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M Morimatsu

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U Albrecht

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D S Lim

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E Regel

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C Dinh

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A Sands

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G Eichele

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P Hasty

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A Bradley

Allele losses in the region 17q12-21 in familial breast and ovarian cancer involve the wild-type chromosome

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language of work or name

English

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publication date

24 April 1997

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published in

Nature

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volume

386

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issue

6627

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page(s)

804-10

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cites work

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Brca2 is coordinately regulated with Brca1 during proliferation and differentiation in mammary epithelial cells

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Association of BRCA1 with Rad51 in mitotic and meiotic cells

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Double-strand break repair in the absence of RAD51 in yeast: a possible role for break-induced DNA replication

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Cloning of human, mouse and fission yeast recombination genes homologous to RAD51 and recA

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Rad51 protein involved in repair and recombination in S. cerevisiae is a RecA-like protein

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A mutation in mouse rad51 results in an early embryonic lethal that is suppressed by a mutation in p53

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DNA strand exchange mediated by a RAD51-ssDNA nucleoprotein filament with polarity opposite to that of RecA

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Human Rad51 protein promotes ATP-dependent homologous pairing and strand transfer reactions in vitro

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RecA homologs Dmc1 and Rad51 interact to form multiple nuclear complexes prior to meiotic chromosome synapsis.

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Roles for two RecA homologs in promoting meiotic chromosome synapsis

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Onset of gastrulation, morphogenesis and somitogenesis in mouse embryos displaying compensatory growth

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Homotypic and heterotypic protein associations control Rad51 function in double-strand break repair

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The tumor suppressor gene Brca1 is required for embryonic cellular proliferation in the mouse

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Inactivation of the mouse Brca1 gene leads to failure in the morphogenesis of the egg cylinder in early postimplantation development.

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The cellular responses to DNA damage

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WT-1 is required for early kidney development

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Association of the APC tumor suppressor protein with catenins

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High susceptibility to ultraviolet-induced carcinogenesis in mice lacking XPC

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Increased susceptibility to ultraviolet-B and carcinogens of mice lacking the DNA excision repair gene XPA

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Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours

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Alpha-inhibin is a tumour-suppressor gene with gonadal specificity in mice

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Gene targeting in embryonic stem cells

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10 Yeast promoters and lacZ fusions designed to study expression of cloned genes in yeast

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