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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술대회자료
- 저자정보
- 발행연도
- 2010.2
- 수록면
- 79 - 83 (5page)
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초록· 키워드
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The tumor suppressor BRCA1 interacts with many proteins, and undergoes multiple modifications upon DNA damage. ATM, a key molecule of the DNA damage response, phosphorylates S1189 of BRCA1 after γ-irradiation. S1189 of BRCA1 is known as a unique ATM phosphorylation site in BRCA1 exon 11. To study the functions of ATM-dependent phosphorylation of BRCA1-S1189, we generated a mouse model carrying a mutation of S1152A (S1152 in mouse Brca1 corresponds to S1189 in human BRCA1) by gene targeting. Brca1<SUP>S1152A/S1152A</SUP> mice were born at the expected ratio, unlike that seen in previous studies of Brca1-null mice. However, 36% of Brca1<SUP>S1152A/S1152A</SUP> mice exhibited aging-like phenotypes including growth retardation, skin abnormalities, delay of the mammary gland morphogenesis with an increase in apoptosis. Mutant mice were hypersensitive to high dose of γ-irradiation, displaying shortening of the lifespan and reduction in intestinal villi size, associated with increased apoptosis. Aging-unaffected 18 month-old Brca1<SUP>S1152A/S1152A</SUP> female mice also showed mammary gland abnormalities with increased level of cyclin D1, and phospho-ER-α such as Brca1-△11 mutation. Upon low dose γ-irradiation, they suffered a marked increase in tumor formation with an abnormal coat pattern. Furthermore Brca1<SUP>S1152A/S1152A</SUP> embryonic fibroblasts failed to accumulate p53 upon γ-irradiation with delayed phosphorylation of p53-S23. These observations indicate that ATM-mediated phosphorylation of S1189 is required for BRCA1 functions to modulate DNA damage response and suppress tumor formation by regulation of p53 and apoptosis.
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UCI(KEPA) : I410-ECN-0101-2010-510-002595231