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SNM1A acts downstream of ATM to promote the G1 cell cycle checkpoint.

Abstract：

:We have shown previously that SNM1A colocalizes with 53BP1 at sites of double-strand breaks (DSBs) induced by IR, and that these proteins interact with or without DNA damage. However, the role of SNM1A in the DNA damage response has not been elucidated. Here, we show that SNM1A is required for an efficient G1 checkpoint arrest after IR exposure. Interestingly, the localization of SNM1A to sites of DSBs does not require either 53BP1 or H2AX, nor does the localization of 53BP1 require SNM1A. However, the localization of SNM1A does require ATM. Furthermore, SNM1A is shown to be a phosphorylation substrate of ATM in vitro, and to interact with ATM in vivo particularly after exposure of cells to IR. In addition, in the absence of SNM1A the activation of the downstream ATM target p53 is reduced. These findings suggest that SNM1A acts with ATM to promote the G1 cell cycle checkpoint.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Akhter S,Legerski RJ

doi

10.1016/j.bbrc.2008.09.130

subject

Has Abstract

pub_date

2008-12-05 00:00:00

pages

236-41

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(08)01886-X

journal_volume

377

pub_type

杂志文章

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