PTIP Regulates 53BP1 and SMC1 at the DNA Damage Sites

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PTIP regulates 53BP1 and SMC1 at the DNA damage sites.

Although PTIP is implicated in the DNA damage response, through interactions with 53BP1, the function of PTIP in the DNA damage response remain elusive. Here, we show that RNF8 controls DNA damage-induced nuclear foci formation of PTIP, which in turn regulates 53BP1 localization to the DNA damage sites. In addition, SMC1, a substrate of ATM, could not be phosphorylated at the DNA damage sites i...

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Dynamic assembly and sustained retention of 53BP1 at the sites of DNA damage are controlled by Mdc1/NFBD1

53BP1 is a key component of the genome surveillance network activated by DNA double strand breaks (DSBs). Despite its known accumulation at the DSB sites, the spatiotemporal aspects of 53BP1 interaction with DSBs and the role of other DSB regulators in this process remain unclear. Here, we used real-time microscopy to study the DSB-induced redistribution of 53BP1 in living cells. We show that w...

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53BP1 exchanges slowly at the sites of DNA damage and appears to require RNA for its association with chromatin.

53BP1 protein is re-localized to the sites of DNA damage after ionizing radiation (IR) and is involved in DNA-damage-checkpoint signal transduction. We examined the dynamics of GFP-53BP1 in living cells. The protein starts to accumulate at the sites of DNA damage 2-3 minutes after damage induction. Fluorescence recovery after photobleaching experiments showed that GFP-53BP1 is highly mobile in ...

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BRCA1-associated exclusion of 53BP1 from DNA damage sites underlies temporal control of DNA repair.

Following irradiation, numerous DNA-damage-responsive proteins rapidly redistribute into microscopically visible subnuclear aggregates, termed ionising-radiation-induced foci (IRIF). How the enrichment of proteins on damaged chromatin actually relates to DNA repair remains unclear. Here, we use super-resolution microscopy to examine the spatial distribution of BRCA1 and 53BP1 proteins within si...

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DNA repair pathway choice--a PTIP of the hat to 53BP1.

hot off the press hot off the press D NA double-stranded breaks (DSBs) are highly cytotoxic lesions that can induce genome rearrangements if not accurately repaired. DSBs can be repaired either through homologous recombination (HR) or non-homologous end-joining (NHEJ). HR is the preferred repair pathway during the S and G2 cell cycle phases because a sister chromatid provides a perfect template...

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ژورنال

عنوان ژورنال: Journal of Biological Chemistry

سال: 2009

ISSN: 0021-9258

DOI: 10.1074/jbc.m109.002527