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this study shows that 53BP1 is required for three-dimensional organization of the immunoglobulin heavy chain locus and provides a plausible explanation for the link with 53BP1 enforcement of deletional immunoglobulin class switch recombination
Genomic instability can be rescued by the deletion of Trp53bp1, which encodes the DNA damage response factor 53BP1, and mice expressing RING-less BRCA1 (show BRCA1 Proteins) do not show an increased susceptibility to tumors in the absence of 53BP1.
Unlike directly induced DSBs, secondary DSBs were not efficiently repaired, although Rad51 (show RAD51 Proteins) and 53BP1 were recruited to these sites. H2AX (show H2AFX Proteins) was dramatically stabilized in response to DSBs directly caused by gamma-rays, enabling gammaH2AX (show H2AFX Proteins) foci formation and DSB repair, whereas H2AX (show H2AFX Proteins) was barely stabilized in response to secondary DSBs, in which gammaH2AX (show H2AFX Proteins) foci were small and DSBs were not efficiently repaired
Study showed that mammalian cells use microtubules in the cytoplasm to promote the mobility of sites of DNA damage in the nucleus; molecular details of this process remain to be determined, the main players, including the MOB (show SGMS1 Proteins) domain of 53BP1, the linker of the nucleoskeleton, and cytoskeleton complex, kinesins, and microtubules are now known, allowing further study.
These experiments define a novel requirement for 53BP1 in the fusions of DNA-PKcs (show PRKDC Proteins)-deficient telomeres throughout the cell cycle.
Study concludes that only the 53BP1 status in DNA lesions, induced by UVA or gamma-rays, is affected by A-type lamin (show LMNA Proteins) deficiency, which was not observed for heterochromatin-related proteins HP1beta (show CBX1 Proteins) and BMI1 (show BMI1 Proteins).
Binding of 53BP1 to methyl K810 occurs on E2 promoter binding factor (show E2F1 Proteins) target genes and allows pRb (show PGR Proteins) activity to be effectively integrated with the DNA damage response.
study uncovers novel ATM (show ATM Proteins)-independent functions for 53BP1 in the suppression of oncogenic translocations and in radioprotection
Study concludes that 53BP1 promotes productive class switch recombination and suppresses mutagenic DNA repair through distinct phosphodependent interactions with RIF1 and PTIP (show PAXIP1 Proteins).
Thus, RIF1 and 53BP1 cooperate to block DSB resection to promote NHEJ in G1, which is antagonized by BRCA1 in S phase to ensure a switch of DSB repair mode to homologous recombination
PAXIP1 (show PAXIP1 Proteins) and 53BP1 protein levels followed gene expression results, i.e., are intrinsically correlated, and also reduced in more advanced breast cancer tumors.
Data indicate that p53-binding protein 1 (53BP1) is required to prevent excessive chromosome missegregation and probably genome hyper-instability, and also for optimal growth in cancer cells.
Study demonstrates a consistent resistance profile to PARPi and a unique cross-resistance profile to non-PARPi drugs in different PARPi-resistant U251 glioblastoma cells and reveals 53BP1 loss and SAMHD1 (show SAMHD1 Proteins) overexpression as the primary mechanisms responsible for their resistance to PARPi and Ara (show FOXC1 Proteins)-C, respectively.
number of gammaH2AX (show H2AFX Proteins) foci did not significantly change following cardiac MR (median foci per cell pre-MR = 0.11, post-MR = 0.11, p = .90), but the number of 53BP1 foci significantly increased following MR
premature maturation of post-replicative chromatin restores Histone h4 lysine 20 methylation and rescues 53BP1 accumulation on replicated chromatin.
UVA-induced progerinlamin A complex formation was largely responsible for suppressing 53BP1-mediated NHEJ DSB repair activity. The present study is the first to demonstrate that UVA-induced progerin upregulation adversely affects 53BP1-mediated NHEJ DSB repair in human keratinocytes via progerinlamin A complex formation.
53BP1/RIF1 (show INSL6 Proteins) has a role in limiting BRCA1/CtIP (show RBBP8 Proteins)-mediated end resection to control double strand break repair pathway choice
It observed a distinct accumulation of 53BP1 protein to UV-induced DNA lesions: in R273C mutants, 53BP1 appeared transiently at DNA lesions, during 10-30 min after irradiation; the mutation R282W was responsible for accumulation of 53BP1 immediately after UVA-damage; and in L194F mutants, the first appearance of 53BP1 protein at the lesions occurred during 60-70 min.
A reciprocal regulation between 53BP1 and APC (show APC Proteins)/C that is required for response to mitotic stress.
The authors identified 53BP1 and USP28 (show USP28 Proteins) as essential components acting upstream of p53 (show TP53 Proteins), evoking p21 (show CDKN1A Proteins)-dependent cell cycle arrest in response not only to centrosome loss, but also to other distinct defects causing prolonged mitosis.
May have a role in checkpoint signaling during mitosis. Enhances TP53-mediated transcriptional activation. Binds to sites of DNA damage. Plays a role in the response to DNA damage (By similarity).
tumor protein p53 binding protein 1
, tumor protein p53 binding protein, 1
, tumor suppressor p53-binding protein 1-like
, tumor protein p53 binding protein 1 (predicted), 5 prime
, tumor protein p53 binding protein 1 (predicted), 3 prime
, murine p53-binding protein
, p53-binding protein 1
, transformation related protein 53 binding-protein 1
, tumor suppressor p53-binding protein 1
, tumor protein 53-binding protein, 1
, tumor protein p53-binding protein, 1
, transformation related protein 53 binding protein 1