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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
Results indicate that 53BP1 is a biomarker of response to anti-PARP therapy in the laboratory, and our DNA damage response gene signature may be used to identify patients who are most likely to respond to PARP inhibition.
the two cell lines exhibited relatively low protein expression levels of p53 (show TP53 Proteins), lower levels of p53 (show TP53 Proteins) and TPp53BP1 transcripts were detected in the K562/G cells. Taken together, these findings suggest that the resistance of CML (show BCR Proteins) to the tyrosine kinase (show TXK Proteins) inhibitor, imatinib, may be associated with persistent STAT5 (show STAT5A Proteins)-mediated ROS (show ROS1 Proteins) production, and the abnormality of the p53 (show TP53 Proteins) pathway
These results reveal two distinct fork restart pathways, which are antagonistically controlled by 53BP1 and BRCA1 in a double-strand DNA break repair-independent manner.
Gamma-H2AX (show H2AFX Proteins), phosphorylated KAP-1 (show CDKN3 Proteins) and 53BP1 play an important role in the repair of heterochromatic radon-induced DNA double-strand breaks.
Data show that the expression of tumor protein p53 binding protein 1 (53BP1) varies at different stages of cell cycle, with high-level expression observed in mitosis.
results further highlight the antagonistic relationship between 53BP1 and BRCA1, and place Nup153 and Nup50 in a molecular pathway that regulates 53BP1 function by counteracting BRCA1-mediated events.
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
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