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mediates changes in chromatin architecture that affect break order.
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 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 and 53BP1 were recruited to these sites. H2AX was dramatically stabilized in response to DSBs directly caused by gamma-rays, enabling gammaH2AX foci formation and DSB repair, whereas H2AX was barely stabilized in response to secondary DSBs, in which gammaH2AX 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 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-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 deficiency, which was not observed for heterochromatin-related proteins HP1beta and BMI1.
Binding of 53BP1 to methyl K810 occurs on E2 promoter binding factor target genes and allows pRb activity to be effectively integrated with the DNA damage response.
study uncovers novel ATM-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.
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
loss of 53BP1 alters the translocatome by increasing rearrangements to intergenic regions.
A mutant lacking the oligomerization domain (53BP1(oligo)) was only modestly impaired in promoting NHEJ of dysfunctional telomeres and showed no defect with regard to the repression of CtIP.
data establish Rif1 as an important contributor to the control of double-strand break repair by 53BP1
deletion of 53BP1 in TRF1-deficient cells impairs the C-NHEJ repair pathway, decreasing the occurrence of chromosome-type end to end telomere fusions while inducing a persistent DNA damage signal that activates the ATR-dependent DDR and HR repair pathways
XLF repair protein and 53BP1 DNA damage response factor have overlapping functions in end joining and lymphocyte development
find that combined XLF/53BP1 deficiency in mice severely impairs C-NHEJ, V(D)J recombination, and lymphocyte development while also leading to general genomic instability and growth defects
Data suggest a link between recruitment of 53BP1, resolution of DNA damage, and increased species lifespan.
A novel pathway regulates the levels of 53BP1 & the repair of DNA DSBs by the NHEJ pathway. The central player is cathepsin L which is impacted upon by the loss of A-type lamins and can be regulated by treatment with vitamin D.
Roles of Dot1L and 53Bp1 in gene expression and the control of DNA double-strand repair pathways in the context of chromatin.
Inhibition of 53BP1 is a robust method to increase efficiency of HDR-based precise genome editing.
This study elucidates the mechanism by which TIRR recognizes 53BP1 Tudor and functions as a cellular inhibitor of the histone methyl-lysine readers.
Data indicate the molecular mechanism underlying Tudor interacting repair regulator (TIRR)-mediated suppression of tumor protein p53 binding protein 1 (53BP1)-dependent DNA damage repair.
GFI1 facilitates efficient DNA repair by regulating PRMT1 dependent methylation of MRE11 and 53BP1.
The results may suggest that TP53BP1 and MFN1 frameshift mutations and their intratumoral heterogeneity (ITH) could contribute to cancer development by inhibiting the TSG activities.
results highlight the interplay of RNF169 with 53BP1 in fine-tuning choice of DSB repair pathways.
Despite the requirement of all three nucleoporins for accurate NHEJ, only Nup153 is needed for proper nuclear import of 53BP1 and SENP1-dependent sumoylation of 53BP1. Data support the role of Nup153 as an important regulator of 53BP1 activity and efficient NHEJ.
Results indicate that integrity of the nuclear localization signal is important for 53BP1 nuclear localization.
As shown in xenograft model of glioblastoma phosphorylation of 53BP1 by GSK3beta was indispensable for DNA double-strand break repair.
results suggest that there is a direct interaction between 53BP1 and MCMs, which is essential for 53BP1 chromatin fraction and foci formation in hepatoma HepG2 cells.
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, lower levels of p53 and TPp53BP1 transcripts were detected in the K562/G cells. Taken together, these findings suggest that the resistance of CML to the tyrosine kinase inhibitor, imatinib, may be associated with persistent STAT5-mediated ROS production, and the abnormality of the p53 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, phosphorylated KAP-1 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 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 overexpression as the primary mechanisms responsible for their resistance to PARPi and Ara-C, respectively.
number of gammaH2AX 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