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anti-Mouse (Murine) TP53BP1 Antibodies:
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Fish Polyclonal TP53BP1 Primary Antibody for ChIP, FACS - ABIN151770
Riballo, Kühne, Rief, Doherty, Smith, Recio, Reis, Dahm, Fricke, Krempler, Parker, Jackson, Gennery, Jeggo, Löbrich: A pathway of double-strand break rejoining dependent upon ATM, Artemis, and proteins locating to gamma-H2AX foci. in Molecular cell 2004
Show all 378 Pubmed References
Human Polyclonal TP53BP1 Primary Antibody for ChIP, ICC - ABIN151771
Silverman, Takai, Buonomo, Eisenhaber, de Lange: Human Rif1, ortholog of a yeast telomeric protein, is regulated by ATM and 53BP1 and functions in the S-phase checkpoint. in Genes & development 2004
Show all 84 Pubmed References
Human Polyclonal TP53BP1 Primary Antibody for ICC, IF - ABIN152191
Murga, Jaco, Fan, Soria, Martinez-Pastor, Cuadrado, Yang, Blasco, Skoultchi, Fernandez-Capetillo: Global chromatin compaction limits the strength of the DNA damage response. in The Journal of cell biology 2007
Show all 80 Pubmed References
Human Polyclonal TP53BP1 Primary Antibody for ICC, FACS - ABIN151311
Kang, Lee, Hoan, Sohn, Chang, You: Protein phosphatase 5 regulates the function of 53BP1 after neocarzinostatin-induced DNA damage. in The Journal of biological chemistry 2009
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Polyclonal TP53BP1 Primary Antibody for IF, WB - ABIN540806
Rothkamm, Balroop, Shekhdar, Fernie, Goh: Leukocyte DNA damage after multi-detector row CT: a quantitative biomarker of low-level radiation exposure. in Radiology 2006
Show all 4 Pubmed References
Polyclonal TP53BP1 Primary Antibody for FACS, IF - ABIN540805
Hockemeyer, Daniels, Takai, de Lange: Recent expansion of the telomeric complex in rodents: Two distinct POT1 proteins protect mouse telomeres. in Cell 2006
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Polyclonal TP53BP1 Primary Antibody for IF, WB - ABIN540255
Yanagawa, Funasaka, Tsutsumi, Hu, Watanabe, Raz: Regulation of phosphoglucose isomerase/autocrine motility factor activities by the poly(ADP-ribose) polymerase family-14. in Cancer research 2007
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Human Monoclonal TP53BP1 Primary Antibody for FACS, IHC - ABIN1724820
Nakada, Yonamine, Matsuo: RNF8 regulates assembly of RAD51 at DNA double-strand breaks in the absence of BRCA1 and 53BP1. in Cancer research 2012
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Human Monoclonal TP53BP1 Primary Antibody for FACS, IHC - ABIN1724821
Mok, Henderson: The in vivo dynamic interplay of MDC1 and 53BP1 at DNA damage-induced nuclear foci. in The international journal of biochemistry & cell biology 2012
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Human Polyclonal TP53BP1 Primary Antibody for IF (p), IHC (p) - ABIN682993
Cai, Cao, Zhang, Xue, Zhang, Zhou, Zhou, Sun, Fu: Oncogenic miR-17/20a Forms a Positive Feed-forward Loop with the p53 Kinase DAPK3 to Promote Tumorigenesis. in The Journal of biological chemistry 2015
53BP1 deficiency promotes pathological neovascularization in proliferative retinopathy attributed to an increased homologous recombination rate.
An absence of 53BP1 leads to defective ATR-Chk1-p53 signaling.
we observed the occurrence of synaptonemal complex bridges between bivalents, most likely representing chromosome translocation events that may involve DMC1, RAD51 or 53BP1.
binding of single-stranded DNA by SHLD2 is critical for shieldin function, consistent with a model in which shieldin protects DNA ends to mediate 53BP1-dependent DNA repair
53BP1 pathway therefore comprises distinct double-strand break repair activities within chromatin and single-stranded DNA compartments, which explains both the immunological differences between 53bp1- and Rev7- deficient mice and the context specificity of the pathway
data suggest that CST-Polalpha-mediated fill-in helps to control the repair of double-strand breaks by 53BP1, RIF1 and shieldin
In pachytenes immediate colocalisation of gammaH2AX and 53BP1, which participates in non-homologous end-joining repair pathway, was followed by dissociation from the major focal area of gH2AX by 4 h demonstrating ongoing DSB repair. These results confirm the differential radiosensitivity and repair kinetics of DSBs in male germ cells at different stages.
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.
X-ray crystal structures of TIRR and a designer protein bound to 53BP1 now reveal a mechanism in which an intricate binding area centered on an essential TIRR arginine residue blocks the methylated-chromatin-binding surface of 53BP1. A 53BP1 separation-of-function mutation that abolishes TIRR-mediated regulation in cells renders 53BP1 hyperactive in response to DSBs, highlighting the key inhibitory function of TIRR.
Study shows that ectopic expression of RAD52 and dn53BP1 improves homology-directed repair during CRISPR-Cas9 genome editing.
Results indicate that the acetylation status of P53-binding protein 1 (53BP1) plays a key role in its recruitment to DNA double strand break (DSB) repair by promoting non-homologous end joining (NHEJ).
structure and function of 53BP1 and its contribution to cancer
Study shows that UTX and 53BP1 directly interact and co-occupy promoters in human embryonic stem cells and differentiating neural progenitor cells. Data suggests that the 53BP1-UTX interaction supports the activation of key genes required for human neurodevelopment.
53BP1 deletion increased HR in BRCA1-mutant COV362 cells and decreased PARPi sensitivity in vitro. In 36 women with relapsed ovarian cancer, responses to the PARPi ABT-767 were observed exclusively in cancers with HR deficiency.
HPV16 E6 and E7 oncoproteins interact with 53BP1 inside nuclear foci after DNA damage
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.
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