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Human TP53BP1 ELISA Kit for Sandwich ELISA - ABIN825076
Jacot, Thezenas, Senal, Viglianti, Laberenne, Lopez-Crapez, Bibeau, Bleuse, Romieu, Lamy: BRCA1 promoter hypermethylation, 53BP1 protein expression and PARP-1 activity as biomarkers of DNA repair deficit in breast cancer. in BMC cancer 2014
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 ELISA Kits) 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 ELISA Kits) and 53BP1 were recruited to these sites. H2AX (show H2AFX ELISA Kits) was dramatically stabilized in response to DSBs directly caused by gamma-rays, enabling gammaH2AX (show H2AFX ELISA Kits) foci formation and DSB repair, whereas H2AX (show H2AFX ELISA Kits) was barely stabilized in response to secondary DSBs, in which gammaH2AX (show H2AFX ELISA Kits) 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 ELISA Kits) 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 ELISA Kits)-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 ELISA Kits) deficiency, which was not observed for heterochromatin-related proteins HP1beta (show CBX1 ELISA Kits) and BMI1 (show BMI1 ELISA Kits).
Binding of 53BP1 to methyl K810 occurs on E2 promoter binding factor (show E2F1 ELISA Kits) target genes and allows pRb (show PGR ELISA Kits) activity to be effectively integrated with the DNA damage response.
study uncovers novel ATM (show ATM ELISA Kits)-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 (show RIF1 ELISA Kits) and PTIP (show PAXIP1 ELISA Kits).
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
BRCA1 promotes PP4C (show PPP4C ELISA Kits)-dependent 53BP1 dephosphorylation and RIF1 (show INSL6 ELISA Kits) release, directing repair toward homologous recombination.
Co-localization of gammaH2AX (show H2AFX ELISA Kits) and 53BP1 indicates promotion of (in)effective nonhomologous end-joining repair mechanisms at sites of DSB. Moreover, gammaH2AX (show H2AFX ELISA Kits)/53BP1 foci distribution presumably reveals a non-random spatial organization of the genome in MDS (show PAFAH1B1 ELISA Kits) and AML (show RUNX1 ELISA Kits).
Results provide evidence that 53BP1 is involved in breast cancer cells resistance for PARP (show COL11A2 ELISA Kits) inhibitor; its depletion causes resistance in ATM (show ATM ELISA Kits)-deficient tumor cells.
Ubiquitin ligases RNF168 (show RNF168 ELISA Kits), RNF169, and RAD18 (show RAD18 ELISA Kits) specifically bind histone H2A Lys13/15-ubiquitylated nucleosomes. 53BP1 chromatin recruitment may be activated by RNF168 (show RNF168 ELISA Kits) and blocked by RNF169 and RAD18 (show RAD18 ELISA Kits).
53BP1 embodies two distinct activities: it can act as a DNA repair factor on the chromatin that flanks double-strand DNA repairs, and it promotes optimal p53 (show TP53 ELISA Kits) activity.
Ras-induced senescent cells are hindered in their ability to recruit BRCA1 and 53BP1 to DNA damage sites. Whereas BRCA1 is downregulated at transcripts levels, 53BP1 loss is caused by activation of cathepsin L-mediated degradation of 53BP1 protein. we discovered a marked downregulation of vitamin D receptor (VDR) during OIS, and a role for the vitamin D/VDR axis regulating the levels of these DNA repair
53BP1-USP28 (show USP28 ELISA Kits) cooperation is essential for normal p53 (show TP53 ELISA Kits)-promoter element interactions and gene transactivation-associated events, yet dispensable for 53BP1-dependent DNA double-strand repair regulation.
TIP60 (show KAT5 ELISA Kits) complex regulates bivalent chromatin recognition/modification by 53BP1 through direct H4K20me binding and H2AK15 acetylation.
findings identify TIRR as a new factor that influences double-strand break repair using a unique mechanism of masking the histone methyl-lysine binding function of 53BP1
Deficiency of 53BP1 inhibits the radiosensitivity of colorectal cancer.
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