Phospho-TP53BP1 (Ser25) Antibody

1. Inhibition of 53BP1 has been demonstrated as a robust method to enhance the efficiency of HDR-based precise genome editing. PMID: 29176614
2. This study elucidates the mechanism by which TIRR recognizes 53BP1 Tudor and functions as a cellular inhibitor of histone methyl-lysine readers. PMID: 29844495
3. Data suggests the molecular mechanism underlying Tudor interacting repair regulator (TIRR)-mediated suppression of tumor protein p53 binding protein 1 (53BP1)-dependent DNA damage repair. PMID: 30002377
4. GFI1 facilitates efficient DNA repair by regulating PRMT1-dependent methylation of MRE11 and 53BP1. PMID: 29651020
5. The findings suggest that TP53BP1 and MFN1 frameshift mutations and their intratumoral heterogeneity (ITH) could contribute to cancer development by inhibiting tumor suppressor gene (TSG) activities. PMID: 30082159
6. Results highlight the interplay of RNF169 with 53BP1 in fine-tuning the selection of DSB repair pathways. PMID: 30104380
7. While all three nucleoporins are required for accurate NHEJ, only Nup153 is needed for proper nuclear import of 53BP1 and SENP1-dependent sumoylation of 53BP1. Data supports the role of Nup153 as a significant regulator of 53BP1 activity and efficient NHEJ. PMID: 28576968
8. Results indicate that the integrity of the nuclear localization signal is crucial for 53BP1 nuclear localization. PMID: 29603287
9. As demonstrated in a xenograft model of glioblastoma, phosphorylation of 53BP1 by GSK3beta is indispensable for DNA double-strand break repair. PMID: 29328365
10. Results indicate a direct interaction between 53BP1 and MCMs, essential for 53BP1 chromatin fraction and foci formation in hepatoma HepG2 cells. PMID: 29990989
11. Results suggest that 53BP1 serves as a biomarker of response to anti-PARP therapy in laboratory settings, and our DNA damage response gene signature can be utilized to identify patients most likely to respond to PARP inhibition. PMID: 28958991
12. These findings reveal two distinct fork restart pathways, antagonistically controlled by 53BP1 and BRCA1 in a double-strand DNA break repair-independent manner. PMID: 29106372
13. Gamma-H2AX, phosphorylated KAP-1, and 53BP1 play a significant role in the repair of heterochromatic radon-induced DNA double-strand breaks. PMID: 27922110
14. Data indicates that the expression of tumor protein p53 binding protein 1 (53BP1) varies across different stages of the cell cycle, with high-level expression observed during mitosis. PMID: 28930533
15. Results further emphasize the antagonistic relationship between 53BP1 and BRCA1, placing Nup153 and Nup50 within a molecular pathway that regulates 53BP1 function by counteracting BRCA1-mediated events. PMID: 28751496
16. PAXIP1 and 53BP1 protein levels mirrored gene expression results, indicating an intrinsic correlation, and were also reduced in more advanced breast cancer tumors. PMID: 28475402
17. Data indicates that p53-binding protein 1 (53BP1) is required to prevent excessive chromosome missegregation and potentially genome hyper-instability, and is also essential for optimal growth in cancer cells. PMID: 29445165
18. This 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, revealing 53BP1 loss and SAMHD1 overexpression as the primary mechanisms responsible for their resistance to PARPi and Ara-C, respectively. PMID: 29274141
19. While the 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), the number of 53BP1 foci significantly increased after MR. PMID: 29309426
20. Premature maturation of post-replicative chromatin restores Histone h4 lysine 20 methylation and rescues 53BP1 accumulation on replicated chromatin. PMID: 28564601
21. UVA-induced progerinlamin A complex formation was primarily responsible for suppressing 53BP1-mediated NHEJ DSB repair activity. This 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. PMID: 28498430
22. 53BP1/RIF1 plays a role in limiting BRCA1/CtIP-mediated end resection to control the choice of double-strand break repair pathway. PMID: 27494840
23. Observations revealed a distinct accumulation of 53BP1 protein at UV-induced DNA lesions: in R273C mutants, 53BP1 appeared transiently at DNA lesions, during 10-30 min after irradiation; the mutation R282W resulted in immediate accumulation of 53BP1 after UVA-damage; and in L194F mutants, the first appearance of 53BP1 protein at the lesions occurred between 60-70 min. PMID: 28397142
24. A reciprocal regulation exists between 53BP1 and APC/C, essential for the response to mitotic stress. PMID: 28228263
25. BRCA1 promotes PP4C-dependent 53BP1 dephosphorylation and RIF1 release, directing repair towards homologous recombination. PMID: 28076794
26. Co-localization of gammaH2AX and 53BP1 indicates the promotion of (in)effective nonhomologous end-joining repair mechanisms at DSB sites. Moreover, gammaH2AX/53BP1 foci distribution likely reflects a non-random spatial organization of the genome in MDS and AML. PMID: 28359030
27. Results provide evidence that 53BP1 is involved in breast cancer cell resistance to PARP inhibitors; its depletion causes resistance in ATM-deficient tumor cells. PMID: 27613518
28. Ubiquitin ligases RNF168, RNF169, and RAD18 specifically bind histone H2A Lys13/15-ubiquitylated nucleosomes. 53BP1 chromatin recruitment can be activated by RNF168 and blocked by RNF169 and RAD18. PMID: 28506460
29. Ras-induced senescent cells are hindered in their ability to recruit BRCA1 and 53BP1 to DNA damage sites. While BRCA1 is downregulated at the transcript level, 53BP1 loss is caused by activation of cathepsin L-mediated degradation of 53BP1 protein. Notably, a marked downregulation of vitamin D receptor (VDR) was observed during OIS, suggesting a role for the vitamin D/VDR axis in regulating the levels of these DNA repair proteins. PMID: 27041576
30. The TIP60 complex regulates bivalent chromatin recognition/modification by 53BP1 through direct H4K20me binding and H2AK15 acetylation. PMID: 27153538
31. 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. PMID: 28241136
32. Deficiency of 53BP1 inhibits the radiosensitivity of colorectal cancer. PMID: 27499037
33. The interplay between 53BP1/NHEJ and BRCA1/HR is highly relevant for tumor treatment, as 53BP1 status would be crucial for the treatment response of BRCA1-associated tumors. PMID: 26615718
34. Exhaustion of 53BP1 by increasing the load of double-strand breaks suppresses RAD51 accumulation in repair foci during S and G2. PMID: 27348077
35. TIRR is a novel 53BP1-interacting protein that participates in the DNA damage response. PMID: 28213517
36. These data suggest that multiple pathways collectively fine-tune the cellular levels of 53BP1 protein to ensure proper DSB repair and cell survival. PMID: 28255090
37. This study reveals that 53BP1 protects both close and distant DSEs from degradation, and that the association of unprotection with distance between DSEs favors ECS capture. Conversely, silencing CtIP lessens ECS capture both in control and 53BP1-depleted cells. It is proposed that close ends are immediately/rapidly tethered and ligated, whereas distant ends first require synapsis of the distant DSEs prior to ligation. PMID: 27798638
38. Increased 53BP1 expression (i.e., "unstable" expression) in nuclear foci of oncocytic follicular adenoma (FA) of the thyroid correlates with a higher incidence of DNA copy numbers compared to conventional FA. PMID: 26935218
39. High 53BP1 mRNA is associated with head and neck cancer. PMID: 27465548
40. During live-cell imaging, 53BP1-GFP focus formation was observed within 10 minutes after UVC irradiation. Most 53BP1 foci resolved by 100 minutes. To block UVC-induced double-strand break repair in cancer cells, poly(ADP-ribose) polymerase (PARP) was targeted with ABT-888 (veliparib). PARP inhibition significantly enhanced UVC-irradiation-induced persistence of 53BP1-foci. PMID: 27466483
41. The combined effect of dynamic recruitment of RNF4 to KAP1 regulates the relative occupancy of 53BP1 and BRCA1 at double-strand break sites to direct DNA repair in a cell cycle-dependent manner. PMID: 26766492
42. The formation of 53BP1, gammaH2AX foci, and their co-localization induced by gamma-rays (2, 5, 10, 50, 200 cGy) in human lymphocytes, was analyzed. PMID: 26243567
43. 5-Hydroxymethylcytosine (5hmC) accumulates at DNA damage foci and colocalizes with major DNA damage response proteins 53BP1 and gH2AX, revealing 5hmC as an epigenetic marker of DNA damage. PMID: 26854228
44. This study shows that XIST and 53BP1 can be used to identify BRCA1-like breast cancer patients who have higher event rates and poorer outcomes after HD chemotherapy. PMID: 26637364
45. The kinetics of accumulation of selected DNA repair-related proteins is protein-specific at locally induced DNA lesions, and the formation of gH2AX- and NBS1-positive foci, but not 53BP1-positive NBs, is cell cycle-dependent in HeLa cells. PMID: 26482424
46. The interaction of 53BP1 with gammaH2AX is required for sustaining the 53BP1-dependent focal concentration of activated ATM, facilitating repair of DNA double-strand breaks in heterochromatin during G1. PMID: 26628370
47. The cryo-EM structure of a dimerized human 53BP1 fragment bound to a H4K20me2-containing and H2AK15ub-containing nucleosome core particle at 4.5 A resolution. PMID: 27462807
48. The study shows higher expression of gamma-H2AX and 53BP1 foci in rectal cancer patients compared to healthy individuals. However, the data in vitro was not predictive in regard to the radiotherapy outcome. PMID: 26541290
49. For both gamma-H2AX and 53BP1, the cellular focus number, as well as the percentage of positive cells, did not differ between patients with clinically isolated syndrome/early relapsing-remitting multiple sclerosis and healthy controls. PMID: 26820970
50. Impaired TIP60-mediated H4K16 acetylation accounts for the aberrant chromatin accumulation of 53BP1 and RAP80 in Fanconi anemia pathway-deficient cells. PMID: 26446986

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HGNC: 11999

OMIM: 605230

KEGG: hsa:7158

STRING: 9606.ENSP00000371475

UniGene: Hs.440968