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TP53BP1 Antibody

  • 货号：
    CSB-PA572150
  • 规格：
    ￥2024
  • 图片：
    • Immunohistochemistry analysis of paraffin-embedded human brain tissue using 53BP1 antibody.
  • 其他：

产品详情

  • 产品名称：
    Rabbit anti-Homo sapiens (Human) TP53BP1 Polyclonal antibody
  • Uniprot No.：
    Q12888
  • 基因名：
  • 宿主：
    Rabbit
  • 反应种属：
    Human
  • 免疫原：
    Synthesized peptide derived from Internal of Human 53BP1.
  • 免疫原种属：
    Homo sapiens (Human)
  • 克隆类型：
    Polyclonal
  • 纯化方式：
    The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
  • 浓度：
    It differs from different batches. Please contact us to confirm it.
  • 产品提供形式：
    Liquid
  • 应用范围：
    ELISA,IHC
  • 推荐稀释比：
    Application Recommended Dilution
    IHC 1:50-1:100
  • Protocols：
  • 储存条件：
    Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
  • 货期：
    Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.

产品评价

靶点详情

  • 功能：
    Double-strand break (DSB) repair protein involved in response to DNA damage, telomere dynamics and class-switch recombination (CSR) during antibody genesis. Plays a key role in the repair of double-strand DNA breaks (DSBs) in response to DNA damage by promoting non-homologous end joining (NHEJ)-mediated repair of DSBs and specifically counteracting the function of the homologous recombination (HR) repair protein BRCA1. In response to DSBs, phosphorylation by ATM promotes interaction with RIF1 and dissociation from NUDT16L1/TIRR, leading to recruitment to DSBs sites. Recruited to DSBs sites by recognizing and binding histone H2A monoubiquitinated at 'Lys-15' (H2AK15Ub) and histone H4 dimethylated at 'Lys-20' (H4K20me2), two histone marks that are present at DSBs sites. Required for immunoglobulin class-switch recombination (CSR) during antibody genesis, a process that involves the generation of DNA DSBs. Participates in the repair and the orientation of the broken DNA ends during CSR. In contrast, it is not required for classic NHEJ and V(D)J recombination. Promotes NHEJ of dysfunctional telomeres via interaction with PAXIP1.
  • 基因功能参考文献：
    1. Inhibition of 53BP1 is a robust method to increase 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 the histone methyl-lysine readers. PMID: 29844495
    3. 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. PMID: 30002377
    4. GFI1 facilitates efficient DNA repair by regulating PRMT1 dependent methylation of MRE11 and 53BP1. PMID: 29651020
    5. 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. PMID: 30082159
    6. results highlight the interplay of RNF169 with 53BP1 in fine-tuning choice of DSB repair pathways. PMID: 30104380
    7. 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. PMID: 28576968
    8. Results indicate that integrity of the nuclear localization signal is important for 53BP1 nuclear localization. PMID: 29603287
    9. As shown in xenograft model of glioblastoma phosphorylation of 53BP1 by GSK3beta was indispensable for DNA double-strand break repair. PMID: 29328365
    10. 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. PMID: 29990989
    11. 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. PMID: 28958991
    12. 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. PMID: 29106372
    13. Gamma-H2AX, phosphorylated KAP-1 and 53BP1 play an important role in the repair of heterochromatic radon-induced DNA double-strand breaks. PMID: 27922110
    14. 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. PMID: 28930533
    15. 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. PMID: 28751496
    16. PAXIP1 and 53BP1 protein levels followed gene expression results, i.e., are intrinsically correlated, and also reduced in more advanced breast cancer tumors. PMID: 28475402
    17. 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. PMID: 29445165
    18. 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. PMID: 29274141
    19. 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 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 largely responsible for suppressing 53BP1-mediated NHEJ DSB repair activity. The present 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 has a role in limiting BRCA1/CtIP-mediated end resection to control double strand break repair pathway choice PMID: 27494840
    23. It observed a distinct accumulation of 53BP1 protein to UV-induced DNA lesions: in R273C mutants, 53BP1 appeared transiently at DNA lesions, during 10-30 min after irradiation; the mutation R282W was responsible for accumulation of 53BP1 immediately after UVA-damage; and in L194F mutants, the first appearance of 53BP1 protein at the lesions occurred during 60-70 min. PMID: 28397142
    24. A reciprocal regulation between 53BP1 and APC/C that is required for response to mitotic stress. PMID: 28228263
    25. BRCA1 promotes PP4C-dependent 53BP1 dephosphorylation and RIF1 release, directing repair toward homologous recombination. PMID: 28076794
    26. Co-localization of gammaH2AX and 53BP1 indicates promotion of (in)effective nonhomologous end-joining repair mechanisms at sites of DSB. Moreover, gammaH2AX/53BP1 foci distribution presumably reveals 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 cells resistance for PARP inhibitor; 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 may 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. 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 PMID: 27041576
    30. 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. interplay between 53BP1/NHEJ and BRCA1/HR is of great relevance for tumor treatment, as the 53BP1 status would be highly important 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. his shows that 53BP1 protects both close and distant DSEs from degradation and that the association of unprotection with distance between DSEs favors ECS capture. Reciprocally, silencing CtIP lessens ECS capture both in control and 53BP1-depleted cells. We propose 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 with 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 markedly enhanced UVC-irradiation-induced persistence of 53BP1-foci PMID: 27466483
    41. 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. we show that XIST and 53BP1 can be used to identify BRCA1-like breast cancer patients that have higher event rates and poor outcome after HD chemotherapy. PMID: 26637364
    45. kinetics of the accumulation of selected DNA repair-related proteins is protein specific at locally induced DNA lesions, and that 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 that facilitates repair of DNA double-strand breaks in heterochromatin in G1. PMID: 26628370
    47. 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 with healthy individuals. Yet the data in vitro were 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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  • 相关疾病：
    A chromosomal aberration involving TP53BP1 is found in a form of myeloproliferative disorder chronic with eosinophilia. Translocation t(5;15)(q33;q22) with PDGFRB creating a TP53BP1-PDGFRB fusion protein.
  • 亚细胞定位：
    Nucleus. Chromosome. Chromosome, centromere, kinetochore.
  • 数据库链接：

    HGNC: 11999

    OMIM: 605230

    KEGG: hsa:7158

    STRING: 9606.ENSP00000371475

    UniGene: Hs.440968