Recombinant Human Tumor suppressor p53-binding protein 1(TP53BP1) ,partial

Code CSB-YP613268HU
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Source Yeast
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Code CSB-EP613268HU
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Source E.coli
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Code CSB-EP613268HU-B
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Source E.coli
Conjugate Avi-tag Biotinylated
E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.
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Code CSB-BP613268HU
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Source Baculovirus
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Code CSB-MP613268HU
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Source Mammalian cell
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Product Details

Purity >85% (SDS-PAGE)
Target Names TP53BP1
Uniprot No. Q12888
Alternative Names 53 BP1; 53BP1; FLJ41424; MGC138366; p202; p53 binding protein 1; p53 BP1; p53-binding protein 1; p53BP1; TP53 BP1; TP53B_HUMAN; Tp53bp1; TRP53 BP1; Tumor protein 53 binding protein 1; Tumor protein p53 binding protein 1; Tumor suppressor p53 binding protein 1; Tumor suppressor p53-binding protein 1
Species Homo sapiens (Human)
Protein Length Partial
Tag Info The following tags are available.
N-terminal His-tagged
Tag-Free
The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
Form Lyophilized powder
Buffer before Lyophilization Tris/PBS-based buffer, 6% Trehalose, pH 8.0
Reconstitution We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting
and FAQs
Protein FAQs
Storage Condition Store at -20°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
Notes Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet Please contact us to get it.

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Target Background

Function
(From Uniprot)
Double-strand break (DSB) repair protein involved in response to DNA damage, telomere dynamics and class-switch recombination (CSR) during antibody genesis
Gene References into Functions
  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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Involvement in disease 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.
Subcellular Location Nucleus, Chromosome, Chromosome, centromere, kinetochore
Database Links

HGNC: 11999

OMIM: 605230

KEGG: hsa:7158

STRING: 9606.ENSP00000371475

UniGene: Hs.440968

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