RBBP8 Antibody

Code CSB-PA192852
Size US$166
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Image
  • The image on the left is immunohistochemistry of paraffin-embedded Human thyroid cancer tissue using CSB-PA192852(RBBP8 Antibody) at dilution 1/45, on the right is treated with fusion protein. (Original magnification: ×200)
  • The image on the left is immunohistochemistry of paraffin-embedded Human breast cancer tissue using CSB-PA192852(RBBP8 Antibody) at dilution 1/45, on the right is treated with fusion protein. (Original magnification: ×200)
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Product Details

Uniprot No.
Target Names
RBBP8
Alternative Names
COM1 antibody; COM1_HUMAN antibody; CtBP interacting protein antibody; CtBP-interacting protein antibody; CtIP antibody; DNA endonuclease RBBP8 antibody; JWDS antibody; RB binding protein 8 endonuclease antibody; RBBP-8 antibody; RBBP8 antibody; Retinoblastoma-binding protein 8 antibody; Retinoblastoma-interacting protein and myosin-like antibody; Rim antibody; SAE2 antibody; SCKL2 antibody; Sporulation in the absence of SPO11 protein 2 homolog antibody
Raised in
Rabbit
Species Reactivity
Human,Mouse,Rat
Immunogen
Fusion protein of Human RBBP8
Immunogen Species
Homo sapiens (Human)
Conjugate
Non-conjugated
Isotype
IgG
Purification Method
Antigen affinity purification
Concentration
It differs from different batches. Please contact us to confirm it.
Buffer
-20°C, pH7.4 PBS, 0.05% NaN3, 40% Glycerol
Form
Liquid
Tested Applications
ELISA,IHC
Recommended Dilution
Application Recommended Dilution
ELISA 1:2000-1:10000
IHC 1:100-1:300
Troubleshooting and FAQs
Storage
Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
Lead Time
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.

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Target Background

Function
Endonuclease that cooperates with the MRE11-RAD50-NBN (MRN) complex in DNA-end resection, the first step of double-strand break (DSB) repair through the homologous recombination (HR) pathway. HR is restricted to S and G2 phases of the cell cycle and preferentially repairs DSBs resulting from replication fork collapse. Key determinant of DSB repair pathway choice, as it commits cells to HR by preventing classical non-homologous end-joining (NHEJ). Functions downstream of the MRN complex and ATM, promotes ATR activation and its recruitment to DSBs in the S/G2 phase facilitating the generation of ssDNA. Component of the BRCA1-RBBP8 complex that regulates CHEK1 activation and controls cell cycle G2/M checkpoints on DNA damage. During immunoglobulin heavy chain class-switch recombination, promotes microhomology-mediated alternative end joining (A-NHEJ) and plays an essential role in chromosomal translocations.
Gene References into Functions
  1. Study identifies the KLHL15 as a new interaction partner of CtIP and show that KLHL15 promotes CtIP protein turnover via the ubiquitin-proteasome pathway. PMID: 27561354
  2. ATM-dependent phosphorylation of CtIP and the epistatic and coordinated actions of MRE11 and CtIP nuclease activities are required to limit the stable loading of Ku on single-ended DNA double-strand breaks. PMID: 27641979
  3. 53BP1/RIF1 has a role in limiting BRCA1/CtIP-mediated end resection to control double strand break repair pathway choice PMID: 27494840
  4. we reveal that reprogramming is associated with high levels of DNA end resection, a critical step in homologous recombination. Moreover, the resection factor CtIP is essential for cell reprogramming and establishment of iPSCs, probably to repair reprogramming-induced DNA damage. PMID: 28065643
  5. Data show that SUMO E3 ligase CBX4 sumoylates subpopulation of CtIP to regulate recruitment to breaks and resection. PMID: 28740167
  6. CtIP/Ctp1/Sae2/Com1 role in removal of DNA double strand breaks through DSB repair by homologous recombination is reviewed. PMID: 28623092
  7. Data delineates the regulatory mechanisms of GATA3 in DNA double-strand breaks repair and strongly suggests that it might act as a tumor suppressor by promoting CtIP expression and homologous recombination to stabilize genomes. PMID: 28481869
  8. The results illuminate the important role of Nbs1 and CtIP in determining the substrates and consequences of human Mre11/Rad50 nuclease activities on protein-DNA lesions. PMID: 27814491
  9. And-1 interacts with CtIP and that these interactions are required for DNA damage checkpoint maintenance, thereby linking DNA processing with prolonged cell cycle arrest to allow sufficient time for DNA repair. PMID: 27940552
  10. 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
  11. Low level of CtIP expression is associated with breast cancer. PMID: 26713604
  12. Homozygous RBBP8 mutation is associated with microcephaly, intellectual disability, short stature and brachydactyly. PMID: 26333564
  13. USP4 cooperates with CtIP in DNA double-strand break end resection. PMID: 26387952
  14. CtIP is a DNA damage response protein at the intersection of DNA metabolism. (Review) PMID: 25957490
  15. Data show that ubiquitin E2 enzymes UBE2D1/2/3 and E3 ligase RNF138 accumulate at DNA-damage sites and act at early resection stages by promoting CtIP protein ubiquitylation and accrual. PMID: 26502057
  16. BRCA1 and CtIP contribute to DSB resection by recruiting Dna2 to damage sites, thus ensuring the robust DSB resection necessary for efficient homologous recombination. PMID: 25909997
  17. The CtIP 3'UTR is directly targeted by miR-19a and miR-19b. PMID: 25308476
  18. CtIP interacts with Cdh1 through a conserved KEN box, mutation of which impedes ubiquitylation and downregulation of CtIP both during G1 and after DNA damage in G2. PMID: 25349192
  19. Possible association of SOX-17 and RBBP8 with brain arteriovenous malformations, genes involved in cell cycle progression, deserves further investigation PMID: 25053769
  20. findings provide strong evidence that CtIP is continuously recruited to DSBs downstream of both the initiation and extension step of resection PMID: 25771978
  21. Data indicate that FANCD2 primes CtIP-dependent resection during HR after ICL induction but that CtIP helps prevent illegitimate recombination in FA cells. PMID: 24794434
  22. Study identified CtIP as a novel interaction partner of FANCD2. CtIP binds and stabilizes FANCD2 in a DNA damage- and FA core complex-independent manner, suggesting that FANCD2 monoubiquitination is dispensable for its interaction with CtIP. PMID: 24556218
  23. Plk3 binds to CtIP phosphorylated at S327 via its Polo box domains, which is necessary for robust damage-induced CtIP phosphorylation at S327 and subsequent CtIP phosphorylation at T847. PMID: 25267294
  24. These studies suggest that an end resection-independent CtIP function is important for processing double-strand break ends with secondary structures to promote homologous recombination. PMID: 24837675
  25. human CtIP is a 5' flap endonuclease and this activity is required in some contexts for the efficient function of CtIP. PMID: 24837676
  26. Low or no expression of RBBP8 correlates with high-grade breast cancer, poor prognosis and with nodal metastasis. PMID: 24403251
  27. our data demonstrate that CtIP is required for DNA damage-induced P21 induction PMID: 24196441
  28. Microsatellite instability dependent mutations were detected in CtIP in myeloid malignancies conferring hypersensitivity to PARP inhibitors. PMID: 23349304
  29. study identified a homozygous mutation in RBBP8, which co-segregates with microcephaly-associated intellectual disability syndrome in a Pakistani family; also identified a heterozygous deletion encompassing the NRXN1 in this family, which is present in 2 affected sibs with complex phenotype and the mother with mild phenotype PMID: 24440292
  30. BRCA1/CtIP-mediated processing of the second end of the break controls the annealing step that normally terminates synthesis-dependent strand annealing, thereby suppressing the error-prone long-tract gene conversion outcome. PMID: 23994874
  31. Taken together, these findings strongly suggest that an ATM-dependent CREB-miR-335-CtIP axis influences the selection of HRR for repair of certain DSB lesions PMID: 23696749
  32. These studies reveal one important mechanism to regulate cell-cycle-dependent activation of HR upon DNA damage by coupling CDK- and ATM-mediated phosphorylation of CtIP through modulating the interaction of CtIP with Nbs1 PMID: 23468639
  33. Data suggest that overexpression of LMO4 may disrupt some of the normal tumour suppressor activities of CtIP, thereby contributing to breast cancer progression. PMID: 23353824
  34. RIF1 accumulation at DSB sites is strongly antagonized by BRCA1 and its interacting partner CtIP PMID: 23333306
  35. CtIP binds to ATM protein proximal promoter, but after DNA damage Ctip is released. PMID: 22832221
  36. show that CHK1 was rapidly and robustly activated before detectable end resection PMID: 22733999
  37. The severe repair defects of CtIP dimerization mutants are likely due to the failure in localization to chromosomal DSBs upon DNA damage. PMID: 22544744
  38. The authors show that, in human and mouse, Mre11 controls these events through a direct interaction with CDK2 that is required for CtIP phosphorylation and BRCA1 interaction in normally dividing cells. PMID: 22231403
  39. the SCKL2 mutation creates an alternative splicing site leading to both the normal and aberrant CtIP proteins coexisting in the cells of patients and carriers PMID: 21998596
  40. Studies indicate that codon-based models of gene evolution yielded statistical support for the recurrent positive selection of five NHEJ genes during primate evolution: XRCC4, NBS1, Artemis, POLlambda, and CtIP. PMID: 20975951
  41. This study identifies new functions of CtIP and EXO1 in DNA end resection and provides new information on the regulation of DNA double-strand breaks repair pathways, which is a key factor in the maintenance of genome integrity. PMID: 21052091
  42. BCR-ABL promotes mutagenic DSB repair with the DSB end-processing protein CtIP acting as the key mediator downstream of BCR-ABL PMID: 20974687
  43. identified double-strand break(DSB) resection protein CtIP as a SIRT6 interaction partner; showed SIRT6-dependent CtIP deacetylation promotes resection;CtIP identified as key substrate by which SIRT6 facilitates DSB processing and homologous recombination PMID: 20829486
  44. Data found that HMGA2, along with a dozen of other genes, was co-repressed by ZBRK1, BRCA1, and CtIP. PMID: 20007691
  45. CtIP facilitates the transition from DSB sensing to processing, by binding to the DNA at double-strand breaks (DSBs) after DSB sensing and ATM activation and then promoting DNA resection, leading to checkpoint activation and homologous recombination. PMID: 20064462
  46. These findings reveal a novel complex between BRCA1, LMO4, and CtIP and indicate a role for LMO4 as a repressor of BRCA1 activity in breast tissue. PMID: 11751867
  47. a corepressor complex containing CtIP/CtBP facilitates RBP-Jkappa/SHARP-mediated repression of Notch target genes PMID: 16287852
  48. CTIP activates its own and cyclin D promoters via the E2F/RB pathway during G1/S progression. PMID: 16581787
  49. Since CtIP plays important roles in cell cycle checkpoint control and it has been implicated in tumorigenesis, our data suggest that TRB3 may be involved in these biological processes through interacting with CtIP. PMID: 17112672
  50. Data show that CtIP expression is induced by AdE1A during viral infection and that reduction of CtIP expression with RNA interference can retard virus replication. PMID: 17546052

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Involvement in disease
Seckel syndrome 2 (SCKL2); Jawad syndrome (JWDS)
Subcellular Location
Nucleus. Chromosome.
Protein Families
COM1/SAE2/CtIP family
Tissue Specificity
Expressed in ER-positive breast cancer lines, but tends to be down-regulated ER-negative cells (at protein level).
Database Links

HGNC: 9891

OMIM: 251255

KEGG: hsa:5932

STRING: 9606.ENSP00000323050

UniGene: Hs.546282

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