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anti-Human Retinoblastoma Binding Protein 8 Antibodies:
anti-Mouse (Murine) Retinoblastoma Binding Protein 8 Antibodies:
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Human Monoclonal Retinoblastoma Binding Protein 8 Primary Antibody for ICC, IF - ABIN2668263
Zhou, Caron, Legube, Paull: Quantitation of DNA double-strand break resection intermediates in human cells. in Nucleic acids research 2014
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Human Polyclonal Retinoblastoma Binding Protein 8 Primary Antibody for ICC, IF - ABIN256682
Quennet, Beucher, Barton, Takeda, Löbrich: CtIP and MRN promote non-homologous end-joining of etoposide-induced DNA double-strand breaks in G1. in Nucleic acids research 2011
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Human Polyclonal Retinoblastoma Binding Protein 8 Primary Antibody for IP - ABIN256681
Yin, Seifert, Chua, Maure, Golebiowski, Hay: SUMO-targeted ubiquitin E3 ligase RNF4 is required for the response of human cells to DNA damage. in Genes & development 2012
Show all 3 Pubmed References
Human Monoclonal Retinoblastoma Binding Protein 8 Primary Antibody for ChIP, ICC - ABIN445506
Liu, Lee: CtIP activates its own and cyclin D1 promoters via the E2F/RB pathway during G1/S progression. in Molecular and cellular biology 2006
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Data sufgest that polo like kinase 1 (PLK1) may target retinoblastoma binding protein 8 (RBBP8; CtIP) to promote error-prone microhomology-mediated end joining (MMEJ) and inactivate the G2/M checkpoint.
Bioinformatics predicted the putative binding site of miR18a5p in the 3' untranslated region of CtIP/RBBP8. Study using nasopharyngeal carcinoma cell line further confirmed that miR18a5p could directly bind with RBBP8 and inhibit RBBP8 expression.
Data demonstrate that RBBP8 is almost exclusively methylated in 45% primary bladder cancer, suggesting the development of methylation in a distinct molecular context. A close association between RBBP8 methylation and its gene expression in primary tumors as well as after demethylation treatment in vitro indicate that RBBP8 methylation could be responsible for its gene inactivation.
Study identifies the KLHL15 as a new interaction partner of CtIP and show that KLHL15 promotes CtIP protein turnover via the ubiquitin-proteasome pathway.
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.
53BP1/RIF1 has a role in limiting BRCA1/CtIP-mediated end resection to control double strand break repair pathway choice
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.
Data show that SUMO E3 ligase CBX4 sumoylates subpopulation of CtIP to regulate recruitment to breaks and resection.
CtIP/Ctp1/Sae2/Com1 role in removal of DNA double strand breaks through DSB repair by homologous recombination is reviewed.
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.
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.
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.
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
Low level of CtIP expression is associated with breast cancer.
Homozygous RBBP8 mutation is associated with microcephaly, intellectual disability, short stature and brachydactyly.
USP4 cooperates with CtIP in DNA double-strand break end resection.
CtIP is a DNA damage response protein at the intersection of DNA metabolism. (Review)
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.
BRCA1 and CtIP contribute to DSB resection by recruiting Dna2 to damage sites, thus ensuring the robust DSB resection necessary for efficient homologous recombination.
The CtIP 3'UTR is directly targeted by miR-19a and miR-19b.
CtIP enhances long-range resection by BLM-DNA2-RPA. CtIP interacts with and stimulates the activity of the BLM helicase and upregulates DNA2 activity.
CtIP is not a tumor suppressor, but has oncogenic properties that can promote tumorigenesis, consistent with its ability to facilitate MMEJ-dependent chromosomal instability.
Q418P nsSNP influences the efficiency of CTIP function in HR repair of DNA DSBs
Ctip1 couples subtype and area specification, enabling specific functional areas to organize precise ratios of appropriate output projections.
work therefore ascribes novel roles for BRCA1 and CtIP in end-processing and fusion reactions at uncapped telomeres
Data indicate that loss of the CtIP-BRCA1 interaction does not detectably affect resection, maintenance of genomic stability or viability.
The phospho-dependent BRCA1-CtIP interaction is not essential for HDR-mediated DSB repair or for tumor suppression.
CtIP contributes to the metabolism of DNA ends during DNA double-strand breaks repair in B lymphocytes.
CtIP-mediated alt-NHEJ has a primary role in translocation formation.
CtIP binds to switch-region DNA and plays a physiological role in microhomology-mediated end joining in a C-NHEJ-proficient environment.
the histone protein H2AX prevents nucleases other than Artemis from processing hairpin-sealed coding ends; in the absence of H2AX, CtIP can efficiently promote the hairpin opening and resection of DNA ends generated by RAG cleavage
CtIP counteracts Rb-mediated G(1) restraint.
Rbbp8 is shown to be upregulated in response to X-irradiation in the AML sensitive CBA strain but not AML resistant C57BL/6 strain
CtiP activates its own and cyclin D promoters via the E2F/RB pathway during G1/S progression.
MRN (Mre11, Rad50, and Nbs1) complex, CtIP, and BRCA1 are required for both the removal of Top2-DNA adducts and the subsequent resection of Top2-adducted DSB ends.
ATM activity is required for an early step in resection, leading to ATR activation, CtIP-T818 phosphorylation, and accumulation of CtIP on chromatin.
By promoting CtIP-dependent resection of double-strand break (DSB) ends while preventing Rad51 chromatin assembly, Cdk1 inhibits both the nonhomologous and homologous modes of DSB repair during mitosis.
The protein encoded by this gene is a ubiquitously expressed nuclear protein. It is found among several proteins that bind directly to retinoblastoma protein, which regulates cell proliferation. This protein complexes with transcriptional co-repressor CTBP. It is also associated with BRCA1 and is thought to modulate the functions of BRCA1 in transcriptional regulation, DNA repair, and/or cell cycle checkpoint control. It is suggested that this gene may itself be a tumor suppressor acting in the same pathway as BRCA1. Three transcript variants encoding two different isoforms have been found for this gene. More transcript variants exist, but their full-length natures have not been determined.
, DNA endonuclease RBBP8
, sporulation in the absence of SPO11 protein 2 homolog
, ctBP-interacting protein
, retinoblastoma-binding protein 8
, retinoblastoma binding protein 8
, CtBP-interacting protein
, retinoblastoma-binding protein 8-like