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抗Human Retinoblastoma Binding Protein 8 抗体:
抗Mouse (Murine) Retinoblastoma Binding Protein 8 抗体:
抗Rat (Rattus) Retinoblastoma Binding Protein 8 抗体:
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 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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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
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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 (显示 ATM 抗体)-dependent phosphorylation of CtIP and the epistatic and coordinated actions of MRE11 (显示 MRE11A 抗体) and CtIP nuclease (显示 DCLRE1C 抗体) activities are required to limit the stable loading of Ku on single-ended DNA double-strand breaks.
53BP1 (显示 TP53BP1 抗体)/RIF1 (显示 INSL6 抗体) 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 (显示 PIAS1 抗体) CBX4 (显示 CBX4 抗体) 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 (显示 GATA3 抗体) 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 (显示 NBN 抗体) and CtIP in determining the substrates and consequences of human Mre11 (显示 MRE11A 抗体)/Rad50 (显示 RAD50 抗体) nuclease (显示 DCLRE1C 抗体) 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 (显示 TP53BP1 抗体) 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 (显示 TP53BP1 抗体)-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
CtIP enhances long-range resection by BLM (显示 BLM 抗体)-DNA2 (显示 DNA2 抗体)-RPA (显示 RPA1 抗体). CtIP interacts with and stimulates the activity of the BLM helicase (显示 BLM 抗体) and upregulates DNA2 (显示 DNA2 抗体) 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 (显示 BCL11A 抗体) couples subtype and area specification, enabling specific functional areas to organize precise ratios of appropriate output projections.
work therefore ascribes novel roles for BRCA1 (显示 BRCA1 抗体) 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 (显示 BRCA1 抗体)-CtIP interaction is not essential for HDR (显示 GATA3 抗体)-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.
MRN (Mre11 (显示 MRE11A 抗体), Rad50 (显示 RAD50 抗体), and Nbs1 (显示 NLRP2 抗体)) complex, CtIP, and BRCA1 are required for both the removal of Top2 (显示 TOP2 抗体)-DNA adducts and the subsequent resection of Top2 (显示 TOP2 抗体)-adducted DSB ends.
ATM (显示 ATM 抗体) activity is required for an early step in resection, leading to ATR (显示 ATR 抗体) 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 (显示 CDK1 抗体) 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