Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human Retinoblastoma Binding Protein 8 Antibodies:
anti-Mouse (Murine) Retinoblastoma Binding Protein 8 Antibodies:
anti-Rat (Rattus) Retinoblastoma Binding Protein 8 Antibodies:
Go to our pre-filtered search.
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
Show all 6 Pubmed References
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
Show all 4 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
Show all 3 Pubmed References
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
53BP1 (show TP53BP1 Antibodies)/RIF1 (show INSL6 Antibodies) 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 (show PIAS1 Antibodies) CBX4 (show CBX4 Antibodies) 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 (show GATA3 Antibodies) 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 (show NBN Antibodies) and CtIP in determining the substrates and consequences of human Mre11 (show MRE11A Antibodies)/Rad50 (show RAD50 Antibodies) nuclease (show DCLRE1C Antibodies) 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 (show TP53BP1 Antibodies) 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 (show TP53BP1 Antibodies)-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.
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 (show BCL11A Antibodies) couples subtype and area specification, enabling specific functional areas to organize precise ratios of appropriate output projections.
work therefore ascribes novel roles for BRCA1 (show BRCA1 Antibodies) 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 (show BRCA1 Antibodies)-CtIP interaction is not essential for HDR (show GATA3 Antibodies)-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.
MRN (Mre11 (show MRE11A Antibodies), Rad50 (show RAD50 Antibodies), and Nbs1 (show NLRP2 Antibodies)) complex, CtIP, and BRCA1 are required for both the removal of Top2 (show TOP2 Antibodies)-DNA adducts and the subsequent resection of Top2 (show TOP2 Antibodies)-adducted DSB ends.
ATM (show ATM Antibodies) activity is required for an early step in resection, leading to ATR (show ATR Antibodies) 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 (show CDK1 Antibodies) 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