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MRN (Mre11 (show MRE11A ELISA Kits), Rad50 (show RAD50 ELISA Kits), and Nbs1) complex, CtIP, and BRCA1 are required for both the removal of Top2 (show TOP2 ELISA Kits)-DNA adducts and the subsequent resection of Top2 (show TOP2 ELISA Kits)-adducted DSB ends.
ATM (show ATM ELISA Kits) activity is required for an early step in resection, leading to ATR (show ATR ELISA Kits) 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 ELISA Kits) inhibits both the nonhomologous and homologous modes of DSB repair during mitosis.
Homozygous RBBP8 mutation is associated with microcephaly, intellectual disability, short stature and brachydactyly.
USP4 (show USP4 ELISA Kits) 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 (show UBE2D1 ELISA Kits)/2/3 and E3 ligase RNF138 (show RNF138 ELISA Kits) 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 (show DNA2 ELISA Kits) to damage sites, thus ensuring the robust DSB resection necessary for efficient homologous recombination.
The CtIP 3'UTR (show UTS2R ELISA Kits) is directly targeted by miR (show MLXIP ELISA Kits)-19a and miR (show MLXIP ELISA Kits)-19b.
CtIP interacts with Cdh1 (show CDH1 ELISA Kits) through a conserved KEN (show PCNT ELISA Kits) box, mutation of which impedes ubiquitylation and downregulation of CtIP both during G1 and after DNA damage in G2.
Possible association of SOX-17 (show SOX17 ELISA Kits) and RBBP8 with brain arteriovenous malformations, genes involved in cell cycle progression, deserves further investigation
findings provide strong evidence that CtIP is continuously recruited to DSBs downstream of both the initiation and extension step of resection
Data indicate that FANCD2 (show FANCD2 ELISA Kits) primes CtIP-dependent resection during HR after ICL induction but that CtIP helps prevent illegitimate recombination in FA cells.
work therefore ascribes novel roles for BRCA1 (show BRCA1 ELISA Kits) 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 ELISA Kits)-CtIP interaction is not essential for HDR (show GATA3 ELISA Kits)-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 (show H2AFX ELISA Kits) prevents nucleases other than Artemis (show DCLRE1C ELISA Kits) from processing hairpin-sealed coding ends; in the absence of H2AX (show H2AFX ELISA Kits), 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 (show RUNX1 ELISA Kits) sensitive CBA strain but not AML (show RUNX1 ELISA Kits) resistant C57BL/6 strain
CtiP activates its own and cyclin D promoters via the E2F (show E2F1 ELISA Kits)/RB pathway during G1/S progression.
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.
retinoblastoma binding protein 8
, CtBP-interacting protein
, DNA endonuclease RBBP8
, ctBP-interacting protein
, retinoblastoma-binding protein 8
, sporulation in the absence of SPO11 protein 2 homolog
, retinoblastoma-binding protein 8-like
, CTBP-interacting protein