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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 ELISA Kits) 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 (show GATA3 ELISA Kits) 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 ELISA Kits) and CtIP in determining the substrates and consequences of human Mre11 (show MRE11A ELISA Kits)/Rad50 (show RAD50 ELISA Kits) nuclease (show DCLRE1C ELISA Kits) 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 ELISA Kits) 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 ELISA Kits)-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 (show USP4 ELISA Kits) cooperates with CtIP in DNA double-strand break end resection.
Q418P nsSNP influences the efficiency of CTIP function in HR repair of DNA DSBs
Ctip1 (show BCL11A ELISA Kits) 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 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
MRN (Mre11 (show MRE11A ELISA Kits), Rad50 (show RAD50 ELISA Kits), and Nbs1 (show NLRP2 ELISA Kits)) 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.
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