Browse our Retinoblastoma Binding Protein 8 Proteins (RBBP8)

Human Retinoblastoma Binding Protein 8 (RBBP8) interaction partners

1. 53BP1 (show TP53BP1 Proteins)/RIF1 (show INSL6 Proteins) has a role in limiting BRCA1/CtIP-mediated end resection to control double strand break repair pathway choice

2. 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.

3. Data show that SUMO E3 ligase (show PIAS1 Proteins) CBX4 (show CBX4 Proteins) sumoylates subpopulation of CtIP to regulate recruitment to breaks and resection.

4. CtIP/Ctp1/Sae2/Com1 role in removal of DNA double strand breaks through DSB repair by homologous recombination is reviewed.

5. Data delineates the regulatory mechanisms of GATA3 (show GATA3 Proteins) 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.

6. The results illuminate the important role of Nbs1 (show NBN Proteins) and CtIP in determining the substrates and consequences of human Mre11 (show MRE11A Proteins)/Rad50 (show RAD50 Proteins) nuclease (show DCLRE1C Proteins) activities on protein-DNA lesions.

7. 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.

8. his shows that 53BP1 (show TP53BP1 Proteins) 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 Proteins)-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

9. Low level of CtIP expression is associated with breast cancer.

10. Homozygous RBBP8 mutation is associated with microcephaly, intellectual disability, short stature and brachydactyly.

Mouse (Murine) Retinoblastoma Binding Protein 8 (RBBP8) interaction partners

1. CtIP is not a tumor suppressor, but has oncogenic properties that can promote tumorigenesis, consistent with its ability to facilitate MMEJ-dependent chromosomal instability.

2. 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.

3. Q418P nsSNP influences the efficiency of CTIP function in HR repair of DNA DSBs

4. Ctip1 (show BCL11A Proteins) couples subtype and area specification, enabling specific functional areas to organize precise ratios of appropriate output projections.

5. work therefore ascribes novel roles for BRCA1 (show BRCA1 Proteins) and CtIP in end-processing and fusion reactions at uncapped telomeres

6. Data indicate that loss of the CtIP-BRCA1 interaction does not detectably affect resection, maintenance of genomic stability or viability.

7. The phospho-dependent BRCA1 (show BRCA1 Proteins)-CtIP interaction is not essential for HDR (show GATA3 Proteins)-mediated DSB repair or for tumor suppression.

8. CtIP contributes to the metabolism of DNA ends during DNA double-strand breaks repair in B lymphocytes.

9. CtIP-mediated alt-NHEJ has a primary role in translocation formation.

10. CtIP binds to switch-region DNA and plays a physiological role in microhomology-mediated end joining in a C-NHEJ-proficient environment.

Xenopus laevis Retinoblastoma Binding Protein 8 (RBBP8) interaction partners

1. MRN (Mre11 (show MRE11A Proteins), Rad50 (show RAD50 Proteins), and Nbs1 (show NLRP2 Proteins)) complex, CtIP, and BRCA1 are required for both the removal of Top2 (show TOP2 Proteins)-DNA adducts and the subsequent resection of Top2 (show TOP2 Proteins)-adducted DSB ends.

2. ATM (show ATM Proteins) activity is required for an early step in resection, leading to ATR activation, CtIP-T818 phosphorylation, and accumulation of CtIP on chromatin.

3. By promoting CtIP-dependent resection of double-strand break (DSB) ends while preventing Rad51 chromatin assembly, Cdk1 (show CDK1 Proteins) inhibits both the nonhomologous and homologous modes of DSB repair during mitosis.