Browse our anti-Retinoblastoma Binding Protein 8 (RBBP8) Antibodies

Human Retinoblastoma Binding Protein 8 (RBBP8) interaction partners

1. HGF/c-Met regulates expression of SAE2 and cirRNA CCDC66 to increase epithelial-to-mesenchymal transition and drug resistance of lung adenocarcinoma cells.

2. We propose that BRCA1-CTIP and MRE11 prepare nascent DNA ends, blocked from synthesis by CTNAs, for further repair.

3. Data sufgest that polo like kinase 1 (PLK1) may target retinoblastoma binding protein 8 (RBBP8; CtIP) to promote error-prone microhomology-mediated end joining (MMEJ) and inactivate the G2/M checkpoint.

4. Bioinformatics predicted the putative binding site of miR18a5p in the 3' untranslated region of CtIP/RBBP8. Study using nasopharyngeal carcinoma cell line further confirmed that miR18a5p could directly bind with RBBP8 and inhibit RBBP8 expression.

5. Data demonstrate that RBBP8 is almost exclusively methylated in 45% primary bladder cancer, suggesting the development of methylation in a distinct molecular context. A close association between RBBP8 methylation and its gene expression in primary tumors as well as after demethylation treatment in vitro indicate that RBBP8 methylation could be responsible for its gene inactivation.

6. Study identifies the KLHL15 as a new interaction partner of CtIP and show that KLHL15 promotes CtIP protein turnover via the ubiquitin-proteasome pathway.

7. ATM-dependent phosphorylation of CtIP and the epistatic and coordinated actions of MRE11 and CtIP nuclease activities are required to limit the stable loading of Ku on single-ended DNA double-strand breaks.

8. 53BP1/RIF1 has a role in limiting BRCA1/CtIP-mediated end resection to control double strand break repair pathway choice

9. 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.

10. Data show that SUMO E3 ligase CBX4 sumoylates subpopulation of CtIP to regulate recruitment to breaks and resection.

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

12. Data delineates the regulatory mechanisms of GATA3 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.

13. The results illuminate the important role of Nbs1 and CtIP in determining the substrates and consequences of human Mre11/Rad50 nuclease activities on protein-DNA lesions.

14. 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.

15. his shows that 53BP1 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-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

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

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

18. USP4 cooperates with CtIP in DNA double-strand break end resection.

19. CtIP is a DNA damage response protein at the intersection of DNA metabolism. (Review)

20. Data show that ubiquitin E2 enzymes UBE2D1/2/3 and E3 ligase RNF138 accumulate at DNA-damage sites and act at early resection stages by promoting CtIP protein ubiquitylation and accrual.

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

1. CtIP enhances long-range resection by BLM-DNA2-RPA. CtIP interacts with and stimulates the activity of the BLM helicase and upregulates DNA2 activity.

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

3. 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.

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

5. Ctip1 couples subtype and area specification, enabling specific functional areas to organize precise ratios of appropriate output projections.

6. work therefore ascribes novel roles for BRCA1 and CtIP in end-processing and fusion reactions at uncapped telomeres

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

8. The phospho-dependent BRCA1-CtIP interaction is not essential for HDR-mediated DSB repair or for tumor suppression.

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

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

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

12. the histone protein H2AX prevents nucleases other than Artemis from processing hairpin-sealed coding ends; in the absence of H2AX, CtIP can efficiently promote the hairpin opening and resection of DNA ends generated by RAG cleavage

13. CtIP counteracts Rb-mediated G(1) restraint.

14. Rbbp8 is shown to be upregulated in response to X-irradiation in the AML sensitive CBA strain but not AML resistant C57BL/6 strain

15. CtiP activates its own and cyclin D promoters via the E2F/RB pathway during G1/S progression.

Xenopus laevis Retinoblastoma Binding Protein 8 (RBBP8) interaction partners

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

2. ATM 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 inhibits both the nonhomologous and homologous modes of DSB repair during mitosis.