anti-REV3L (REV3L) Antikörper

Human REV3-Like, Polymerase (DNA Directed), Zeta, Catalytic Subunit (REV3L) Interaktionspartner

1. These data provide a model whereby interbase H-bonding interactions at the DNA terminus promote lesion bypass and extension by human DNA polymerase zeta.

2. Results suggest a pivotal role of miR29a in mediating NSCLC cell sensitivity towards cisplatin through the regulation of REV3L.

3. We have identified and characterised a novel DNA damage response mechanism in melanoma. Instead of increasing levels of RAD51 on encountering cisplatin-induced interstrand crosslinks during replication, melanoma cells shut down RAD51 synthesis and instead boost levels of translesion synthesis DNA polymerase zeta to allow replication to proceed

4. Following challenge with AFB1, survival of mouse cells deficient in pol zeta (Rev3L(-/-)) was significantly reduced relative to Rev3L(+/-) cells or Rev3L(-/-) cells complemented through expression of the wild-type human REV3L

5. These results demonstrate a previously unrecognized relationship between p53 and REV3L in cancer cell metabolism and may lead to improvements in chemotherapy treatment plans that reduce cisplatin resistance in lung cancer.

6. REV3/ATR knockdown enhances the cytotoxicity of cisplatin in non-small cell lung cells.

7. The data directly show that, in the human genome, DNA Pol-eta and Rev1 bypass cyclobutane pyrimidine dimers and 6-4PP at replication forks, while only 6-4PP are also tolerated by a Rev3L-dependent gap-filling mechanism, independent of S phase.

8. The results indicate that human DNA polymerase zeta plays important roles in induction of mutations, clastogenicity and in cellular survival of the damaged human cells.

9. loss-of-function of REV3L dramatically enhanced the sensitivity of SCCHN cells to dacomitinib by the loss of both translesion synthesis and homologous recombination pathways.

10. REV3L plays an important role in esophageal squamous cell carcinoma (ESCC) progression and chemoresistance, and is a potential diagnostic marker and therapeutic target for ESCC

11. REV3 functions in mammalian mitochondria and that mitochondrial REV3 is associated with the tumorigenic potential of cells.

12. Taken together, we demonstrated that inhibition of REV3L sensitized lung cancer H1299 cells to cisplatin treatment

13. finding that PLXND1 and REV3L mutations are responsible for a proportion of MBS patients suggests that de novo mutations in other genes might account for other MBS patients

14. data suggest that REV3L plays an important role in regulating cervical cancer cellular response to cisplatin

15. Rev3, the catalytic subunit of polymerase zeta (Pol zeta), is involved in DNA replication under conditions of replication stress caused by deoxyribonucleotide shortage and/or imbalance in human lung adenocarcinoma cells.

16. Single nucleotide polymorphisms in RBPJ, IL1R1, REV3L, TRAF3IP2, IRF1 and ICOS showed association with rheumatoid arthritis in black South Africans.

17. Our results suggest for the first time that REV1 and REV3L SNPs might serve as potential predictive markers of outcome of cisplatin-based chemotherapy

18. Human Pol eta inserts a nucleotide opposite the lesion, followed by Pol zeta extending the DNA primer; thus, the two complement each other to fully bypass the cisplatin cross-link.

19. DNA polymerase zeta is a predictor of poor prognosis for cervical cancer patients who are resistant to chemoradiation.

20. A long-term depletion of Rev3 in cultured human cells results in massive genomic instability and severe cell cycle arrest.

Mouse (Murine) REV3-Like, Polymerase (DNA Directed), Zeta, Catalytic Subunit (REV3L) Interaktionspartner

1. Following challenge with AFB1, survival of mouse cells deficient in pol zeta (Rev3L(-/-)) was significantly reduced relative to Rev3L(+/-) cells or Rev3L(-/-) cells complemented through expression of the wild-type human REV3L

2. A single aspartate mutation in the conserved catalytic site of Rev3L generates a hypomorphic phenotype in vivo and in vitro.

3. the functions of REV3L in maintaining cell viability, embryonic viability and genomic stability are directly dependent on its polymerase activity, and cannot be ameliorated by an additional deletion of pol eta

4. results can be unified by a model in which slowly dividing cells accumulate replication-associated DNA breaks but otherwise survive Rev3L deletion, but functional polzeta is essential for responses requiring rapid proliferation

5. Structural basis of Rev1-mediated assembly of a quaternary vertebrate translesion polymerase complex consisting of Rev1, heterodimeric polymerase (Pol) zeta, and Pol kappa

6. DNA polymerase zeta generates tandem mutations in immunoglobulin variable regions

7. Pol zeta was determined to be necessary for proliferation of normal cells using conditions in which Rev3L could be conditionally inactivated by Cre recombinase.

8. REV7 subunit of pol zeta mediated the interaction between REV3 and the REV1 C terminus.

9. In the presence of reduced levels of Rev3, an essential component of Polzeta, tumors exhibited pronounced sensitivity to cisplatin, leading to a significant extension in overall survival of treated recipient mice.

10. found that Rev3 is important for a post-replication repair pathway of helix-distorting [6-4]pyrimidine-pyrimidone photoproducts

11. Involvement of mouse Rev3 in tolerance of endogenous and exogenous DNA damage

12. An essential role for REV3 in cell survival: absence of REV3 induces p53-independent embryonic death

13. data support a central role for DNA polymerase eta in the error-free bypass of UV photoproducts

14. Immortalized mouse cell lines that lack a functional Rev3 gene are hypersensitive to UV irradiation and cisplatin treatment.

15. REV3 and REV1 play major roles in recombination-independent repair of DNA interstrand cross-links mediated by monoubiquitinated PCNA

16. Pol zeta ablation in B cells impairs the germinal center reaction, class switch recombination, DNA break repair, and genome stability.