Recently I am researching about HISTONE H2AX; BRCT DOMAINS; S-PHASE; DNA; PROTEIN; REPAIR; MDC1; LOCALIZATION; LIGASE; REGION, Saw an article supported by the National Institute of HealthUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) – USA [R21CA184996, P20GM121316, P30CA036727, T32CA009476]; NATIONAL CANCER INSTITUTEUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) – USANIH National Cancer Institute (NCI) [P30CA036727, T32CA009476] Funding Source: NIH RePORTER; NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCESUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) – USANIH National Institute of General Medical Sciences (NIGMS) [P20GM121316] Funding Source: NIH RePORTER. Product Details of 61-82-5. Published in MDPI in BASEL ,Authors: Krieger, KL; Hu, WF; Ripperger, T; Woods, NT. The CAS is 61-82-5. Through research, I have a further understanding and discovery of 1H-1,2,4-Triazol-5-amine
Deleterious mutations in Breast Cancer 1 (BRCA1) are associated with an increased risk of breast and ovarian cancer. Mutations in the tandem BRCA1 C-terminal (tBRCT) protein domain disrupt critical protein interactions required for the faithful repair of DNA through homologous recombination, which contributes to oncogenesis. Our studies have identified RICTOR, PRR5, and SIN1 subunits of the mammalian target of rapamycin complex 2 (mTORC2) as interacting partners with the tBRCT domain of BRCA1 leading to the disruption of the mTORC2 complex. However, the interplay between mTORC2 signaling and BRCA1 function in the DNA damage response (DDR) remains to be determined. In this study, we used protein interaction assays to determine the binary interactions between the tBRCT domain and mTORC2 subunits, evaluated the impact of mTOR inhibition on the transcriptional function of the tBRCT, evaluated the impact of mTOR signaling on BRCA1 recruitment to DNA damage-induced foci and determined the breast cancer cell line response to mTOR inhibition dependent upon BRCA1 expression and mutation. This study determined that PRR5, RICTOR, and SIN1 could each independently interact with the BRCA1 tBRCT. Inhibition of mTORC1, but not mTORC1/2, increases BRCA1 transcriptional activation activity. Treatment with pan-mTOR inhibitor PP242 diminishes DNA damage-induced gamma H2AX and BRCA1 foci formation. Breast cancer cells lacking expression of functional BRCA1 are more sensitive to mTOR inhibitors. These data suggest that mTOR signaling is required for BRCA1 response to DNA damage and breast cancer cells lacking BRCA1 are more sensitive to pan-mTOR inhibition. This work suggests chemotherapeutic strategies using mTOR inhibitors could be tailored for patients that lack functional BRCA1.
Welcome to talk about 61-82-5, If you have any questions, you can contact Krieger, KL; Hu, WF; Ripperger, T; Woods, NT or send Email.. Product Details of 61-82-5
Reference:
Article; Safari, Niloufar; Shirini, Farhad; Tajik, Hassan; Journal of Molecular Structure; vol. 1201; (2020);,
1,2,3-Triazole – Wikipedia,
Triazoles – an overview | ScienceDirect Topics