S6K1 gene is closely related to obesity and aging

S6K1 plays a role in many key metabolic processes, and previous studies have shown that S6K1 is closely related to obesity. On Feb. 8, Spanish scientists published a report in the journal Nature, where they identified downstream effectors of mTORC1-S6K1. S6K1 kinase mediates obesity and aging in mice by affecting metabolic pathways by EPRS and FATP1. This research using recombinant human proteins will promote the development of biomarkers and promote targeted therapies for obesity and aging.

S6K1 gene can determine the number of adipocytes in our childhood, and adipose cells are differentiated from stem cells. The authors of the study, Dr. George Thomas and Dr. Sara Kozma, were heads of the Metabolic and Cancer Research Group. Their previous work has shown that S6K1 differentiates into adipocytes through transcriptional regulation of mesenchymal stem cells (MSC) and plays a key role in the expansion of adipose tissue. S6K1 can determine the number of fat cells. S6K1 tends to be active in the process of stem cell differentiation. It will inhibit the differentiation of WNT signaling in adipocytes, and ultimately promoting the differentiation of adipocytes.

The researchers found that glutamylprolyl tRNA synthetase (EPRS) can serve as a target for mTORC1-S6K1, promoting obesity and aging. MTORCl-S6Kl induces the phosphorylation of EPRS, which is released from the aminoacyl tRNA multiple synthetase complex. It is necessary to perform the unconventional function of EPRS outside of protein synthesis.

To investigate the physiological role of EPRS phosphorylation, the researchers constructed knock-in mutant mice carrying Eprs-deficient phosphate. Homozygous Eprs knock-in mutant mice showed low weight, reduced adipose tissue and prolonged lifespan, similar to the phenotype of S6K1-deficient mice and adipose tissue-deficient mice.

EPRS phosphorylation mediates S6K1-dependent metabolic reactions. In adipocytes, insulin stimulates the release of S6K1-dependent EPRS phosphorylation from multiple complex enzyme complexes. Furthermore, screening by interaction showed that phosphorylation of EPRS combined with fatty acid transporter 1 (FATP1) induced its localization on the cell membrane and stimulated the uptake of long chain fatty acids. EPRS and FATP1 are downstream effectors of mTORC1-S6K1 and are essential for the metabolic phenotype.

These findings provide further evidence that S6K1 can serve as a predictor of obesity or as a drug target for obesity suppression. Flarebio offers high-quality recombinant proteins like recombinant COLEC12 at good prices.