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SESN3 encodes a member of the sestrin family of stress-induced proteins. Additionally we are shipping Sestrin 3 Antibodies (71) and Sestrin 3 Proteins (7) and many more products for this protein.
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in FOXO3-death-resistant cells no point mutations in the TP53-DBD were found-in these cells FOXO3-TP53 complexes are formed and FOXO3-binding to the BIM-promoter, but not the induction of the detoxifying protein SESN3, were prevented, which in turn increased chemo-protection in this type of high-stage-derived neuroblastoma (NB)cells
Treatment with cucurbitacin B to sestrin-3 siRNA treated EGFR (show EGFR ELISA Kits)-mutant cells further amplified the decrease in cell-viability and caused more sustained G2-phase cell cycle arrest, suggesting that these effects are mediated partly through sestrin-3.
study revealed high confidence set of BMos (integrated with DNase I hypersensitivity sites) in the upstream regulatory regions of SESN3 that could be bound by transcription factors from multiple families including FOXOs, SMADs, SOXs, TCFs and HNF4A. TF-TF network analysis established hubs of interaction that include SMAD3, TCF3, SMAD2, HDAC2, SOX2, TAL1 and TCF12 as well as the likely protein complexes formed between them
SESN3 positively regulates the gene network module in macrophages, microglia and neurons.
Suggest that inhibitory effect of ethanol on Sesn3 may play an important role in the development of ethanol-induced fatty liver.
findings suggest the existence of a novel mechanism for the generation of antileukemic responses in CML (show BCR ELISA Kits) cells, involving upregulation of SESN3 expression.
Sestrin 3 is upregulated in T2D and could influence skeletal muscle differentiation without altering glucose and lipid metabolism.
HSF1 (show HSF1 ELISA Kits)/SESN3/reactive oxygen species/p21(Cip1/WAF1 (show CDKN1A ELISA Kits))-mediated deceleration of cell growth may contribute to cell defense systems protecting the organism from excessive proliferation of cells that overexpress activated Ras oncoproteins.
FoxOs inhibit mTORC1 and activate Akt (show AKT1 ELISA Kits) by inducing the expression of Sestrin3 and Rictor (show RICTOR ELISA Kits)
Sesn3 liver-specific knockout mice exhibit insulin (show INS ELISA Kits) resistance and glucose intolerance. Sesn3 interacts with and activates mTORC2 and subsequently stimulates Akt (show AKT1 ELISA Kits) phosphorylation at Ser473.
Study found that Sestrins (1,2 and 3) can inhibit mTORC1 signaling in the absence of AMPK or TSC2. Surprisingly, when coexpressed with a GTP-bound constitutively active form of RagB (RagBQ99L), Sestrins potentiate mTORC1 signaling in the absence of amino acids.
Concomitant ablation of Sesn2 (show SESN2 ELISA Kits) and Sesn3 provokes hepatic mTORC1-S6K (show RPS6KB1 ELISA Kits) activation and insulin (show INS ELISA Kits) resistance even in the absence of nutritional overload and obesity.
This gene encodes a member of the sestrin family of stress-induced proteins. The encoded protein reduces the levels of intracellular reactive oxygen species induced by activated Ras downstream of RAC-alpha serine/threonine-protein kinase (Akt) and FoxO transcription factor. The protein is required for normal regulation of blood glucose, insulin resistance and plays a role in lipid storage in obesity. Alternative splicing results in multiple transcript variants.
, sestrin 3