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SESN3 encodes a member of the sestrin family of stress-induced proteins. Zusätzlich bieten wir Ihnen Sestrin 3 Antikörper (71) und Sestrin 3 Kits (22) und viele weitere Produktgruppen zu diesem Protein an.
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in FOXO3 (zeige FOXO3 Proteine)-death-resistant cells no point mutations in the TP53 (zeige TP53 Proteine)-DBD were found-in these cells FOXO3 (zeige FOXO3 Proteine)-TP53 (zeige TP53 Proteine) complexes are formed and FOXO3 (zeige FOXO3 Proteine)-binding to the BIM (zeige BCL2L11 Proteine)-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 (zeige ARHGEF16 Proteine) (NB)cells
Treatment with cucurbitacin B to sestrin-3 siRNA treated EGFR (zeige EGFR Proteine)-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 (zeige DNASE1 Proteine) 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 (zeige HNF4A Proteine). TF-TF network analysis established hubs of interaction that include SMAD3 (zeige SMAD3 Proteine), TCF3 (zeige TCF3 Proteine), SMAD2 (zeige SMAD2 Proteine), HDAC2 (zeige HDAC2 Proteine), SOX2 (zeige SOX2 Proteine), TAL1 (zeige TAL1 Proteine) and TCF12 (zeige TCF12 Proteine) 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 (zeige BCR Proteine) 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 (zeige HSF1 Proteine)/SESN3/reactive oxygen species/p21(Cip1/WAF1 (zeige CDKN1A Proteine))-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 by inducing the expression of Sestrin3 and Rictor
Sesn3 liver-specific knockout mice exhibit insulin (zeige INS Proteine) resistance and glucose intolerance. Sesn3 interacts with and activates mTORC2 (zeige CRTC2 Proteine) and subsequently stimulates Akt (zeige AKT1 Proteine) phosphorylation at Ser473.
Study found that Sestrins (1,2 and 3) can inhibit mTORC1 signaling in the absence of AMPK (zeige PRKAA1 Proteine) or TSC2. Surprisingly, when coexpressed with a GTP (zeige AK3 Proteine)-bound constitutively active form of RagB (zeige RRAGB Proteine) (RagBQ99L), Sestrins potentiate mTORC1 signaling in the absence of amino acids.
Concomitant ablation of Sesn2 (zeige SESN2 Proteine) and Sesn3 provokes hepatic mTORC1-S6K (zeige RPS6KB1 Proteine) activation and insulin (zeige INS Proteine) 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