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SESN2 encodes a member of the sestrin family of PA26-related proteins. Additionally we are shipping Sestrin 2 Antibodies (53) and Sestrin 2 Kits (17) and many more products for this protein.
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The data are the first to indicate that SESN2 might be a novel prognostic marker for hepatocellular carcinoma
The up-regulation of SESN2 by mitochondrial dysfunction requires binding to ATF4 (show ATF4 Proteins).
Sesn2 has two subdomains. The N-terminal domain reduces alkylhydroperoxide radicals through its helix-turn-helix oxidoreductase (show TXNRD1 Proteins) motif, and the C-terminal domain interacts with GATOR2 and subsequently inhibits mTORC1.
SESN2-AMPK (show PRKAA1 Proteins) signaling could exert a protective effect against glucose deprivation-induced cell death and that this effect is mediated by restoration of mitochondrial function.
Sesn2 is a potential tumor suppressor in lung epithelial cells. The expression level of Sesn2 may serve as a prognostic marker for Chinese lung cancer patients in the clinic.
The findings suggested that a decreased expression of sestrin 2 is associated with an unfavorable prognosis, which suggests that it is a novel and crucial predictor for colorectal cancer metastasis.
an AMPK (show PRKAA1 Proteins)-independent mechanism of mTORC1 inhibition by Sestrins mediated by their interaction with GATOR2, is reported.
GAA (show GAA Proteins) promotes FoxO3 (show FOXO3 Proteins) nuclear translocation and binding to the SESN2 enhancer.
Data indicate that inactivation of Sestrin 2 (Sesn2) or nuclear factor erythroid 2-related factor 2 (Nrf2 (show NFE2L2 Proteins)) induced reactive oxygen species-mediated proteasomal inhibition and platelet-derived growth factor receptor beta (show PDGFRB Proteins) (Pdgfrbeta) accumulation.
Sesn2 is oncogenic in skin squamous cell carcinoma and melanoma.
SESN2 suppressed ER stress-mediated apoptosis. SESN2 attenuated hepatic injury in mice.
Decreased Sesn2 levels in aging lead to a blunted ischemic AMPK (show PRKAA1 Proteins) activation, alterations in substrate metabolism, and an increased sensitivity to ischemic insults.
p53 (show TP53 Proteins)-dependent coordination with SESN2 regulates AMPK (show PRKAA1 Proteins) and mTORC1 signaling and controls parturition timing
Our findings further revealed that Sesn2-induced autophagy contributed to restore the impaired insulin (show INS Proteins) signaling through the activation of AMPK (show PRKAA1 Proteins) signal. Even in the presence of palmitate, Sesn2 up-regulation maintained insulin (show INS Proteins) sensitivity and glucose metabolism via AMPK (show PRKAA1 Proteins)-dependent autophagic activation.
Oleanolic acid can attenuate hepatic ischemia reperfusion injury via HO-1 (show HMOX1 Proteins)/Sesn2 signaling pathway.
suggest that TLR-mediated Sesn2 induction is dependent on AP-1 (show JUN Proteins), Nrf2 (show NFE2L2 Proteins), and the inhibition of ubiquitin-mediated degradation of Sesn2 and might protect cells against endotoxin toxicity
Study found that Sestrins (1,2 and 3) can inhibit mTORC1 signaling in the absence of AMPK (show PRKAA1 Proteins) or TSC2. Surprisingly, when coexpressed with a GTP (show AK3 Proteins)-bound constitutively active form of RagB (show RRAGB Proteins) (RagBQ99L), Sestrins potentiate mTORC1 signaling in the absence of amino acids.
Sestrin2 plays an important role in cardioprotection against I/R injury, serving as an LKB1 (show STK11 Proteins)-AMPK (show PRKAA1 Proteins) scaffold to initiate AMPK (show PRKAA1 Proteins) activation during ischemic insults
Data indicate that sestrin2 expression is upregulated by dopamine D2 receptor (show DRD2 Proteins).
This gene encodes a member of the sestrin family of PA26-related proteins. The encoded protein may function in the regulation of cell growth and survival. This protein may be involved in cellular response to different stress conditions.
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