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SESN2 encodes a member of the sestrin family of PA26-related proteins. Additionally we are shipping Sestrin 2 Antibodies (54) and Sestrin 2 Kits (11) and many more products for this protein.
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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.
knockdown of SESN2 using small RNA interference promotes cellular toxicity of angiotensin II, as well as a reduction in cell viability, exacerbation of oxidative stress, and stimulation of apoptosis.
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 study identifies ULK1 as a new p62 Ser403 kinase and establishes Sestrin2 as a promoter of ULK1-mediated p62 phosphorylation.
Sesn2 controls reactive oxygen species-dependent neuropathic pain signaling after peripheral nerve injury.
results imply that SESN2 could serve as both a biomarker and as a drug target in the clinical management of COPD (show ARCN1 Proteins)
Ablation of Sesn2 blocked Keap1 (show KEAP1 Proteins) degradation and Nrf2 (show NFE2L2 Proteins) activation induced by refeeding and thereby increased the susceptibility of the liver to oxidative damage resulting from the acute stimulation of lipogenesis associated with refeeding.
Sestrin2--encoded by the Sesn2 locus, whose expression is induced upon hypernutrition--maintains metabolic homeostasis in liver of obese mice.
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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