anti-Sestrin 2 (SESN2) Antibodies

Human Sestrin 2 (SESN2) interaction partners

1. High serum Sestrin 2 levels are associated with metabolic synfrome.

2. Knockdown of sesn2 aggravates atherosclerotic processes by increasing pro-inflammatory reactions and ER stress in the endothelium via an AMPK-dependent mechanism, suggesting that sesn2 might be a novel therapeutic target for atherosclerosis.

3. SESN2 is critical to protect cells against detrimental effect of mitochondrial damage and RBX1 is a negative regulator of SESN2 which hampers its stabilization.

4. Sesn2 ablation increased UVA-induced Nrf2 induction and inhibits UVA-induced ROS production, indicating that Sesn2 acts as an upstream regulator of Nrf2

5. tribbles pseudokinase 3(TRB3) and sestrin 2 may contribute to the development of obesity and its complications and can be considered interesting therapeutic target for the treatment of obesity

6. Overexpression of Sesn2 downregulated the expression of autophagy genes, upregulated pro-apoptotic gene expression, and downregulated specific extracellular matrix markers in stress-induced cells.

7. These results suggest that sestrin 2 suppresses CRC cell growth through activation of the AMPK/mTORC1 pathway and induction of apoptosis, and could be a novel pharmacological target for the treatment of CRC.

8. This study shows that differential Sestrin2-mediated regulation of mTORC1 and mTORC2 is necessary for the survival of glutamine-depleted lung cancer cells.

9. There was significant overexpression of serum sesn2 protein and mRNA levels in the Alzheimer's Disease group compared to Mild Cognitive Impairment and the control group.

10. isorhapontigenin treatment induces autophagy and inhibits bladder cancer growth through MAPK8-JUN-dependent transcriptional induction of SESN2

11. The results suggest that SESN2 increases degradation of HIF-1A via AMPK-PHD regulation that contributes to inhibition of in vitro and in vivo tumorigenesis.

12. simple analysis of the reported "apo"-Sestrin2 structure reveals the clear presence of prominent, unmodeled electron density in the leucine-binding pocket that exactly accommodates the leucine observed in the higher resolution structure.

13. Mass spectrometry analysis, western blot and surface plasmon resonance (SPR) of affinity purified sesn1 and sesn2 proteins confirmed their identity; biophysical characteristics were observed using circular dichroism (CD) showing that sesn1 and sesn2 have a predominant a-helical structure.

14. the results support a model in which leucine selectively promotes dephosphorylation of Sestrin2.

15. The data are the first to indicate that SESN2 might be a novel prognostic marker for hepatocellular carcinoma

16. These results highlight Sestrin2 as a novel tumor suppressor, whose downregulation can accelerate both colitis and colon carcinogenesis.

17. The up-regulation of SESN2 by mitochondrial dysfunction requires binding to ATF4.

18. Sestrin2 silencing strongly inhibits cytokine-induced cell death.

19. Sesn2 has two subdomains. The N-terminal domain reduces alkylhydroperoxide radicals through its helix-turn-helix oxidoreductase motif, and the C-terminal domain interacts with GATOR2 and subsequently inhibits mTORC1.

20. Sestrin2 inhibits mTORC1 through modulation of GATOR complexes

Mouse (Murine) Sestrin 2 (SESN2) interaction partners

1. Sestrin 2 may attenuate the activation of Hepatic Stellate Cell and ameliorate liver fibrosis, most likely via upregulation of AMPK phosphorylation and suppression of the mTOR signaling pathway.

2. sesn2 has a role in lipopolysaccharide-induced oxidative stress in mice and in H9c2 cells

3. Knockdown of sesn2 aggravates atherosclerotic processes by increasing pro-inflammatory reactions and ER stress in the endothelium via an AMPK-dependent mechanism, suggesting that sesn2 might be a novel therapeutic target for atherosclerosis.

4. Sesn2/AMPK/mTOR signaling mediates balance between survival and apoptosis in sensory hair cells under stress.

5. Sesn2 KO mice displayed enhanced expression of proinflammatory genes and activation of basilar membrane macrophages, suggesting that loss of SESN2 function provokes the immune response

6. Aerobic physical exercise recovers Sestrin 2 protein content and induces autophagy in the skeletal muscle of old mice.

7. While acute aerobic exercise increased Sesn1 accumulation and induced a discrete augment of Sesn2 protein content and AMPK threonine phosphorylation, chronic exercise reduced the basal levels of Sesn1 and Sesn2 as well as of AMPK threonine phosphorylation in the quadriceps muscles of C57BL/6J mice.

8. sestrin2 has a role in suppressing sepsis by inducing mitophagy and inhibiting NLRP3 activation in macrophages

9. SESN2 suppressed ER stress-mediated apoptosis. SESN2 attenuated hepatic injury in mice.

10. Decreased Sesn2 levels in aging lead to a blunted ischemic AMPK activation, alterations in substrate metabolism, and an increased sensitivity to ischemic insults.

11. p53-dependent coordination with SESN2 regulates AMPK and mTORC1 signaling and controls parturition timing

12. Our findings further revealed that Sesn2-induced autophagy contributed to restore the impaired insulin signaling through the activation of AMPK signal. Even in the presence of palmitate, Sesn2 up-regulation maintained insulin sensitivity and glucose metabolism via AMPK-dependent autophagic activation.

13. Oleanolic acid can attenuate hepatic ischemia reperfusion injury via HO-1/Sesn2 signaling pathway.

14. propose that Sestrin2 protects cells from glucose starvation-induced cell death via regulation of mitochondrial homeostasis

15. Sestrin2 involved in the regulation of cardiomyopathy (such as myocardial fibrosis) after irradiation

16. Sestrin2 inhibits mTORC1 through modulation of GATOR complexes

17. suggest that TLR-mediated Sesn2 induction is dependent on AP-1, Nrf2, and the inhibition of ubiquitin-mediated degradation of Sesn2 and might protect cells against endotoxin toxicity

18. Sestrin2 has a hepatoprotective role against chronic ER stress

19. an AMPK-independent mechanism of mTORC1 inhibition by Sestrins mediated by their interaction with GATOR2, is reported.

20. 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.