anti-Sestrin 2 (SESN2) Antibodies

Human Sestrin 2 (SESN2) interaction partners

1. Sesn2 ablation increased UVA-induced Nrf2 (show GABPA Antibodies) induction and inhibits UVA-induced ROS (show ROS1 Antibodies) production, indicating that Sesn2 acts as an upstream regulator of Nrf2 (show GABPA Antibodies)

2. tribbles (show TRIB1 Antibodies) pseudokinase 3(TRB3 (show TAS2R13 Antibodies)) 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

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

4. These results suggest that sestrin 2 suppresses CRC (show CALR Antibodies) cell growth through activation of the AMPK (show PRKAA1 Antibodies)/mTORC1 pathway and induction of apoptosis, and could be a novel pharmacological target for the treatment of CRC (show CALR Antibodies).

5. This study shows that differential Sestrin2-mediated regulation of mTORC1 and mTORC2 (show CRTC2 Antibodies) is necessary for the survival of glutamine (show GFPT1 Antibodies)-depleted lung cancer cells.

6. 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.

7. isorhapontigenin treatment induces autophagy and inhibits bladder cancer growth through MAPK8 (show MAPK8 Antibodies)-JUN (show JUN Antibodies)-dependent transcriptional induction of SESN2

8. The results suggest that SESN2 increases degradation of HIF-1A (show HIF1A Antibodies) via AMPK (show PRKAA1 Antibodies)-PHD (show PDC Antibodies) regulation that contributes to inhibition of in vitro and in vivo tumorigenesis.

9. simple analysis of the reported "apo (show C9orf3 Antibodies)"-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.

10. Mass spectrometry analysis, western blot and surface plasmon resonance (SPR (show SPR Antibodies)) of affinity purified sesn1 (show SESN1 Antibodies) and sesn2 proteins confirmed their identity; biophysical characteristics were observed using circular dichroism (CD) showing that sesn1 (show SESN1 Antibodies) and sesn2 have a predominant a-helical structure.

Mouse (Murine) Sestrin 2 (SESN2) interaction partners

1. 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

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

3. While acute aerobic exercise increased Sesn1 (show SESN1 Antibodies) accumulation and induced a discrete augment of Sesn2 protein content and AMPK (show PRKAA1 Antibodies) threonine phosphorylation, chronic exercise reduced the basal levels of Sesn1 (show SESN1 Antibodies) and Sesn2 as well as of AMPK (show PRKAA1 Antibodies) threonine phosphorylation in the quadriceps muscles of C57BL/6J mice.

4. sestrin2 has a role in suppressing sepsis by inducing mitophagy and inhibiting NLRP3 (show NLRP3 Antibodies) activation in macrophages

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

6. Decreased Sesn2 levels in aging lead to a blunted ischemic AMPK (show PRKAA1 Antibodies) activation, alterations in substrate metabolism, and an increased sensitivity to ischemic insults.

7. p53 (show TP53 Antibodies)-dependent coordination with SESN2 regulates AMPK (show PRKAA1 Antibodies) and mTORC1 signaling and controls parturition timing

8. Our findings further revealed that Sesn2-induced autophagy contributed to restore the impaired insulin (show INS Antibodies) signaling through the activation of AMPK (show PRKAA1 Antibodies) signal. Even in the presence of palmitate, Sesn2 up-regulation maintained insulin (show INS Antibodies) sensitivity and glucose metabolism via AMPK (show PRKAA1 Antibodies)-dependent autophagic activation.

9. Oleanolic acid can attenuate hepatic ischemia reperfusion injury via HO-1 (show HMOX1 Antibodies)/Sesn2 signaling pathway.

10. suggest that TLR-mediated Sesn2 induction is dependent on AP-1 (show JUN Antibodies), Nrf2 (show NFE2L2 Antibodies), and the inhibition of ubiquitin-mediated degradation of Sesn2 and might protect cells against endotoxin toxicity