Sestrin 3 Proteins (SESN3)

Human Sestrin 3 (SESN3) interaction partners

1. Results suggest that Sesn3 is a target gene for rno-miR-155. Moreover, the rno-miR-155 antagonist may induce the expression of Sesn3, and then indirectly decrease the damage of oxidative stress to protect the brain from epileptogenesis-associated impairments.

2. The expression of SESN3 and (TSC2 and FOXO1) was identified in Lewy bodies from brainstem.

3. in FOXO3-death-resistant cells no point mutations in the TP53-DBD were found-in these cells FOXO3-TP53 complexes are formed and FOXO3-binding to the BIM-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 (NB)cells

4. Treatment with cucurbitacin B to sestrin-3 siRNA treated EGFR-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.

5. study revealed high confidence set of BMos (integrated with DNase I 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. TF-TF network analysis established hubs of interaction that include SMAD3, TCF3, SMAD2, HDAC2, SOX2, TAL1 and TCF12 as well as the likely protein complexes formed between them

6. SESN3 positively regulates the gene network module in macrophages, microglia and neurons.

7. Suggest that inhibitory effect of ethanol on Sesn3 may play an important role in the development of ethanol-induced fatty liver.

8. findings suggest the existence of a novel mechanism for the generation of antileukemic responses in CML cells, involving upregulation of SESN3 expression.

9. Sestrin 3 is upregulated in T2D and could influence skeletal muscle differentiation without altering glucose and lipid metabolism.

10. HSF1/SESN3/reactive oxygen species/p21(Cip1/WAF1)-mediated deceleration of cell growth may contribute to cell defense systems protecting the organism from excessive proliferation of cells that overexpress activated Ras oncoproteins.

11. FoxOs inhibit mTORC1 and activate Akt by inducing the expression of Sestrin3 and Rictor

Mouse (Murine) Sestrin 3 (SESN3) interaction partners

1. Sesn3 liver-specific knockout mice exhibit insulin resistance and glucose intolerance. Sesn3 interacts with and activates mTORC2 and subsequently stimulates Akt phosphorylation at Ser473.

2. 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.

3. Suggest that inhibitory effect of ethanol on Sesn3 may play an important role in the development of ethanol-induced fatty liver.

4. Concomitant ablation of Sesn2 and Sesn3 provokes hepatic mTORC1-S6K activation and insulin resistance even in the absence of nutritional overload and obesity.

5. FoxOs inhibit mTORC1 and activate Akt by inducing the expression of Sestrin3 and Rictor