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SESN1 encodes a member of the sestrin family. De plus, nous expédions Sestrin 1 Anticorps (78) et Sestrin 1 Protéines (7) et beaucoup plus de produits pour cette protéine.
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identify SESN1 as an indispensable gene for vertebrate left-right asymmetry and a new player in mediating Nodal signaling
identified new interactions between miR-200 and the oxidative stress response SESN proteins that affect anoikis resistance in human endometrial cancer cells.
mRNA expression of SESN1 was upregulated in older men.
Study shows that SESN1 mRNA, UHRF1BP11 mRNA and miRNA-377-3p levels are prognostically relevant in human papillomavirus-negative head and neck squamous cell carcinoma patients.
The antitumor efficacy of pharmacological EZH2 inhibition depends on SESTRIN1, indicating that mTORC1 control is a critical function of EZH2 in lymphoma.
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.
this study shows that sestrin1 genetic ablation results in broad reconstitution of immune function in stressed T cells and enhanced vaccine responsiveness in old mice
Rapamycin may prohibit sestrin1 downregulation through targeting mTORC2 in appeasing low shear stress induced EC oxidative apoptosis
PA26 mutations are an infrequent cause of heterotaxia (situs inversus) in humans.
results show that sestrins, a family of proteins whose expression is modulated by p53, are required for regeneration of peroxiredoxins containing Cys-SO(2)H
Sestrin 1 targets at the AMPK/mTORC1/autophagy pathway to inhibit cardiac hypertrophy by interaction with AMPK which is responsible for autophagy regulation. Taken together, our data indicate that Sestrin 1 regulates AMPK/mTORC1/autophagy axis to attenuate cardiac hypertrophy.
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.
The enhanced tumor susceptibility of p53+/- mice has made them one of several transgenic mouse models that are being considered as substitutes for standard 2-year rodent carcinogenicity assays.
Sestrin1 and Sestrin2 therefore provide an important link between genotoxic stress, p53 and the mTOR signaling pathway.
This gene encodes a member of the sestrin family. Sestrins are induced by the p53 tumor suppressor protein and play a role in the cellular response to DNA damage and oxidative stress. The encoded protein mediates p53 inhibition of cell growth by activating AMP-activated protein kinase, which results in the inhibition of the mammalian target of rapamycin protein. The encoded protein also plays a critical role in antioxidant defense by regenerating overoxidized peroxiredoxins, and the expression of this gene is a potential marker for exposure to radiation. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
, nuclear factor XPA26-T2
, p53 activated gene 26
, p53 regulated PA26 nuclear protein
, p53 regulated Pa26 nuclear protein
, p53-regulated protein PA26
, sestrin 1,nuclear factor XPA26-T2