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Sestrin 1

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. [provided by RefSeq, Dec 2010] (from NCBI)
Top mentioned proteins: p53, CAN, POLYMERASE, Ros, Sestrin2
Papers on PA26
Gene expression profiling of lung adenocarcinoma in Xuanwei, China.
Zhang et al., Kunming, China. In Eur J Cancer Prev, Jan 2016
The tendency of changes in the expression of 12 selected DEGs (five downregulated genes, PIK3R1, RARB, HGF, MAPK11, and SESN1, and seven upregulated genes, PAK1, E2F1, CCNE1, EGF, CDC25A, PTTG1, and UHRF1) in RTq-PCR was consistent with the expression profiling data.
Taxonomic reassessment of N4-like viruses using comparative genomics and proteomics suggests a new subfamily - "Enquartavirinae".
Kropinski et al., Braunschweig, Germany. In Arch Virol, Dec 2015
We propose to create four new genera: "G7cvirus" (consisting of phages G7C, IME11, KBNP21, vB_EcoP_PhAPEC5, vB_EcoP_PhAPEC7, Bp4, EC1-UPM and pSb-1), "Lit1virus" (LIT1, PA26 and vB_PaeP_C2-10_Ab09), "Sp58virus" (SP058 and SP076), and "Dss3virus" (DSS3φ2 and EE36φ1).
Constitutive autophagy contributes to resistance to TP53-mediated apoptosis in Epstein-Barr virus-positive latency III B-cell lymphoproliferations.
Wiels et al., Villejuif, France. In Autophagy, Nov 2015
However the process of autophagy was only triggered in the latter and was associated with an upregulation of SESN1/sestrin 1 and inhibition of MTOR more rapid than in EBV-negative cells.
Actinomycin D and nutlin-3a synergistically promote phosphorylation of p53 on serine 46 in cancer cell lines of different origin.
Rusin et al., Gliwice, Poland. In Cell Signal, Sep 2015
Other p53 target genes (SESN1, SESN2, TIGAR, DRAM1) were also efficiently upregulated; however, a marker of apoptosis (active caspase-3) appeared only in some cancer cell lines (e.g., A375 and other cell lines derived from melanoma) indicating that phosphorylation of p53 on serine 46 is not straightforwardly associated with induction of apoptosis.
Arsenic-induced S phase cell cycle lengthening is associated with ROS generation, p53 signaling and CDC25A expression.
Garrido et al., Mexico. In Chem Biol Interact, Sep 2015
Furthermore, for the first time, we demonstrate that arsenic activates p53-dependent transcription of ROS detoxification genes, such as SESN1, and by an indirect mechanism involving ATF3, genes that could be responsible for the S phase cell cycle arrest, such as CDC25A.
Time, dose and ataxia telangiectasia mutated (ATM) status dependency of coding and noncoding RNA expression after ionizing radiation exposure.
Badie et al., United Kingdom. In Radiat Res, Mar 2015
The majority of genes investigated responded rapidly to radiation exposure, with the peak up-regulation (CDKN1A, SESN1, ATF3, MDM2, PUMA and GADD45A) or down-regulation (CCNB1) occurring 2-3 h postirradiation, while DDB2, FDXR and CCNG1 responded with slower kinetics reaching a peak of expression between 5 and 24 h.
Analysis of genes involved in response to doxorubicin and a GD2 ganglioside-specific 14G2a monoclonal antibody in IMR-32 human neuroblastoma cells.
Rokita et al., Kraków, Poland. In Acta Biochim Pol, 2014
Then, we applied western blot and analyzed levels of RPS27L, PPM1D, sestrin 1 proteins after DOX-treatment.
Oxidative stress preferentially induces a subtype of micronuclei and mediates the genomic instability caused by p53 dysfunction.
Shao et al., In Mutat Res, 2014
Depletion of p53-regulated antioxidant gene SESN1 by RNA interference also resulted in an elevation of MN-γ-H2AX (+).
Essential function of the N-termini tails of the proteasome for the gating mechanism revealed by molecular dynamics simulations.
Ishida, Kyoto, Japan. In Proteins, 2014
To understand the gating mechanism of the CP for the translocation of the substrate, four different molecular dynamics simulations were carried out: ordered- and Tyr8Gly/Asp9Gly disordered-gate models of the CP complexed with an ATP-independent PA26 and ordered- and disordered-gate models of the CP complexed with an ATP-dependent PAN-like activator.
Therapeutic delivery of miR-200c enhances radiosensitivity in lung cancer.
Welsh et al., Houston, United States. In Mol Ther, 2014
We found that miR-200c overexpression increased cellular radiosensitivity by direct regulation of the oxidative stress response genes PRDX2, GAPB/Nrf2, and SESN1 in ways that inhibits DNA double-strand breaks repair, increase levels of reactive oxygen species, and upregulate p21.
Acute L-glutamine deprivation affects the expression of TP53-related protein genes in U87 glioma cells.
Minchenko et al., In Fiziol Zh, 2013
We have studied the effect of acute L-glutamine deprivation on the expression oftumor protein 53 (TP53)-related genes such as TOPORS (topoisomerase I binding, arginine/serine-rich, E3 ubiquitin protein ligase), TP53BPI (TP53 bindingprotein 1), TP53TG1 (TP53 inducible gene 1), SESN1 (p53 regulatedPA26 nuclear protein), NME6 (NME/NM23 nucleoside diphosphate kinase 6), and ZMAT3 (zinc finger Matrin-type 3) in glioma cells with ERN1 knockdown.
Impact of α-targeted radiation therapy on gene expression in a pre-clinical model for disseminated peritoneal disease when combined with paclitaxel.
Brechbiel et al., Bethesda, United States. In Plos One, 2013
Differentially expressed genes following therapy with Pac/²¹²Pb-trastuzumab included those involved in apoptosis (BRCA1, CIDEA, GADD45α, GADD45γ, GML, IP6K3, PCBP4, PPP1R15A, RAD21, and p73), cell cycle (BRCA1, CHK1, CHK2, GADD45α, GML, GTSE1, NBN, PCBP4, PPP1R15A, RAD9A, and SESN1), and damaged DNA repair (ATRX, BTG2, EXO1, FEN1, IGHMBP2, OGG1, MSH2, MUTYH, NBN, PRKDC, RAD21, and p73).
Sesn1 is a novel gene for left-right asymmetry and mediating nodal signaling.
Devriendt et al., Leuven, Belgium. In Hum Mol Genet, 2006
identify SESN1 as an indispensable gene for vertebrate left-right asymmetry and a new player in mediating Nodal signaling
Comprehensive mass spectrometric analysis of the 20S proteasome complex.
Burlingame et al., Irvine, United States. In Methods Enzymol, 2004
Using the same approach, we also identified and characterized an activator protein, PA26, from T. brucei.
Regeneration of peroxiredoxins by p53-regulated sestrins, homologs of bacterial AhpD.
Chumakov et al., Cleveland, United States. In Science, 2004
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
PA26 is a candidate gene for heterotaxia in humans: identification of a novel PA26-related gene family in human and mouse.
Devriendt et al., Leuven, Belgium. In Hum Genet, 2003
PA26 mutations are an infrequent cause of heterotaxia (situs inversus) in humans.
The 11S regulators of 20S proteasome activity.
Whitby et al., Salt Lake City, United States. In Curr Top Microbiol Immunol, 2001
Higher resolution data are needed to discern important structural details of the PA26/20S proteasome complex.
Structural basis for the activation of 20S proteasomes by 11S regulators.
Hill et al., Salt Lake City, United States. In Nature, 2000
11S regulators (also called PA26 (ref.
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