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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 18 Mar 2014.

Signal transducer and activator of transcription 2, 113kDa

STAT2
The protein encoded by this gene is a member of the STAT protein family. In response to cytokines and growth factors, STAT family members are phosphorylated by the receptor associated kinases, and then form homo- or heterodimers that translocate to the cell nucleus where they act as transcription activators. In response to interferon (IFN), this protein forms a complex with STAT1 and IFN regulatory factor family protein p48 (ISGF3G), in which this protein acts as a transactivator, but lacks the ability to bind DNA directly. Transcription adaptor P300/CBP (EP300/CREBBP) has been shown to interact specifically with this protein, which is thought to be involved in the process of blocking IFN-alpha response by adenovirus. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Mar 2010] (from NCBI)
Top mentioned proteins: STAT1, STAT3, CAN, IFN-gamma, Janus kinase
Papers on STAT2
Genetic manipulation of the ApoF/Stat2 locus supports an important role for type I interferon signaling in atherosclerosis.
New
Rader et al., Philadelphia, United States. In Atherosclerosis, 31 Mar 2014
These effects were attributable to hypomorphic expression of Stat2 in the ApoF KO mice, a critical gene in the Type I IFN pathway that is situated just 425 base pairs downstream of ApoF.
Downregulation of microRNA-431 by human interferon-β inhibits viability of medulloblastoma and glioblastoma cells via upregulation of SOCS6.
New
Yokosuka et al., Chiba, Japan. In Int J Oncol, 28 Mar 2014
Addition of HuIFN-β and transient transfection with miR-431 to medulloblastoma and glioblastoma cells did not reduce viability, downregulated expression of SOCS6, and concomitantly activated the JAK1 and STAT2.
3Cpro of FMDV antagonizes IFN signaling pathway by blocking STAT1/STAT2 nuclear translocation.
New
Wang et al., Jinan, China. In J Virol, 19 Mar 2014
The protein level, tyrosine phosphorylation of STAT1 and STAT2 and their heterodimerization were not affected.
Respiratory Syncytial Virus NS1 Protein Degrades STAT2 by Inducing SOCS1 Expression.
New
Zhao et al., Wuhan, China. In Intervirology, 25 Feb 2014
STAT2 and pSTAT2 expression was determined with Western blotting.
Innate Immunity to Dengue Virus Infection and Subversion of Antiviral Responses.
Review
New
Harris et al., Berkeley, United States. In J Mol Biol, Jan 2014
Finally, DENV NS2A, NS4A, and NS4B complex together to block STAT1 phosphorylation, while NS5 binds and promotes degradation of human STAT2, thus preventing formation of the STAT1/STAT2 heterodimer and its transcriptional induction of interferon stimulating genes.
IL-4 Suppresses the Responses to TLR7 and TLR9 Stimulation and Increases the Permissiveness to Retroviral Infection of Murine Conventional Dendritic Cells.
New
Gallucci et al., Philadelphia, United States. In Plos One, Dec 2013
IL-4 also inhibited IFN-dependent MHC Class I expression and amplification of IFN signaling pathways triggered upon TLR stimulation, as indicated by the suppression of IRF7 and STAT2.
STATs get their move on.
Review
New
Reich, Stony Brook, United States. In Jakstat, Nov 2013
Following STAT2 tyrosine phosphorylation, it can form dimers with STAT1 to affect nuclear import as the trimeric complex (ISGF3).
STAT2 phosphorylation and signaling.
Review
New
Gamero et al., Philadelphia, United States. In Jakstat, Nov 2013
Evidence of additional STAT2 phosphorylation sites has emerged as well as novel roles for STAT2 separate from the classical ISGF3-signaling.
STAT2 and IRF9: Beyond ISGF3.
Review
New
Grandvaux et al., Montréal, Canada. In Jakstat, Nov 2013
Among STATs, STAT2 is classically known to dimerize with STAT1 and together with IRF9 forms the ISGF3 transcription factor complex that has long been considered a hallmark of activation by type I and type III interferons.
Paramyxovirus evasion of innate immunity: Diverse strategies for common targets.
Review
New
Moseley et al., Australia. In World J Virol, Jun 2013
Although paramyxovirus IFN antagonists generally target common factors of the IFN system, including melanoma differentiation associated factor 5, retinoic acid-inducible gene-I, signal transducers and activators of transcription (STAT)1 and STAT2, and IFN regulatory factor 3, the mechanisms of antagonism show remarkable diversity between different genera and even individual members of the same genus; the reasons for this diversity, however, are not currently understood.
A variant upstream of IFNL3 (IL28B) creating a new interferon gene IFNL4 is associated with impaired clearance of hepatitis C virus.
New
Impact
O'Brien et al., Bethesda, United States. In Nat Genet, Feb 2013
Transient overexpression of IFNL4 in a hepatoma cell line induced STAT1 and STAT2 phosphorylation and the expression of interferon-stimulated genes.
A haplotype at STAT2 Introgressed from neanderthals and serves as a candidate of positive selection in Papua New Guinea.
GeneRIF
Hammer et al., Tucson, United States. In Am J Hum Genet, 2012
A haplotype at STAT2 introgressed from neanderthals serves as a candidate of positive selection in Papua New Guinea.
HSV-2 inhibits type-I interferon signaling via multiple complementary and compensatory STAT2-associated mechanisms.
GeneRIF
Foster et al., New Orleans, United States. In Virus Res, 2012
These results indicate the importance that herpes simplex virus 2 has assigned to STAT2, investing significant genomic currency throughout its replicative lifecycle for continuous targeted destruction and inhibition of this protein.
Mice deficient in STAT1 but not STAT2 or IRF9 develop a lethal CD4+ T-cell-mediated disease following infection with lymphocytic choriomeningitis virus.
GeneRIF
Campbell et al., Sydney, Australia. In J Virol, 2012
STAT1, not STAT2 or IRF9, prevent the emergence of a lethal antiviral CD4(+) T-cell response after lymphocytic choriomeningitis virus infection.
The JAK-STAT pathway at twenty.
Review
Impact
Darnell et al., Cleveland, United States. In Immunity, 2012
We look back on the discoveries that the tyrosine kinases TYK2 and JAK1 and the transcription factors STAT1, STAT2, and IRF9 are required for the cellular response to type I interferons.
Gene expression profile reveals that STAT2 is involved in the immunosuppressive function of human bone marrow-derived mesenchymal stem cells.
GeneRIF
Song et al., Inch'ŏn, South Korea. In Gene, 2012
STAT2 is functionally involved in the immunosuppressive activity of hcMSCs as a novel regulator under inflammatory conditions.
The transcription factor STAT2 enhances proteasomal degradation of RCAN1 through the ubiquitin E3 ligase FBW7.
GeneRIF
Chung et al., Seoul, South Korea. In Biochem Biophys Res Commun, 2012
Co-immunoprecipitation/immunoblot analyses showed that STAT2 enhanced RCAN1 ubiquitination through the ubiquitin E3 ligase FBW7..
NLRX1 protein attenuates inflammatory responses to infection by interfering with the RIG-I-MAVS and TRAF6-NF-κB signaling pathways.
Impact
Ting et al., Chapel Hill, United States. In Immunity, 2011
We showed that Nlrx1(-/-) mice exhibited increased expression of antiviral signaling molecules IFN-β, STAT2, OAS1, and IL-6 after influenza virus infection.
Nonconventional initiation complex assembly by STAT and NF-kappaB transcription factors regulates nitric oxide synthase expression.
Impact
Decker et al., Vienna, Austria. In Immunity, 2010
Here we showed sequential and cooperative contributions of the transcription factors ISGF3 (a complex containing STAT1, STAT2, and IRF9 subunits) and NF-kappaB to the transcriptional induction of the Nos2 gene in macrophages infected with the intracellular bacterial pathogen Listeria monocytogenes.
Acetylation-dependent signal transduction for type I interferon receptor.
Impact
Chin et al., Providence, United States. In Cell, 2007
IRF9 interacts with the acetyl-Lys399 motif by means of its IRF homology2 (IH2) domain, leading to formation of the ISGF3 complex that includes IRF9, STAT1, and STAT2.
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