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Tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, gamma polypeptide

14-3-3gamma, 14-3-3 protein gamma, YWHAG
This gene product belongs to the 14-3-3 family of proteins which mediate signal transduction by binding to phosphoserine-containing proteins. This highly conserved protein family is found in both plants and mammals, and this protein is 100% identical to the rat ortholog. It is induced by growth factors in human vascular smooth muscle cells, and is also highly expressed in skeletal and heart muscles, suggesting an important role for this protein in muscle tissue. It has been shown to interact with RAF1 and protein kinase C, proteins involved in various signal transduction pathways. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: HIP1, 14-3-3zeta, TBP, OUT, SET
Papers on 14-3-3gamma
miR-200 promotes the mesenchymal to epithelial transition by suppressing multiple members of the Zeb2 and Snail1 transcriptional repressor complexes.
Lieberman et al., Boston, United States. In Oncogene, Feb 2016
Twelve targets of miR-200c (Crtap, Fhod1, Smad2, Map3k1, Tob1, Ywhag/14-3-3γ, Ywhab/14-3-3β, Smad5, Zfp36, Xbp1, Mapk12, Snail1) were experimentally validated by identifying their 3'UTR miR-200 recognition elements.
Epilepsy is a possible feature in Williams-Beuren syndrome patients harboring typical deletions of the 7q11.23 critical region.
Verrotti et al., Roma, Italy. In Am J Med Genet A, Jan 2016
In WBS, epilepsy should be considered both in case of typical and atypical deletions, which do not involve HIP1, YWHAG or MAGI2.
Critical genes in head and neck squamous cell carcinoma revealed by bioinformatic analysis of gene expression data.
Li et al., Hangzhou, China. In Genet Mol Res, 2014
Five PPI networks were constructed from which hub genes were acquired, such as minichromosome maintenance complex component 7 (MCM7), MCM2, decorin (DCN), retinoblastoma 1 (RB1), and tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein gamma (YWHAG).
Selecting key genes associated with osteosarcoma based on a differential expression network.
Jia et al., Jinan, China. In Genet Mol Res, 2014
Six hub genes (APP, UBC, CAND1, RPA, YWHAG, and NEDD8) were discovered; of these, two genes (UBC and RPA) were also found to be disease genes.
Smaller and larger deletions of the Williams Beuren syndrome region implicate genes involved in mild facial phenotype, epilepsy and autistic traits.
Merla et al., San Giovanni Rotondo, Italy. In Eur J Hum Genet, 2014
Two carry ~3.5 Mb larger deletion towards the telomere that includes Huntingtin-interacting protein 1 (HIP1) and tyrosine 3-monooxygenase/tryptophan 5-monooxigenase activation protein gamma (YWHAG) genes.
Gene set analysis of GWAS data for human longevity highlights the relevance of the insulin/IGF-1 signaling and telomere maintenance pathways.
Beekman et al., Leiden, Netherlands. In Age (dordr), 2013
Analysis of gene SNP sets from these pathways indicates that the association of the IIS pathway is scattered over several genes (AKT1, AKT3, FOXO4, IGF2, INS, PIK3CA, SGK, SGK2, and YWHAG), while the association of the TM pathway seems to be mainly determined by one gene (POT1).
Promyelocytic leukemia (PML) protein plays important roles in regulating cell adhesion, morphology, proliferation and migration.
Lee et al., Hong Kong, Hong Kong. In Plos One, 2012
In contrast, ten proteins (CIAPIN1, FAM50A, SUMO2 HSPB1 NSFL1C, PCBP2, YWHAG, STMN1, TPD52L2 and PDAP1) were found up-regulated.
Computational prediction of the polyQ and CAG repeat spinocerebellar ataxia network based on sequence identity to untranslated regions.
Wallihan et al., United States. In Gene, 2012
UGUUU repeats were identified as an abundant motif in the SCA network and PAXIP1, CELF2, CREBBP, EBF1, PLEKHG4, SRSF4, C5orf42, NFIA, STK24, and YWHAG were identified as statistically significant proteins in the polyQ and PPP2R2B network.
Quantitative proteomic Isotope-Coded Protein Label (ICPL) analysis reveals alteration of several functional processes in the glioblastoma.
Pineau et al., Rennes, France. In J Proteomics, 2012
The core of this network is mainly constituted of interactions between beta-actin (ACTB) with heat shock proteins (HSP90AA1, HSPA8) and 14-3-3 proteins (YWHAZ, YWHAG, YWHAB).
Hypoxia activates tumor suppressor p53 by inducing ATR-Chk1 kinase cascade-mediated phosphorylation and consequent 14-3-3γ inactivation of MDMX protein.
Lu et al., Indianapolis, United States. In J Biol Chem, 2012
hypoxia can activate p53 through inactivation of MDMX by the ATR-Chk1-MDMX-14-3-3gamma pathway.
miRNA and protein expression profiles of visceral adipose tissue reveal miR-141/YWHAG and miR-520e/RAB11A as two potential miRNA/protein target pairs associated with severe obesity.
Sacchetti et al., Napoli, Italy. In J Proteome Res, 2012
Bioinformatics integration of miRNA expression and proteomic data highlighted two potential miRNA/protein target pairs: miR-141/YWHAG (tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, gamma polypeptide) and miR-520e/RAB11A (Ras-related protein RAB-11A); the functional interaction between these miRNAs and their target sequences on the corresponding mRNAs was confirmed by luciferase assays.
Tissue-specific selection of stable reference genes for real-time PCR normalization in an obese rat model.
Del Ry et al., Pisa, Italy. In J Mol Endocrinol, 2012
The aim of this study was to select among ten candidates (Actb, Gapdh, Polr2a, Ywhag, Rpl13a, Sdha, Ppia, Tbp, Hprt1 and Tfrc) a set of reference genes that can be used for the normalization of mRNA expression data obtained by real-time PCR in obese and lean Zucker rats both at fasting and during acute hyperglycemia.
Hormone-induced 14-3-3γ adaptor protein regulates steroidogenic acute regulatory protein activity and steroid biosynthesis in MA-10 Leydig cells.
Papadopoulos et al., Montréal, Canada. In J Biol Chem, 2012
Data show that binding motifs of 14-3-3gamma were identified in components of the transduceosome, including STAR.
A 14-3-3γ dimer-based scaffold bridges CtBP1-S/BARS to PI(4)KIIIβ to regulate post-Golgi carrier formation.
Corda et al., Napoli, Italy. In Nat Cell Biol, 2012
description of a protein complex that mediates carrier formation and contains budding and fission molecules, as well as other molecules, such as the adaptor protein 14-3-3gamma
Gene expression profiling of B-CLL in Ukrainian patients in post-Chernobyl period.
Koval et al., Kocaeli, Turkey. In Exp Oncol, 2011
CONCLUSION: In B-CLL patients, gene networks around MYC, HNF1A and HNF4A, YWHAG, NF-κB1 and SP1 are identified as up-regulated; CEBPA, YWHAG, SATB1 and RB1 -- as down-regulated.
The binding of 14-3-3γ to membranes studied by intrinsic fluorescence spectroscopy.
Martinez et al., Bergen, Norway. In Febs Lett, 2011
results support that membrane binding involves the non-conserved, convex area of 14-3-3gamma, and that Trp residues do not intercalate in the bilayer.
14-3-3Gamma inhibition of MDMX-mediated p21 turnover independent of p53.
Lu et al., Indianapolis, United States. In J Biol Chem, 2011
a new role for 14-3-3gamma in protecting p21 from MDMX-mediated proteasomal turnover, which may partially account for DNA damage-induced elevation of p21 levels independent of p53.
Application of systems biology approach identifies and validates GRB2 as a risk gene for schizophrenia in the Irish Case Control Study of Schizophrenia (ICCSS) sample.
Zhao et al., Nashville, United States. In Schizophr Res, 2011
We tested the association of four genes (GRB2, HSPA5, YWHAG, and YWHAZ) in the Irish Case-Control Study of Schizophrenia (ICCSS) sample (1021 cases and 626 controls).
Recurrent distal 7q11.23 deletion including HIP1 and YWHAG identified in patients with intellectual disabilities, epilepsy, and neurobehavioral problems.
Stankiewicz et al., Houston, United States. In Am J Hum Genet, 2011
data do not exclude the possibility that YWHAG loss of function is also sufficient to cause neurological phenotypes
P53 suppresses expression of the 14-3-3 gamma oncogene.
Martinez et al., Tucson, United States. In Bmc Cancer, 2010
Increased expression of 14-3-3 gamma in lung cancer coincides with loss of functional p53.
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