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Protein kinase, cAMP-dependent, catalytic, gamma

PRKACG, serine(threonine) protein kinase, cAMP-dependent protein kinase catalytic subunit C alpha
Cyclic AMP-dependent protein kinase (PKA) consists of two catalytic subunits and a regulatory subunit dimer. This gene encodes the gamma form of its catalytic subunit. The gene is intronless and is thought to be a retrotransposon derived from the gene for the alpha form of the PKA catalytic subunit. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, OUT, protein kinase A catalytic subunit, CalDAG-GEFI, ACID
Papers on PRKACG
Update on the inherited platelet disorders.
Lambert, Philadelphia, United States. In Curr Opin Hematol, Sep 2015
RECENT FINDINGS: The description of novel mechanisms of disease including mutations in PRKACG, in a family with severe macrothrombocytopenia, RUNX1 and FLI1 mutations in patients with inherited mild platelet function disorders and CalDAG-GEFI resulting in a severe platelet bleeding phenotype show that there is still much to be learned from studying families and molecular sequencing of patients with well phenotyped platelet disorders.
Inherited disorders of platelet function: selected updates.
Nurden et al., Pessac, France. In J Thromb Haemost, Jun 2015
Next-generation sequencing technology (NGST), mainly exome sequencing, has highlighted genes responsible for defects in platelet secretion (NBEAL2, gray platelet syndrome), procoagulant activity (STIM1, Stormorken syndrome), and activation pathways (RASGRP2, CalDAG-GEFI deficiency and integrin dysfunction; PRKACG, cyclic adenosine monophosphate-dependent protein kinase deficiency).
A closer look at evolution: Variants (SNPs) of genes involved in skin pigmentation, including EXOC2, TYR, TYRP1, and DCT, are associated with 25(OH)D serum concentration.
Reichrath et al., Homburg, Germany. In Endocrinology, 2015
Serum 25(OH)D and SNPs (n = 960) related to genes with relevance for skin pigmentation (tyrosinase [TYR], TYR-related protein 1 [TYRP1], dopachrome tautomerase [DCT], oculocutaneous albinism II [OCA2], two pore segment channel 2 [TPCN2], solute carrier family 24 A4 [SLC24A4], solute carrier family 45 A2 [SLC45A2], agouti signalling peptide [ASIP], cyclic AMP-dependent transcription factor [ATF1], microphthalmia-associated transcription factor [MITF], proopiomelanocortin [POMC], cAMP-dependent protein kinase catalytic subunit beta [PRKACB], cAMP-dependent protein kinase catalytic subunit gamma [PRKACG], cAMP-dependent protein kinase type I-alpha regulatory subunit [PRKAR1A], cAMP-dependent protein kinase type II-alpha regulatory subunit [PRKAR2A], cAMP-dependent protein kinase type II-beta regulatory subunit [PRKAR2B], tubulin beta-3 chain/melanocortin receptor 1 [TUBB3/MC1R], Cadherin-1 [CDH1], catenin beta 1 [CTNNB1], Endothelin 1 [EDN1], endothelin 3 [EDN3], endothelin receptor type B [EDNRB], fibroblast growth factor 2 [FGF2], KIT, KIT ligand [KITLG], nerve growth factor [NGF], interferon regulatory factor 4 [IRF4], exocyst complex component 2 [EXOC2], and tumor protein 53 [TP53]) were analyzed in a cohort of participants of the Ludwigshafen Risk and Cardiovascular Health Study (n = 2970).
A new form of macrothrombocytopenia induced by a germ-line mutation in the PRKACG gene.
Raslova et al., Villejuif, France. In Blood, 2014
Exome sequencing identified a c.222C>G mutation (missense p.74Ile>Met) in PRKACG, a gene encoding the γ-catalytic subunit of the cyclic adenosine monophosphate-dependent protein kinase, the mutated allele cosegregating with the macrothrombocytopenia.
Inherited macrothrombocytopenias on the rise.
Kahr et al., Toronto, Canada. In Blood, 2014
In this issue of Blood, Manchev et al describe a consanguineous family with severe macrothrombocytopenia and bleeding symptoms where exome sequencing revealed a homozygous missense mutation in the PRKACG gene (p.74Ile>Met)
Novel candidate genes for 46,XY gonadal dysgenesis identified by a customized 1 M array-CGH platform.
Barbaro et al., Stockholm, Sweden. In Eur J Med Genet, 2013
A large duplication highlighting PIP5K1B, PRKACG and FAM189A2 as candidates for 46,XY GD, were also detected.
[Application of genome-wide genechip for screening and identifying genes related to CD133(+)CD200(+) colorectal cancer stem cells].
Xiao et al., Guangzhou, China. In Nan Fang Yi Ke Da Xue Xue Bao, 2013
Bioinformatics analysis and gene co-expression network building identified 3 genes (MDM2, PRKACG, and CACNA1G) with specific expression in CD133(+)CD200(+) colorectal cancer stem cells, and this result was confirmed by real-time quantitative PCR analysis.
A genetic dissection of antipsychotic induced movement disorders.
Serretti et al., Messina, Italy. In Curr Med Chem, 2012
RESULTS: Variations located within PIK3CA (phosphoinositide-3- kinase, catalytic, alpha polypeptide), PLA2G4A (phospholipase A2, group IVA, cytosolic, calcium-dependent), PRKCA (protein kinase C, alpha), PRKACG (Phosphatidylinositol-4,5-bisphosphate 3-kinase 110 kDa catalytic subunit gamma), ERK-1 (extracellular signalregulated kinase 1 (MAPK3)), ERK-2 (extracellular signal-regulated kinase 2 (MAPK1)), GNAS (guanine nucleotide binding protein (G protein), alpha stimulating activity polypeptide 1), PLCB1 (phospholipase C, beta 1 (phosphoinositide-specific)) and ITPR1 (inositol 1,4,5-triphosphate receptor type 1) were found to be relevant for APM induced EPS.
Evolutionary paths of the cAMP-dependent protein kinase (PKA) catalytic subunits.
Laerdahl et al., Oslo, Norway. In Plos One, 2012
The evolution of the PRKACG retroposon in simians was also investigated.
Overexpressing PKIB in prostate cancer promotes its aggressiveness by linking between PKA and Akt pathways.
Nakagawa et al., Tokyo, Japan. In Oncogene, 2009
Findings show that PKIB and PKA-C kinase can have critical functions of aggressive phenotype of PCs through Akt phosphorylation and that they should be a promising molecular target for PC treatment.
PKA-mediated stabilization of FoxH1 negatively regulates ERalpha activity.
Yeo et al., Seoul, South Korea. In Mol Cells, 2009
Results suggest that PKA can negatively regulate ERalpha, at least in part, through FoxH1.
The paradoxical increase in cortisol secretion induced by dexamethasone in primary pigmented nodular adrenocortical disease involves a glucocorticoid receptor-mediated effect of dexamethasone on protein kinase A catalytic subunits.
Lefebvre et al., Mont-Saint-Aignan, France. In J Clin Endocrinol Metab, 2009
In human primary pigmented nodular adrenocortical disease tissues, dexamethasone paradoxically stimulates cortisol release through a glucocorticoid receptor-mediated effect on PKA catalytic subunits.
Visual screening and analysis for kinase-regulated membrane trafficking pathways that are involved in extensive beta-amyloid secretion.
Murata et al., Tokyo, Japan. In Genes Cells, 2009
As the result of our visual screening, which examined the effect of kinase inhibitors and a kinase siRNA library, we identified five kinases (CDC42BPB, PRKACA, PRKACG, GSK3 beta and CSNK2A1) that regulate CI-M6PR trafficking.
Mutation in the catalytic domain of protein kinase C gamma and extension of the phenotype associated with spinocerebellar ataxia type 14.
Durr et al., Paris, France. In Arch Neurol, 2004
A novel missense mutation, F643L, which maps to a highly conserved amino acid of the catalytic domain of protein kinase C gamma, extends the phenotype associated with the spinocerebellar ataxia type 14 (SCA14) locus.
Characterization of the cAMP-dependent protein kinase catalytic subunit Cgamma expressed and purified from sf9 cells.
Beebe et al., Chicago, United States. In Protein Expr Purif, 2004
Results suggest that Cgamma and Calpha differ in structure and function in vitro, supporting the hypothesis that functionally different C-subunit isozymes could affect cAMP signal transduction downstream of protein kinase A activation.
Exon-intron structure of a 2.7-kb transcript of the STM7 gene with phosphatidylinositol-4-phosphate 5-kinase activity.
Chamberlain et al., London, United Kingdom. In Genomics, 1997
We now report the exon-intron structure of STM7.I and primer sequences designed to facilitate full characterization, including details relating to a novel exon (STM7; exon 17) derived from the 3'-UTR of the PRKACG gene.
Molecular cloning and characterization of a conserved nuclear serine(threonine) protein kinase.
Hemmings et al., Basel, Switzerland. In Proc Natl Acad Sci U S A, 1995
Human, Drosophila melanogaster, and Caenorhabditis elegans cDNA clones encoding homologues of a serine(threonine) protein kinase (EC
Activation of YRP kinase by v-Src and protein kinase C-mediated signal transduction pathways.
Hanafusa et al., New York City, United States. In Proc Natl Acad Sci U S A, 1995
We have previously reported that a serine(threonine) protein kinase that phosphorylates histone H1 in vitro is activated by tyrosine phosphorylation in v-Src-transformed rat 3Y1 fibroblasts.
Localization of the catalytic subunit C gamma of the cAMP-dependent protein kinase gene (PRKACG) to human chromosome region 9q13.
Jahnsen et al., Oslo, Norway. In Cytogenet Cell Genet, 1991
Southern blot analysis of genomic DNA from human x mouse somatic cell hybrids allowed us to assign this gene (PRKACG) to human chromosome 9.
Identification of a 42-kilodalton phosphotyrosyl protein as a serine(threonine) protein kinase by renaturation.
Martin et al., Berkeley, United States. In Mol Cell Biol, 1990
We have surveyed fibroblast lysates for protein kinases that might be involved in mitogenesis.
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