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Ectopic expression of the human gain-of-function mutation GNAS(R201C) in mice supported transplantable HSC (show FUT1 ELISA Kits) activity and improved lymphoid output in secondary recipients. Because declining lymphoid output is a hallmark of aging, GNAS(R201C) mutations may sustain lymphoid-biased HSCs over time and maintain them in a developmental state favorable for transformation.
This is the first report to show that PLEKHG2 is a novel effector of Galphas, and is negatively regulated by the Galphas subunit through direct interaction.
The presence of a mutation in GNAS is helpful in identifying a mucin (show SLC13A2 ELISA Kits)-producing Pancreatic cyst and is found in more than 90% of Intraductal Papillary Mucinous Pancreas Neoplasms .
pseudomyxoma peritonei patients with GNAS mutations had a significantly shorter median progression-free survival as compared to GNAS wild-type ones.
GNAS mutation is associated with gastric cancer.
Mechanical stress affects methylation pattern of GNAS isoforms and osteogenic differentiation of human adipose tissue-derived mesenchymal stem cells.
patients with Pseudohypoparathyroidism type 1A, parathormone (show PTH ELISA Kits) resistance and hypocalcemia develop over time. These findings highlight the importance of screening for maternal GNAS mutations in the presence of ectopic ossifications or family history, even in the absence of parathormone (show PTH ELISA Kits) resistance and hypocalcemia.
Mutation in GNAS gene is associated with Pancreatic Ductal Adenocarcinoma.
activating mutations in GNAS and Kras cooperatively promote murine pancreatic tumorigenesis
These results indicate that the ICL2 region of the EP2 receptor is its potential interaction site with Galphas, and that the aromatic side chain moiety at position 143 is a determinant for the accessibility of the ICL2 to the Galphas protein.
The Galphas and Galphaq (show GNAQ ELISA Kits) peptides adopt different orientations in beta2-AR and V1AR (show AVPR1A ELISA Kits), respectively. The beta2-AR/Galphas peptide interface is dominated by electrostatic interactions, whereas the V1AR (show AVPR1A ELISA Kits)/Galphaq (show GNAQ ELISA Kits) peptide interactions are predominantly hydrophobic.
Target RNA interference of GNAS in porcine fibroblast cells leads to lower mRNA expression of Bcl-2 (show BCL2 ELISA Kits), Fas (show FAS ELISA Kits), and Caspase-3 (show CASP3 ELISA Kits), which are recognized as apoptosis related markers.
study did not find any significant associations for polymorphisms in insulin (show INS ELISA Kits)-like grwoth factor 2, GTP Binding Protein (show RND1 ELISA Kits) alpha Subunits, Gs and melanocortin receptor 4 (show MC4R ELISA Kits) genes with reproductive traits of Polish Landrace and Large White pigs
Genetic inhibition of GNAS protein in the atrioventricular node reduced heart rate and prevented atrial fibrillation-associated reduction of cardiac function in a porcine model.
Imprinting analysis showed that NESP55 is maternally expressed in young and adult pigs.
Review article on the human GNAS complex locus.
results show that most of the PatDp(dist2) phenotype is due to overexpression of Gnasxl combined with loss of expression of Gnas, and suggest that Gnasxl and Gnas may act antagonistically in a number of tissues and to cause a wide range of phenotypic effects
results suggest that the T1R3 (show TAS1R3 ELISA Kits) homomeric sweet taste receptor negatively regulates adipogenesis through Galphas-mediated microtubule disassembly and consequent activation of the Rho/ROCK pathway.
results show that Gsalpha imprinting in the dorsomedial nucleus of the hypothalamus (DMH (show DST ELISA Kits)) underlies the parent-of-origin metabolic phenotype that results from Gsalpha mutations and that DMH (show DST ELISA Kits) MC4R (show MC4R ELISA Kits)/Gsalpha signaling is important for regulation of energy expenditure and brown adipose tissue activation, but not the metabolic response to cold.
Authors demonstrated that Nesp55 is co-localized with serotonin and then went on to show that in midbrain regions there were reductions in mRNA expression of the serotonin-specific genes Tph2 (show TPH2 ELISA Kits) and Slc6a4 (show SLC6A4 ELISA Kits), but not the dopamine-specific gene Th in Nesp(m/+) mice.
Disruption of Gnas in smooth muscle of mice reduced intestinal motility and led to death within 4 weeks. GNAS disruption in adults impaired contraction of intestinal smooth muscle and peristalsis with features of intestinal pseudo-obstruction characterized by chronic intestinal dilation and dysmotility.
Data show that inhibitory (Galphai2 (show GNAI2 ELISA Kits)) and stimulatory (GalphasL) G-protein subunits produced minor atrophic and hypertrophic changes in muscle mass, and Galphai2 (show GNAI2 ELISA Kits) over-expression prevented AAV:beta2-adrenoceptor (beta2-AR) mediated hypertrophy.
Galphas depletion blocks the S1PR1 (show S1PR1 ELISA Kits)-activation induced VE-cadherin (show CDH5 ELISA Kits) stabilization at junctions.
demonstrate that the ability of an MC4R (show MC4R ELISA Kits) agonist delivered to PVN to inhibit food intake is lost in mice lacking G(q/11)alpha in the paraventricular nucleus of the hypothalamus but not in animals deficient for G(s)alpha
Regulation of G-protein signaling via Gnas is required to regulate proximal tubular growth in the Xenopus pronephros.
application of peptide amide hydrogen-deuterium exchange mass spectrometry to probe changes in the structure of the heterotrimeric bovine G protein, Gs on formation of a complex with agonist-bound human beta(2) adrenergic receptor (show ADRB2 ELISA Kits)
crystal structure of the active state ternary complex composed of agonist-occupied monomeric beta2 adrenergic receptor (show ADRB2 ELISA Kits) and nucleotide-free Gs heterotrimer
the results presented here indicate an important role for the imprinted GNAS cluster in underlying complex
a nucleotide-free state of Galphas is induced by Cu2+ and Zn2+
This locus has a highly complex imprinted expression pattern. It gives rise to maternally, paternally, and biallelically expressed transcripts that are derived from four alternative promoters and 5' exons. Some transcripts contain a differentially methylated region (DMR) at their 5' exons, and this DMR is commonly found in imprinted genes and correlates with transcript expression. An antisense transcript is produced from an overlapping locus on the opposite strand. One of the transcripts produced from this locus, and the antisense transcript, are paternally expressed noncoding RNAs, and may regulate imprinting in this region. In addition, one of the transcripts contains a second overlapping ORF, which encodes a structurally unrelated protein - Alex. Alternative splicing of downstream exons is also observed, which results in different forms of the stimulatory G-protein alpha subunit, a key element of the classical signal transduction pathway linking receptor-ligand interactions with the activation of adenylyl cyclase and a variety of cellular reponses. Multiple transcript variants encoding different isoforms have been found for this gene. Mutations in this gene result in pseudohypoparathyroidism type 1a, pseudohypoparathyroidism type 1b, Albright hereditary osteodystrophy, pseudopseudohypoparathyroidism, McCune-Albright syndrome, progressive osseus heteroplasia, polyostotic fibrous dysplasia of bone, and some pituitary tumors.
adenylate cyclase-stimulating G alpha protein
, alternative gene product encoded by XL-exon
, extra large alphas protein
, guanine nucleotide binding protein (G protein), alpha stimulating activity polypeptide 1
, guanine nucleotide regulatory protein
, guanine nucleotide-binding protein G(s) subunit alpha isoforms XLas
, neuroendocrine secretory protein
, protein ALEX
, secretogranin VI
, GNAS complex locus
, GTP-binding regulatory protein alpha subunit exon 1
, guanine nucleotide binding protein, alpha stimulating activity polypeptide 1
, guanine nucleotide-binding protein G(s) subunit alpha
, stimulatory GTP binding protein
, Galpha olf1
, guanine nucleotide-binding protein G(olf) subunit alpha
, alpha-stimulatory subunit of GTP-binding protein
, guanine nucleotide-binding protein, alpha-stimulating activity polypeptide 1
, Gs alpha subunit
, neuroendocrine secretory protein 55
, stimulatory G-protein alpha subunit
, guanine nucleotide-binding protein G(s) subunit alpha isoforms
, GNAS (guanine nucleotide binding protein, alpha stimulating) complex locus
, guanine nucleotide binding protein alpha s
, guanine nucleotide-binding protein G-s, alpha subunit
, guanine nucleotide binding protein, alpha stimulating, olfactory type
, guanine nucleotide-binding protein G(s) subunit alpha isoforms XLas-like
, Galpha s