Recombinant Mouse Protein ALEX (Gnas)

1. In mice that express activated KRAS in the pancreas, we found expression of GNAS(R201C) to cause development of more differentiated tumors, with gene expression pattern associated with the ductal phenotype. PMID: 30142336
2. Gsalpha regulates osteoclast differentiation and function through cAMP/PKA and Wnt/beta-catenin pathways. PMID: 28338087
3. Related GPCRs couple differently to Gs: preassociation between G protein and 5-HT7 serotonin receptor reveals movement of Galphas upon receptor activation PMID: 29079700
4. This study demonstrates that induced expression of the fibrous dysplasia (FD) Galphas mutant from the mouse endogenous Gnas locus exhibits human FD phenotypes in vivo, and that inhibitors of Wnt/beta-catenin signaling may be repurposed for treating FD and other bone diseases caused by Galphas activation. PMID: 29158412
5. high osteoblastic GalphaS expression results in aberrant skeletal development in which bone production is favored at the cost of bone quality. PMID: 28727179
6. Our findings suggest that a cis-acting factor could be implicated in reducing paternal Galphas expression in brown adipose tissue PMID: 28694163
7. Our data revealed a positive correlation between hepatic Gsalpha-cAMP signal axis and fasting blood glucose (FBG) in slight insulin resistance stage of HIgh Sugar High Fat-diet rats and diabetic db/db mice. The current finding thus suggested hepatic Gsalpha-cAMP signal axis plays a central role in regulating of FBG during the developing and development of T2DM. PMID: 28260721
8. retrograde trafficking to the trans-Golgi network induces local Gs-protein activation and cAMP/PKA signaling at a critical position near the nucleus, which appears required for efficient CREB phosphorylation and gene transcription PMID: 28874659
9. Gsalpha deficiency in JG cells of adult mice results in kidney injury, suggesting that JG cells are critically involved in the maintenance and protection of the renal microvascular endothelium. PMID: 28775003
10. 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 PMID: 23822972
11. results suggest that the T1R3 homomeric sweet taste receptor negatively regulates adipogenesis through Galphas-mediated microtubule disassembly and consequent activation of the Rho/ROCK pathway. PMID: 28472098
12. results show that Gsalpha imprinting in the dorsomedial nucleus of the hypothalamus (DMH) underlies the parent-of-origin metabolic phenotype that results from Gsalpha mutations and that DMH MC4R/Gsalpha signaling is important for regulation of energy expenditure and brown adipose tissue activation, but not the metabolic response to cold. PMID: 27991864
13. activating mutations in GNAS and Kras cooperatively promote murine pancreatic tumorigenesis PMID: 26257060
14. 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 and Slc6a4, but not the dopamine-specific gene Th in Nesp(m/+) mice. PMID: 27509352
15. 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. PMID: 28043906
16. Gsalpha signaling in adipose tissues may therefore affect whole-body glucose metabolism in the absence of an effect on body weight. PMID: 26712027
17. Ventromedial hypothalamic Gsalpha/cyclic AMP signaling regulates glucose homeostasis and alters leptin sensitivity in mice, particularly in the setting of excess caloric intake. PMID: 26671183
18. findings suggest that XLalphas enhances Gq/11 signaling to mediate the renal actions of PTH during early postnatal development. PMID: 26307011
19. These data demonstrate that effects of Gsalpha mutations underpinning FD-defining tissue changes and morbidity do not reflect the effects of the mutations on osteoblasts proper. PMID: 25487351
20. a novel role of Galphas in control of neural progenitor asymmetric cell division via suppressing Numb mediated Notch signaling inhibition PMID: 25916881
21. This study highlights an important tumour suppressive function of Galphas-PKA, limiting the proliferation of epithelial stem cells and maintaining proper hair follicle homeostasis. PMID: 25961504
22. Gsalpha mutations are sufficient to cause FD, and are per se compatible with germline transmission and normal embryonic development in mice. Our novel murine lines constitute the first model of FD. PMID: 24764158
23. targeted ablation of Gs alpha in early osteoblast precursors, but not in differentiated osteocytes, results in a dramatic increase in bone marrow adipocytes. PMID: 24806274
24. a paternally inherited Gnas cluster showing ectopic expression of Nesp is "maternalised" in terms of Gnasxl and Gnas expression. PMID: 25659103
25. Altered gene dosages for Galphas and alpha- NAC in compound heterozygous mice result in reduced bone mass, increased numbers of osteocytes, and enhanced expression of Sost. PMID: 24550008
26. study concludes that XLalphas is required for the inhibition of sympathetic outflow towards cardiovascular and metabolically relevant tissues PMID: 23748904
27. Here we describe maternal inheritance of a new Gnas mutation, Ex1A-T, which gives rise to a small but highly significant overgrowth phenotype which we attribute to reduction of maternally expressed NESP55. PMID: 23839232
28. In animal models, genetically-mediated ectopic Hedgehog signaling is sufficient to induce heterotopic ossification, whereas inhibition of this signaling pathway by genetic or pharmacological means strongly reduces the severity of this condition. PMID: 24076664
29. The effects of Gnas dysregulation on osteoblast differentiation, were examined. PMID: 22903279
30. Data indicate that mice lacking Gsalpha in osteocytes showed a dramatic increase in myeloid cells in bone marrow, spleen, and peripheral blood. PMID: 23160461
31. Results indicate that although G(s)alpha deficiency in PVN partially contributes to the metabolic phenotype, G(s)alpha imprinting in other CNS regions is also important in mediating the CNS effects of G(s)alpha mutations. PMID: 22733970
32. Supporting a role for Gnas in adipogenesis in vivo, fat tissue weight and expression of adipogenic genes from multiple types of adipose tissues from Gsalpha(+/p-) mice were significantly decreased. PMID: 22511293
33. in mice with loss of imprinting of Gnas, NREM and complex cognitive processes are enhanced while REM and REM-linked behaviors are inhibited PMID: 22589743
34. Umami taste receptor functions as an amino acid sensor via Galphas subunit in N1E-115 neuroblastoma cells. PMID: 22189795
35. The neonatal phenotype of mutant mice appears to be due to a transient role of XLalphas in muscle tissues. PMID: 22253771
36. Galphas and cAMP has a divergent requirement in the differentiation and inflammatory profile of distinct mouse Th subsets PMID: 22326954
37. Findings indicate that stimulatory G-protein G(alphas)-wt transfected cells showed more sensitization of adenylyl cyclase (AC) and mu1-opioid receptor interacted with G(alphas) after chronic morphine exposure. PMID: 22177524
38. XLalphas is involved in the regulation of bone and adipocyte metabolism PMID: 22215617
39. GalphaS protein coupling to adenylate cyclase mediates membrane-tethered amyloid precursor protein intracellular domain-induced neurite outgrowth. PMID: 22302812
40. Gnas is a key regulator of fate decisions in adipose-derived mesenchymal progenitor cells. PMID: 21812029
41. Fast-to-slow-fiber-type switch in G(s)alpha deficiency at older ages is likely an adaptive response, allowing higher fatigue resistance in adaption to metabolic deficiency and aging. PMID: 21680879
42. activated XLalphas and Galphas traffic differently, and this may form the basis for the differences in their cellular actions PMID: 21890629
43. creatine loss ins a near normal DeltaG approximately (ATP) in transgenic mouse hearts with cardiomyopathy caused by overexpressing Gsalpha PMID: 19913550
44. Gnas gene exhibits a complex imprinted pattern, giving rise to transcripts that are maternally, paternally, or biallelically expressed. PMID: 10097123
45. long-term effect on renal function, blood pressure, and renal pathology in Gsapha deletion low renin and diuretic mouse model PMID: 20551626
46. G(s)alpha deficiency in adipose tissue leads to a lean phenotype with divergent effects on cold tolerance and diet-induced thermogenesis. PMID: 20374964
47. THe Nesp55 differentially methylated region is an additional principal imprinting control region, which directs Gnas methylation and thereby affects expression of all maternal Gnas-derived transcripts. PMID: 20427744
48. Ric-8B plays a critical and specific role in the control of G alpha(s) protein levels by modulating G alpha(s) ubiquitination and positively regulates G(s) signaling PMID: 20133939
49. XLalpha(s) is capable of functionally coupling to receptors that normally act via Gs(alpha). PMID: 12145344
50. results indicate that Gs activity in the oocyte is required to maintain meiotic arrest within the ovarian follicle and suggests that the follicle may keep the cell cycle arrested by activating Gs PMID: 12193786

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UniGene: Mm.125770