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Recombinant Mouse Protein ALEX (Gnas)

  • 中文名稱:
    小鼠Gnas重組蛋白
  • 貨號(hào):
    CSB-YP747529MO
  • 規(guī)格:
  • 來源:
    Yeast
  • 其他:
  • 中文名稱:
    小鼠Gnas重組蛋白
  • 貨號(hào):
    CSB-EP747529MO
  • 規(guī)格:
  • 來源:
    E.coli
  • 其他:
  • 中文名稱:
    小鼠Gnas重組蛋白
  • 貨號(hào):
    CSB-EP747529MO-B
  • 規(guī)格:
  • 來源:
    E.coli
  • 共軛:
    Avi-tag Biotinylated

    E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.

  • 其他:
  • 中文名稱:
    小鼠Gnas重組蛋白
  • 貨號(hào):
    CSB-BP747529MO
  • 規(guī)格:
  • 來源:
    Baculovirus
  • 其他:
  • 中文名稱:
    小鼠Gnas重組蛋白
  • 貨號(hào):
    CSB-MP747529MO
  • 規(guī)格:
  • 來源:
    Mammalian cell
  • 其他:

產(chǎn)品詳情

  • 純度:
    >85% (SDS-PAGE)
  • 基因名:
  • Uniprot No.:
  • 別名:
    Gnas; Gnas1; Protein ALEX; Alternative gene product encoded by XL-exon
  • 種屬:
    Mus musculus (Mouse)
  • 蛋白長(zhǎng)度:
    full length protein
  • 表達(dá)區(qū)域:
    1-725
  • 氨基酸序列
    MSPSPTRLAV RSVDPQKTPN LTSKAPARPS RKSEWVETTA HLRRKPCHSR HNSPAWEISG PPWSSQDHLG PHQASKPSTQ RFWSPGPPLA RAQAWEPIPP HQKKLCHLSS TSLPRETIAS LPCKSQTLRQ EVRKHWSPEL FPRSPGTSDL KTLASEKTTA LPLKNLCHFR SVEKNSGAIA HPQDSRESSH KSALAASSRQ SRSRVRSASL PPRTRLPSGS EAPLTDHSAR LSDLLLTSHA TAPRWRSPDP CLRLAEPPLG STTTPLSIWT APQSQVMARP SKSREPQIRA SAQRDPQLSE KQPRWKEALP PPLRWKEKSP LRREGTDLPP SLKQWMPSQP LLPKPSLPDL MLELLRIPRC SQIARAMPEK TGQPQERLQI SSRILKNSKK PQLSAPILTE GQPQSPQPLL PSPSLKAAEI QPPSQPPRQS LPPRPSLPPG QPLSPRWSPQ PRQSLPPWRS LPPGQPLSPP RSPLPGQSPL LEPIRPLEQS LAPQQCQPLL GQLPLGQPMQ VHWSGEPGHS QLLPPLGHPF LPAQQLPPGQ PLLPAQSLLA GQPLPPPAGP ILDPPAPRSR LLTRLLRGLL RGRLPGLTST SGAEAAAGTR HRLASARSSP PVMSRKKGPP AASSGFCGET AALACPGATR SGATQSATSS PEPSEAASVY PSVPDHDPSA PGRPRILWRR GANRCAKKPL RCESRSAQIR NAASSSTSNW RRRRWTTCVH TACCF
  • 蛋白標(biāo)簽:
    Tag?type?will?be?determined?during?the?manufacturing?process.
    The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
  • 產(chǎn)品提供形式:
    Lyophilized powder
    Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
  • 復(fù)溶:
    We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
  • 儲(chǔ)存條件:
    Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
  • 保質(zhì)期:
    The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
    Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
  • 貨期:
    Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
    Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
  • 注意事項(xiàng):
    Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
  • Datasheet :
    Please contact us to get it.

產(chǎn)品評(píng)價(jià)

靶點(diǎn)詳情

  • 功能:
    May inhibit the adenylyl cyclase-stimulating activity of guanine nucleotide-binding protein G(s) subunit alpha which is produced from the same locus in a different open reading frame.
  • 基因功能參考文獻(xiàn):
    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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  • 亞細(xì)胞定位:
    Cell membrane; Peripheral membrane protein. Cell projection, ruffle.
  • 蛋白家族:
    ALEX family
  • 數(shù)據(jù)庫(kù)鏈接:

    UniGene: Mm.125770



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