06-237 | Anti-Gsα Antibody

06-237
50 µL  
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      Overview

      Replacement Information

      Key Spec Table

      Species ReactivityKey ApplicationsHostFormatAntibody Type
      B, H, MICC, IP, WBRbSerumPolyclonal Antibody
      Description
      Catalogue Number06-237
      ReplacesAB1639
      Brand Family Upstate
      Trade Name
      • Upstate
      DescriptionAnti-Gsα Antibody
      References
      Product Information
      FormatSerum
      Control
      • Widely expressed
      PresentationSerum diluted 1:1 in PBS.
      Applications
      ApplicationAnti-Gsα Antibody is an antibody against Gsα for use in IC, IP & WB.
      Key Applications
      • Immunocytochemistry
      • Immunoprecipitation
      • Western Blotting
      Biological Information
      Immunogenpeptide corresponding to the c-terminus of bovine Gsα (RMHLRQYELL); this sequence is present in all three isoforms of human Gsα (Gsα1, Gsα2, and GsαXL)
      ConcentrationPlease refer to the Certificate of Analysis for the lot-specific concentration.
      HostRabbit
      SpecificityRecognizes the large and small forms of Gsα; does not cross-react with other G proteins.
      IsotypeIgG
      Species Reactivity
      • Bovine
      • Human
      • Mouse
      Antibody TypePolyclonal Antibody
      Entrez Gene Number
      Entrez Gene SummaryThis 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 contains 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 exists, and this antisense transcript and one of the transcripts are paternally expressed, produce 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 have been found for this gene, but the full-length nature and/or biological validity of some variants have not been determined. 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.
      Gene Symbol
      • GNAS
      • NESP55
      • GNASXL
      • C20orf45
      • GPSA
      • dJ309F20.1.1
      • GSA
      • PHP1B
      • CARD3
      • SCG6
      • MGC33735
      • GSP
      • dJ806M20.3.3
      • PHP1A
      • GNAS1
      • POH
      • AHO
      • NESP
      • XLalphas
      Purification MethodProtein A Purfied
      UniProt Number
      UniProt SummaryFUNCTION: SwissProt: P63092 # Guanine nucleotide-binding proteins (G proteins) are involved as modulators or transducers in various transmembrane signaling systems. The G(s) protein is involved in hormonal regulation of adenylate cyclase: it activates the cyclase in response to beta-adrenergic stimuli.| Q5JWF2 # Guanine nucleotide-binding proteins (G proteins) are involved as modulators or transducers in various transmembrane signaling systems. The G(s) protein is involved in hormonal regulation of adenylate cyclase: it activates the cyclase in response to beta-adrenergic stimuli. XLas isoforms interact with the same set of receptors as Gnas isoforms (By similarity).| P84996 # 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.
      SIZE: 394 amino acids; 45665 Da
      SUBUNIT: G proteins are composed of 3 units; alpha, beta and gamma. The alpha chain contains the guanine nucleotide binding site.DOMAIN:SwissProt: P63092
      DISEASE: "SwissProt: P63092 # Defects in GNAS are the cause of Albright hereditary osteodystrophy (AHO) [MIM:103580]. AHO is an autosomal dominant disorder characterized by a short stature, brachydactyly, subcutaneous ossifications. AHO is often associated with pseudohypoparathyoidism, hypocalcemia, and elevated PTH levels. The expression or the activity of GNAS is reduced in AHO. & Defects in GNAS are the cause of pseudohypoparathyroidism type 1A (PHP1A) [MIM:103580]. Pseudohypoparathyroidism is a term applied to a heterogeneous group of disorders whose common feature is resistance to parathyroid hormone. & Defects in GNAS are the cause of McCune-Albright syndrome (MAS) [MIM:174800]. MAS is characterized by polyostotic fibrous dysplasia, cafe-au-lait lesions, and a variety of endocrine disorders, including precocious puberty, hyperthyroidism, hypercortisolism, growth hormone excess, and hyperprolactinemia. The mutations producing MAS lead to constitutive activation of GS alpha. & Defects in GNAS are the cause of a subset of growth hormone secreting pituitary tumors (somatotrophinoma) [MIM:102200]. & Defects in GNAS are the cause of progressive osseous heteroplasia (POH) [MIM:166350]. POH is a rare autosomal dominant disorder characterized by extensive dermal ossification during childhood, followed by disabling and widespread heterotopic ossification of skeletal muscle and deep connective tissue. & Defects in GNAS are a cause of ACTH-independent macronodular adrenal hyperplasia (AIMAH) [MIM:219080]; also known as adrenal Cushing syndrome due to AIMAH. AIMAH is an endogenous form of adrenal Cushing syndrome characterized by multiple bilateral adrenocortical nodules that cause a striking enlargement of the adrenal glands. & Genetic variations in GNAS are the cause of pseudohypoparathyroidism type 1B (PHP1B) [MIM:603233]. PHP1B is characterized by parathyroid hormone (PTH)-resistant hypocalcemia and hyperphosphatemia. Patients affected with PHP1B have normal activity of the product of GNAS, lack developmental defects characteristic of AHO, and typically show no other endocrine abnormalities besides resistance to PTH. Most affected individuals have defects in methylation of the gene. In some cases microdeletions involving the STX16 appear to cause loss of methylation at exon A/B of GNAS, resulting in PHP1B. Paternal uniparental isodisomy have also been observed.| Q5JWF2 # Defects in GNAS are the cause of GNAS hyperfunction [MIM:139320]. This condition is characterized by increased trauma- related bleeding tendency, prolonged bleeding time, brachydactyly and mental retardation. Both the XLas isoforms and the ALEX protein are mutated which strongly reduces the interaction between them and this may allow unimpeded activation of the XLas isoforms. & Defects in GNAS are a cause of ACTH-independent macronodular adrenal hyperplasia (AIMAH) [MIM:219080]; also known as adrenal Cushing syndrome due to AIMAH. AIMAH is an endogenous form of adrenal Cushing syndrome characterized by multiple bilateral adrenocortical nodules that cause a striking enlargement of the adrenal glands. & Genetic variations in GNAS are the cause of pseudohypoparathyroidism type 1B (PHP1B) [MIM:603233]. PHP1B is characterized by parathyroid hormone (PTH)-resistant hypocalcemia and hyperphosphatemia. Patients affected with PHP1B have normal activity of the product of GNAS, lack developmental defects characteristic of AHO, and typically show no other endocrine abnormalities besides resistance to PTH. Most affected individuals have defects in methylation of the gene. In some cases microdeletions involving the STX16 appear to cause loss of methylation at exon A/B of GNAS, resulting in PHP1B. Paternal uniparental isodisomy have also been observed.| O95467 # Defects in GNAS are a cause of ACTH-independent macronodular adrenal hyperplasia (AIMAH) [MIM:219080]; also known as adrenal Cushing syndrome due to AIMAH. AIMAH is an endogenous form of adrenal Cushing syndrome characterized by multiple bilateral adrenocortical nodules that cause a striking enlargement of the adrenal glands. & Genetic variations in GNAS are the cause of pseudohypoparathyroidism type 1B (PHP1B) [MIM:603233]. PHP1B is characterized by parathyroid hormone (PTH)-resistant hypocalcemia and hyperphosphatemia. Patients affected with PHP1B have normal activity of the product of GNAS, lack developmental defects characteristic of AHO, and typically show no other endocrine abnormalities besides resistance to PTH. Most affected individuals have defects in methylation of the gene. In some cases microdeletions involving the STX16 appear to cause loss of methylation at exon A/B of GNAS, resulting in PHP1B. Paternal uniparental isodisomy have also been observed.| P84996 # Defects in GNAS are the cause of GNAS hyperfunction [MIM:139320]. This condition is characterized by increased trauma- related bleeding tendency, prolonged bleeding time, brachydactyly and mental retardation. Both the XLas isoforms and the ALEX protein are mutated which strongly reduces the interaction between them and this may allow unimpeded activation of the XLas isoforms. & Defects in GNAS are a cause of ACTH-independent macronodular adrenal hyperplasia (AIMAH) [MIM:219080]; also known as adrenal Cushing syndrome due to AIMAH. AIMAH is an endogenous form of adrenal Cushing syndrome characterized by multiple bilateral adrenocortical nodules that cause a striking enlargement of the adrenal glands. & Genetic variations in GNAS are the cause of pseudohypoparathyroidism type 1B (PHP1B) [MIM:603233]. PHP1B is characterized by parathyroid hormone (PTH)-resistant hypocalcemia and hyperphosphatemia. Patients affected with PHP1B have normal activity of the product of GNAS, lack developmental defects characteristic of AHO, and typically show no other endocrine abnormalities besides resistance to PTH. Most affected individuals have defects in methylation of the gene. In some cases microdeletions involving the STX16 appear to cause loss of methylation at exon A/B of GNAS, resulting in PHP1B. Paternal uniparental isodisomy have also been observed. & Defects in GNAS may be a cause of colorectal cancer (CRC) [MIM:114500]."
      SIMILARITY: SwissProt: P63092 ## Belongs to the G-alpha family. G(s) subfamily.| Q5JWF2 ## Belongs to the G-alpha family. G(s) subfamily.| O95467 ## Belongs to the NESP55 family. | P84996 ## Belongs to the ALEX family.
      MISCELLANEOUS: This protein is produced by a bicistronic gene which also produces the ALEX protein from an overlapping reading frame. & The GNAS locus is imprinted in a complex manner, giving rise to distinct paternally, maternally and biallelically expressed proteins. The XLas isoforms are paternally derived, the Gnas isoforms are biallelically derived and the Nesp55 isoforms are maternally derived.
      Molecular Weightlarge isoform (52 kDa) and small isoform (45 kDa)
      Physicochemical Information
      Dimensions
      Materials Information
      Toxicological Information
      Safety Information according to GHS
      Safety Information
      Product Usage Statements
      Quality Assuranceroutinely evaluated by immunoblot on rat brain microsomal preparation (Catalog #12-144)
      Usage Statement
      • Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
      Storage and Shipping Information
      Storage ConditionsMaintain for 2 years at -20°C from date of shipment. Aliquot to avoid repeated freezing and thawing. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.
      Packaging Information
      Material Size50 µL
      Transport Information
      Supplemental Information
      Specifications

      Documentation

      SDS

      Title

      Safety Data Sheet (SDS) 

      Certificates of Analysis

      TitleLot Number
      Anti-Gs Alpha_2844100 2844100
      Anti-Gsa (rabbit polyclonal IgG) - DAM1776428 DAM1776428
      Anti-Gsa (rabbit polyclonal IgG) - JBC1878059 JBC1878059
      Anti-Gsa - 2040092 2040092
      Anti-Gsa - 2172457 2172457
      Anti-Gsa - 2201659 2201659
      Anti-Gsa - DAM1493406 DAM1493406
      Anti-Gsa - DAM1588232 DAM1588232
      Anti-Gsa - DAM1641090 DAM1641090
      Anti-Gsa - DAM1734760 DAM1734760

      References

      Reference overviewPub Med ID
      Differential effects of antidepressants escitalopram versus lithium on Gs alpha membrane relocalization.
      Donati, RJ; Schappi, J; Czysz, AH; Jackson, A; Rasenick, MM
      BMC neuroscience  16  40  2015

      Show Abstract
      26162823 26162823
      Parathyroid hormone signaling via Gαs is selectively inhibited by an NH(2)-terminally truncated Gαs: implications for pseudohypoparathyroidism.
      Svetlana Puzhko,Cynthia Gates Goodyer,Mohammad Amin Kerachian,Lucie Canaff,Madhusmita Misra,Harald Jüppner,Murat Bastepe,Geoffrey N Hendy
      Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research  26  2011

      Show Abstract
      21713996 21713996
      Transmembrane adenylyl cyclase regulates amphibian sperm motility through protein kinase A activation.
      O'Brien, ED; Krapf, D; Cabada, MO; Visconti, PE; Arranz, SE
      Developmental biology  350  80-8  2011

      Show Abstract
      21126515 21126515
      Arrestin-3 is essential for the activation of Fyn by the luteinizing hormone receptor (LHR) in MA-10 cells.
      Colette Galet,Mario Ascoli
      Cellular signalling  20  2008

      Show Abstract Full Text Article
      18647647 18647647