货号：06-237

品牌：Merck Millipore

规格：50UL

目录价：￥5974.00

市场价格：￥5077.90

会员价格：￥4779.20

金山科研平台，产品价格货期咨询微信：jinshanbio Description: Anti-Gsα Antibody | 06-237 View All» Replaces: AB1639 View All» Promotional Text: Special Shipping Offer on Antibodies100% Performance Guaranteed View All» Trade Name: Upstate (Millipore) View All» Specificity: Recognizes the large and small forms of Gsα; does not cross-react with other G proteins. View All» Molecular Weight: large isoform (52 kDa) and small isoform (45 kDa) View All» Immunogen: peptide corresponding to the c-terminus of bovine Gsα (RMHLRQYELL); this sequence is present in all three isoforms of human Gsα (Gsα1, Gsα2, and GsαXL) View All» Isotype: IgG View All» Species Reactivity:

• Bovine

• Human

• Mouse
  View All» Control: Widely expressed View All» Quality Assurance: routinely evaluated by immunoblot on rat brain microsomal preparation (Catalog #12-144) View All» Purification Method: Protein A purfied View All» Presentation: Serum diluted 1:1 in PBS. View All» Storage Conditions: Maintain 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. View All» UniProt Number: Q5JWF2 View All» Entrez Gene Number:
  • NM_000516.4

  • NM_001077488.1

  • NM_001077489.1

  • NM_001077490.1

  • NM_016592.2

  • NM_080425.2

  • NM_080426.2
    View All» 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
      View All» 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. View All» Key Applications:
      • Immunocytochemistry

      • Immunoprecipitation

      • Western Blotting
        View All» Entrez Gene Summary: 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 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. View All» UniProt Summary: FUNCTION: 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. View All» Brand Family: Upstate View All» Product Name: Anti-Gsα Antibody | 06-237 View All» Concentration: Variable View All» Antibody Type: Polyclonal Antibody View All» Qty/Pk: 50 μL View All» Format: Serum View All» Host: Rabbit View All»
        © 金山科研平台是专业的授权总代理区域代理经销平台。
        © 如需询价，请加客服QQ：1749072012 、客服微信：jinshanbio，或发送邮件到1749072012@qq.com
        © 平台为生命科学研究相关领域提供一站式耗材试剂仪器解决方案和采购服务，数据资源基于CC协议。
        © 本文地址：https://www.16ao.com/thread-134345.htm
        © Merck Millipore代理06-237 Anti-Gsα Antibody;store at -20℃，产品报价联系微信jinshanbio