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品种反应性 主要应用 宿主 格式 抗体类型 M, B, H WB, ICC Rb Serum Polyclonal Antibody 描述 产品目录编号 06-237 Replaces AB1639 品牌系列 Upstate
商名 - Upstate
描述 Anti-Gsα Antibody 产品信息 格式 Serum 控制 - Widely expressed
演示 Serum diluted 1:1 in PBS. 应用 应用 Anti-Gsα Antibody is an antibody against Gsα for use in IC, IP & WB. 主要应用 - Western Blotting
- Immunocytochemistry
生物信息 免疫原品种 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) 浓缩 Please refer to the Certificate of Analysis for the lot-specific concentration. 宿主 Rabbit 特异性 Recognizes the large and small forms of Gsα; does not cross-react with other G proteins. 同种型 IgG 品种反应性 MouseBovineHuman 抗体类型 Polyclonal Antibody Entrez基因编号 - NM_080426.2
- NM_000516.4
- NM_001077488.1
- NM_001077489.1
- NM_001077490.1
- NM_016592.2
- NM_080425.2
Entrez基因汇总 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. 基因符号 - XLalphas
- GNAS
- NESP55
- GNASXL
- C20orf45
- GPSA
- dJ309F20.1.1
- GSA
- PHP1B
- CARD3
- SCG6
- MGC33735
- GSP
- dJ806M20.3.3
- PHP1A
- GNAS1
- POH
- AHO
- NESP
纯化方法 Protein A purfied UniProt编号 - Q5JWF2
UniProt汇总 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.产品使用声明 质量保证 routinely evaluated by immunoblot on rat brain microsomal preparation (Catalog #12-144) 使用声明 - 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.
储存和货运信息 存储条件 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. 包装信息 数量 50 µL
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