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>   首页   >   产品   >   一抗   >   心血管   >   GSK3A Antibody (Center)   

GSK3A Antibody (Center)

Purified Rabbit Polyclonal Antibody (Pab)

     
  • 1 - GSK3A Antibody (Center) AP21095a
    Western blot analysis of lysates from mouse NIH/3T3 cell line, rat brain tissue lysate(from left to right), using GSK3A Antibody (Center)(Cat. #AP21095a). AP21095a was diluted at 1:1000 at each lane. A goat anti-rabbit IgG H&L(HRP) at 1:10000 dilution was used as the secondary antibody. Lysates at 20ug per lane.
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Product info
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB, E
Primary Accession P49840
Reactivity Mouse, Rat
Host Rabbit
Clonality Polyclonal
Isotype Rabbit Ig
Calculated MW 50981 Da
Additional info
Gene ID 2931
Other Names Glycogen synthase kinase-3 alpha, GSK-3 alpha, Serine/threonine-protein kinase GSK3A, GSK3A
Target/Specificity This GSK3A antibody is generated from a rabbit immunized with a KLH conjugated synthetic peptide between 348-382 amino acids from the Central region of human GSK3A.
Dilution WB~~1:1000
StorageMaintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
PrecautionsGSK3A Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name GSK3A
Function Constitutively active protein kinase that acts as a negative regulator in the hormonal control of glucose homeostasis, Wnt signaling and regulation of transcription factors and microtubules, by phosphorylating and inactivating glycogen synthase (GYS1 or GYS2), CTNNB1/beta-catenin, APC and AXIN1. Requires primed phosphorylation of the majority of its substrates. Contributes to insulin regulation of glycogen synthesis by phosphorylating and inhibiting GYS1 activity and hence glycogen synthesis. Regulates glycogen metabolism in liver, but not in muscle. May also mediate the development of insulin resistance by regulating activation of transcription factors. In Wnt signaling, regulates the level and transcriptional activity of nuclear CTNNB1/beta-catenin. Facilitates amyloid precursor protein (APP) processing and the generation of APP-derived amyloid plaques found in Alzheimer disease. May be involved in the regulation of replication in pancreatic beta-cells. Is necessary for the establishment of neuronal polarity and axon outgrowth. Through phosphorylation of the anti-apoptotic protein MCL1, may control cell apoptosis in response to growth factors deprivation.
Research Areas
Involvement of Protein Acyltransferase ZDHHC3 in Maintaining Oocyte Meiotic Arrest in Xenopus laevis.
Author : Fang J1,Wang H2,Miao L2,Kuang X1,Ma W2,Wang C3,Zhang J4,Xia G5.
Biol Reprod. 2016 Sep;95(3):67. Epub 2016 Aug 10.
27512151

BACKGROUND

Constitutively active protein kinase that acts as a negative regulator in the hormonal control of glucose homeostasis, Wnt signaling and regulation of transcription factors and microtubules, by phosphorylating and inactivating glycogen synthase (GYS1 or GYS2), CTNNB1/beta-catenin, APC and AXIN1. Requires primed phosphorylation of the majority of its substrates. Contributes to insulin regulation of glycogen synthesis by phosphorylating and inhibiting GYS1 activity and hence glycogen synthesis. Regulates glycogen metabolism in liver, but not in muscle. May also mediate the development of insulin resistance by regulating activation of transcription factors. In Wnt signaling, regulates the level and transcriptional activity of nuclear CTNNB1/beta-catenin. Facilitates amyloid precursor protein (APP) processing and the generation of APP-derived amyloid plaques found in Alzheimer disease. May be involved in the regulation of replication in pancreatic beta-cells. Is necessary for the establishment of neuronal polarity and axon outgrowth. Through phosphorylation of the anti-apoptotic protein MCL1, may control cell apoptosis in response to growth factors deprivation.

REFERENCES

He X.,et al.Submitted (MAR-1995) to the EMBL/GenBank/DDBJ databases.
Hoshino T.,et al.Submitted (NOV-1997) to the EMBL/GenBank/DDBJ databases.
Grimwood J.,et al.Nature 428:529-535(2004).
Nikoulina S.E.,et al.Diabetes 49:263-271(2000).
Phiel C.J.,et al.Nature 423:435-439(2003).

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