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Rabbit anti-Human GIPR Polyclonal Antibody

The antibody against GIPR was raised in rabbit using the Synthetic peptide of Human GIPR as the immunogen. This antibody exists as a non-conjugated isotype IgG, Antigen affinity purified. This antibody has been validated on ELISA, WB.

ADC-27186A

The antibody against GIPR was raised in rabbit using the Synthetic peptide of Human GIPR as the immunogen. This antibody exists as a non-conjugated isotype IgG, Antigen affinity purified. This antibody has been validated on ELISA, WB.

$299.00

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Specifications


Cat.No ADC-27186A ClonalityPolyclonal
Host SpeciesRabbitTarget NameGIPR
Target SynonymsGIPR; Gastric inhibitory polypeptide receptor; GIP-R; Glucose-dependent insulinotropic polypeptide receptorFormLiquid
Species ReactivityHuman, MouseIsotypeIgG
Storage Buffer0.05% NaN3, 40% Glycerol., pH7.4 PBSPurification MethodAntigen affinity purified
ConjugateNon-conjugatedApplicationELISA, WB
StorageUpon receipt

Immunogen Information


Immunogen DescriptionSynthetic peptide of Human GIPRTarget SpeciesHuman
Immunogen SequenceComplete sequences for the immunogen, target protein, and peptides are available upon request.Uniprot IDP48546
Background Information
  • Uniprot Id

    P48546

  • Target Species

    Human

  • Target Name

    GIPR

  • Target Full Name

    Gastric inhibitory polypeptide receptor

  • Target Function

    This is a receptor for GIP. The activity of this receptor is mediated by G proteins which activate adenylyl cyclase.

  • Target Subcellular Location

    Cell membrane; Multi-pass membrane protein.

  • Target Protein Families

    G-protein coupled receptor 2 family

  • Target Research Area

    Others

  • Target Synonyms

    GIPR; Gastric inhibitory polypeptide receptor; GIP-R; Glucose-dependent insulinotropic polypeptide receptor

  • Target Background

    This gene encodes a G-protein coupled receptor for gastric inhibitory polypeptide (GIP), which was originally identified as an activity in gut extracts that inhibited gastric acid secretion and gastrin release, but subsequently was demonstrated to stimulate insulin release in the presence of elevated glucose. Mice lacking this gene exhibit higher blood glucose levels with impaired initial insulin response after oral glucose load. Defect in this gene thus may contribute to the pathogenesis of diabetes.

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