GIPr
Anti-GIPr Recombinant Antibody Products
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- Species Reactivity: Human
- Type: Human IgG
- Application: ELISA, Block, FuncS
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- Species Reactivity: Mouse
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- Derivation: Mouse
- Species Reactivity: Human
- Type: Mouse IgG1
- Application: FC
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- Species Reactivity: Human
- Type: ADCC enhanced antibody
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- Species Reactivity: Mouse
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- Species Reactivity: Human
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- Species Reactivity: Human
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- Species Reactivity: Human; Nonhuman primate
- Type: Human IgG
- Application: Inhib, FuncS
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- Species Reactivity: Mouse
- Type: Human IgG1
- Application: ELISA, FuncS
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- Species Reactivity: Mouse
- Type: Human IgG1
- Application: ELISA, FuncS
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- Species Reactivity: Human
- Type: Mouse IgG1
- Application: Block, FC, IHC, CyTOF®
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- Species Reactivity: Human
- Type: Mouse IgG2a
- Application: Neut, FC, CyTOF®
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- Species Reactivity: Human
- Type: Mouse IgG1
- Application: Neut, FC, CyTOF®
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- Species Reactivity: Mouse
- Type: Mouse IgG1
- Application: ELISA, FC
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- Species Reactivity: Mouse
- Type: Human scFv
- Application: ELISA, FuncS
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- Species Reactivity: Mouse
- Type: Human scFv
- Application: ELISA, FuncS
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- Species Reactivity: Human
- Type: Human Fab
- Application: ELISA, Block, FuncS
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- Species Reactivity: Mouse
- Type: Mouse scFv
- Application: ELISA, FC
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- Species Reactivity: Mouse
- Type: Mouse Fab
- Application: ELISA, FC
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- Species Reactivity: Human
- Type: Llama VHH
- Application: IP, ChiP, IHC, ELISA
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- Species Reactivity: Human
- Type: Antibody
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- Species Reactivity: Mouse
- Type: Human Fab
- Application: ELISA, FuncS
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- Species Reactivity: Mouse
- Type: Human Fab
- Application: ELISA, FuncS
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- Species Reactivity: Human
- Type: Human scFv
- Application: ELISA, Block, FuncS
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- Derivation: Phage display library
- Species Reactivity: Human
- Type: Rabbit IgG
- Application: WB, IHC, ICC, FC
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For Research Use Only. Not For Clinical Use.
GIPR 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.