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Human GIPR Protein, His Tag (MALS verified)

Related Products: Cell line CHEK-ATP205 and CHEK-ATF104
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GIR-H52H3-100ug
$500.00
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GIR-H52H3-1mg (500ug X 2)
$3,640.00
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GIR-H52H3
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Product Details
Performance Data
Reviews & Citations
Resources
  • Product Details
  • Performance Data
  • Reviews & Citations
  • Important Statement
  • Resources
Synonyms

PGQTL2

Source

Human GIPR Protein, His Tag (GIR-H52H3) is expressed from human 293 cells (HEK293). It contains AA Gly 26 - Gln 138 (Accession # P48546-1).

Predicted N-terminus: Gly 26

Molecular Characterization
Other Tags and Version Biotin & Other Labeled Version

This protein carries a polyhistidine tag at the C-terminus.

The protein has a calculated MW of 14.9 kDa. The protein migrates as 20-28 kDa when calibrated against Star Ribbon Pre-stained Protein Marker under reducing (R) condition (SDS-PAGE) due to glycosylation.

Endotoxin

Less than 1.0 EU per μg by the LAL method / rFC method.

Purity

>95% as determined by SDS-PAGE.

>95% as determined by SEC-MALS.

Formulation

Lyophilized from 0.22 μm filtered solution in PBS, pH7.4 with trehalose as protectant.

Contact us for customized product form or formulation.

Reconstitution

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

Shipping and Storage

This product is shipped at ambient temperature.

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:
  • -20°C to -70°C for 12 months in lyophilized state;
  • -70°C for 3 months under sterile conditions after reconstitution.
ACRO Quality Management System

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. [provided by RefSeq, Oct 2011]