Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

GCG, Mouse, Clone: HGL-B5, Abnova™

Mouse monoclonal antibody raised against full-length GCG.

Supplier:  Abnova Corporation MAB8497

Catalog No. 89-113-474

This item is not returnable. View return policy

Description

Description

The protein encoded by this gene is actually a preproprotein that is cleaved into four distinct mature peptides. One of these, glucagon, is a pancreatic hormone that counteracts the glucose-lowering action of insulin by stimulating glycogenolysis and gluconeogenesis. Glucagon is a ligand for a specific G-protein linked receptor whose signalling pathway controls cell proliferation. Two of the other peptides are secreted from gut endocrine cells and promote nutrient absorption through distinct mechanisms. Finally, the fourth peptide is similar to glicentin, an active enteroglucagon. [provided by RefSeq

Specifications

Specifications

GCG
Monoclonal
Unconjugated
The optimal working dilution should be determined by the end user.
GCG
GCG
Full length (31 amino acids) synthetic human GCG.
RUO
2641
Store at -20°C. For long term storage store at -80°C.
Aliquot to avoid repeated freezing and thawing.
IgG1
ELISA, Immunofluorescence
HGL-B5
Mouse monoclonal antibody raised against full length GCG.
In PBS (0.05% sodium azide)
GLP1/GLP2/GRPP
Mouse
100 μg
Primary
Human
Liquid
Product Suggestions

Product Suggestions

Videos
SDS
Documents

Documents

Product Certifications
Promotions

Promotions

Product Content Correction

Your input is important to us. Please complete this form to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Your feedback has been submitted: Thank you for helping us improve our website.