Human Glycogen Phosphorylase (GP) ELISA Kit | GP elisa kit

Human Glycogen Phosphorylase (GP) ELISA Kit

Cat. Num. AAA9714682

• Gene Names: PYGL; GSD6
• Reactivity: Human
• Synonyms: Glycogen Phosphorylase (GP); Human Glycogen Phosphorylase (GP) ELISA Kit; PYGL; GSD6; liver glycogen phosphorylase; GP elisa kit

• Reactivity: Human
• Specificity: Human Glycogen phosphorylase (GP) ELISA Kit has high sensitivity and excellent specificity for detection of Human PYGL. No significant cross-reactivity or interference between Human PYGL and analogues was observed.
• Sequence Length: 248

• Assay Type: Sandwich ELISA (Quantitative)
• Samples: Cell Culture Supernatants, Serum, Plasma, Other Biological Fluids
• Detection Method: Colorimetric
• Usage Notes: * Do not mix components from different kit lots or use reagents beyond the kit expiration date.; * Allow all reagents to warm to room temperature for at least 30 minutes before opening.; * Pre-rinse the pipet tip with reagent, use fresh pipet tips for each sample, standard and reagent to avoid contamination.; * Unused wells must be kept desiccated at 4 degree C in the sealed bag provided.; * Mix Thoroughly is very important for the result. It is recommended using low frequency oscillator or slight hand shaking every 10 minutes.; * It is recommended that all samples and standards be assayed in duplicate or triplicate.
• Preparation and Storage: Store at 2-8 degree C.

Typical Testing Data/Standard Curve (for reference only)

(Fig.1. Human Glycogen phosphorylase (GP) Standard Curve.)

Related Product Information for GP elisa kit

Description: This Human Glycogen phosphorylase (GP) ELISA Kit employs a two-site sandwich ELISA to quantitate PYGL in samples. An antibody specific for PYGL has been pre-coated onto a microplate. Standards and samples are pipetted into the wells and any PYGL present is bound by the immobilized antibody. After removing any unbound substances, a biotin-conjugated antibody specific for PYGL is added to the wells. After washing, Streptavidin conjugated Horseradish Peroxidase (HRP) is added to the wells. Following a wash to remove any unbound avidin-enzyme reagent, a substrate solution is added to the wells and color develops in proportion to the amount of PYGL bound in the initial step. The color development is stopped and the intensity of the color is measured.

Background: Glycogen phosphorylase is one of the phosphorylase enzymes (EC 2.4.1.1). Glycogen phosphorylase catalyzes the rate-limiting step in glycogenolysis in animals by releasing glucose-1-phosphate from the terminal alpha-1,4-glycosidic bond. Glycogen phosphorylase is also studied as a model protein regulated by both reversible phosphorylation and allosteric effects

NCBI and Uniprot Product Information

• NCBI GI #: 40675618
• NCBI GeneID: 5836
• UniProt Accession #: P06737
• NCBI Official Full Name: PYGL protein, partial
• NCBI Official Synonym Full Names: glycogen phosphorylase L
• NCBI Official Symbol: PYGL
• NCBI Official Synonym Symbols: GSD6
• NCBI Protein Information: glycogen phosphorylase, liver form
• UniProt Protein Name: Glycogen phosphorylase, liver form
• Protein Family: Envelopment polyprotein
• UniProt Gene Name: PYGL
• UniProt Entry Name: PYGL_HUMAN

NCBI Description

This gene encodes a homodimeric protein that catalyses the cleavage of alpha-1,4-glucosidic bonds to release glucose-1-phosphate from liver glycogen stores. This protein switches from inactive phosphorylase B to active phosphorylase A by phosphorylation of serine residue 15. Activity of this enzyme is further regulated by multiple allosteric effectors and hormonal controls. Humans have three glycogen phosphorylase genes that encode distinct isozymes that are primarily expressed in liver, brain and muscle, respectively. The liver isozyme serves the glycemic demands of the body in general while the brain and muscle isozymes supply just those tissues. In glycogen storage disease type VI, also known as Hers disease, mutations in liver glycogen phosphorylase inhibit the conversion of glycogen to glucose and results in moderate hypoglycemia, mild ketosis, growth retardation and hepatomegaly. Alternative splicing results in multiple transcript variants encoding different isoforms.[provided by RefSeq, Feb 2011]