GlycoFlux™ Human PHKA2 Overexpression HEK293 Cell Line

GlycoFlux™ human PHKA2 overexpression HEK293 cell line boosts PHKA2, the hepatic α-subunit of phosphorylase kinase. Defects lead to glycogen storage disease IXa, and this engineered system provides a model for liver glycogen metabolism and X-linked glycogenosis.

Overexpression Cell Lines

Human

Epithelial-like, adherent

1:2~1:4

HEK293

Embryonic kidney

>90%

The sterility test indicated an absence of microbial growth.

STR identification

Negative

Negative for HIV, HBV and HCV.

We conduct cell genetic stability studies in full compliance with ICH guidelines. Our expertise enables us to design and execute a comprehensive testing program tailored to your specific needs and regulatory requirements.

qPCR, Sanger Sequencing

FBS & Penicillin/Streptomycin & Proline & DMEM

Mechanistic studies; Exploration of glycosylation and signaling pathways in cancer, metabolic, and immune-related diseases; Drug target validation and other functional assays.

1 M cells/vial*2

Frozen

Dry ice

Made to order

Upon receipt, this product must be immediately transferred from dry ice to liquid nitrogen (-150°C to -190°C) and stored in a liquid nitrogen tank. Cell viability is critically dependent on proper handling. We cannot guarantee viability if these instructions are not strictly adhered to.

This product is provided for research only, not suitable for human or animal use. Due to the inherent limitations of infectious agent testing, investigators must exercise extreme caution when handling cells provided by Creative Biolabs, treating all cells as potentially biohazardous.

PHKA2

Phosphorylase Kinase Regulatory Subunit Alpha 2

PHK; PYK; XLG; PYKL; XLG2; GSD9A

Xp22.13

Phosphorylase kinase is a 16-subunit enzyme composed of four alpha, beta, gamma, and delta subunits. The alpha subunit includes skeletal muscle and hepatic isoforms, with the hepatic form encoded by this gene. The gamma subunit holds the active site, while alpha and beta are regulatory. The delta subunit, a calmodulin, mediates calcium dependence. Mutations cause glycogen storage disease type 9A (X-linked liver glycogenosis). Alternative splice variants have been reported, though full-length forms are not defined.