GlycoErase™ PYGL Knockout HEK293T Cell Line (CAT#: GLJF-0825-JF595)

Description	GlycoErase™ PYGL knockout HEK293T cell line eliminates PYGL, the liver isoform of glycogen phosphorylase responsible for mobilizing glycogen to maintain systemic glucose balance. Mutations cause glycogen storage disease type VI (Hers disease). The knockout provides a system for studying hepatic glycogen metabolism, energy release, and hypoglycemia mechanisms.
Product Type	KO Cell Lines
Species	Human
Cell Morphology	Epithelial-like, adherent
Passage Ratio	1:2~1:4
Cell Line	HEK293T
Lineage	Embryonic kidney

Cell Viability	>90%
Sterility Test	The sterility test indicated an absence of microbial growth.
Identity Test	STR identification
Mycoplasma Test	Negative
Virus Test	Negative for HIV, HBV and HCV.
Genetic Stability Testing	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.
Validation	PCR, Sanger Sequencing
Culture Medium	DMEM & FBS & Penicillin/Streptomycin
Application	Functional assay
Size	1 M cells/vial*2
Product Format	Frozen
Shipping	Dry ice
Availability Status	Made to order
Handling Notes	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.
Product Disclaimer	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.

Target	PYGL
Full Name	Glycogen Phosphorylase L
Alternative Name	GSD6
Location	14q22.1
Gene ID	5836
Summary	This homodimeric enzyme cleaves alpha-1,4-glucosidic bonds in liver glycogen, releasing glucose-1-phosphate. It is activated from phosphorylase B to A through phosphorylation at serine 15 and further regulated by hormonal and allosteric factors. Mutations cause Hers disease (glycogen storage disease VI), characterized by hypoglycemia, mild ketosis, slowed growth, and liver enlargement. Multiple isoforms arise from alternative splicing.