GlycoErase™ PYGL Knockout HepG2 Cell Line (CAT#: GLJF-0825-JF711)

Description	GlycoErase™ PYGL knockout HepG2 cell line eliminates PYGL, the liver glycogen phosphorylase isoform. PYGL mobilizes glycogen to maintain glucose homeostasis. Mutations cause glycogen storage disease type VI (Hers disease). This knockout model supports research on hepatic glycogen metabolism, energy mobilization, and hypoglycemia-associated mechanisms in liver cells.
Product Type	KO Cell Lines
Species	Human
Cell Morphology	Epithelial-like, adherent
Passage Ratio	1:4~1:6
Cell Line	HepG2
Primary Disease	Hepatoblastoma
Lineage	Liver
Lineage Subtype	Hepatoblastoma

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 & Glutamine
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 gene encodes the liver glycogen phosphorylase, which releases glucose-1-phosphate from glycogen via alpha-1,4 bond cleavage. Phosphorylation at serine 15 activates it, with hormonal and allosteric regulation. Mutations cause Hers disease (GSD VI) with hypoglycemia, mild ketosis, growth delay, and enlarged liver. Alternative splicing yields multiple isoforms.