GlycoErase™ FBP1 Knockout HEK293 Cell Line

GlycoErase™ FBP1 knockout HEK293 cell line is a human embryonic kidney (HEK293) model lacking FBP1 expression. FBP1 encodes fructose-1,6-bisphosphatase, a key enzyme in gluconeogenesis that catalyzes the conversion of fructose-1,6-bisphosphate to fructose-6-phosphate. Deficiency of FBP1 is associated with hypoglycemia and metabolic acidosis. The knockout of FBP1 in the HEK293 background provides a functional system to study gluconeogenesis, energy homeostasis, and metabolic disease, supporting applications in glucose metabolism research, rare metabolic disorder modeling, and therapeutic development.

KO 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.

PCR, Sanger Sequencing

FBS & Penicillin/Streptomycin & Proline & RPMI

Functional assay

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.

FBP1

Fructose-Bisphosphatase 1

FBP

9q22.32

Fructose-1,6-bisphosphatase 1 is a gluconeogenesis enzyme that hydrolyzes fructose-1,6-bisphosphate into fructose 6-phosphate and inorganic phosphate. Deficiency results in hypoglycemia and metabolic acidosis.