GlycoErase™ SLC35A2 Knockout Human Osteosarcoma Cell 143B (CAT#: GLJF-0525-JF207)

Description	The SLC35A2 knockout 143B cell line, deficient in solute carrier family 35 member A2 (a nucleotide sugar transporter), enables the study of nucleoside-sugar transport disruption in bone sarcoma, potentially broadly impacting nucleotide sugar availability for glycosylation and glycosylatioN-related metabolic processes in osteosarcoma.
Product Type	KO Cell Lines
Species	Human
Cell Morphology	Epithelial-like, adherent
Passage Ratio	1:2~1:3
Cell Line	143B
Primary Disease	Osteosarcoma
Lineage	Bone

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	Bromodeoxyuridine & EMEM & 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	SLC35A2
Full Name	Solute carrier family 35 member A2
Alternative Name	UGT, UDP-Gal-Tr, UGT1, UGAT, UGT2, UGTL, UGALT
Location	Xp11.23
Gene ID	7355
Summary	Transports UDP-galactose from the cytosol into Golgi vesicles for glycan synthesis; mutations cause congenital disorder of glycosylation type IIm (CDG2M).