SLC2A12 Knockout Cell Line (HEK293)

The choice depends on whether you are studying SLC2A12 (GLUT12)'s role as a class III facilitative glucose transporter or its functions in insulin-responsive glucose uptake in non-classical contexts. The Knockout line is the standard tool for asking whether GLUT12 is required for glucose uptake — GLUT12 is principally expressed in cardiac and skeletal muscle, adipose tissue, prostate, and small intestine, and has been characterized as an insulin-responsive glucose transporter, distinct from but complementary to GLUT4. Overexpression is useful for testing transport activity in heterologous systems or for studying GLUT12 trafficking dynamics. For GLUT12 research, the EDITGENE Knockout in HEK293 is a standard mechanistic platform — HEK293 has been extensively used for GLUT family biochemistry and structure-function characterization. Note that physiological insulin-responsive GLUT12 trafficking research benefits from muscle (L6, C2C12) or adipocyte (3T3-L1) models. GLUT12 has emerging relevance in prostate cancer where it has been reported as upregulated and contributing to glucose handling in tumor cells. Rescue with wild-type or transport-deficient GLUT12 is the standard specificity control.

Primary applications: • Glucose uptake assays: ³H-2-deoxyglucose uptake assays under basal and insulin-stimulated conditions (where applicable) to quantify GLUT12-dependent transport activity. • Substrate specificity: comparative uptake of glucose, fructose, and 2-deoxyglucose to characterize GLUT12 substrate scope relative to other class III GLUTs (GLUT8, GLUT10, GLUT13). • Trafficking studies: GLUT12 has both intracellular and plasma membrane pools — imaging-based analysis of trafficking determinants and insulin-induced translocation in rescue cell lines. • Prostate cancer biology: where applicable, studies of GLUT12's emerging role in prostate cancer glucose metabolism. EDITGENE recommends this model for researchers investigating class III GLUT biology, insulin-responsive glucose transport mechanisms, and GLUT12-related cancer metabolism. Physiological insulin-stimulated translocation studies benefit from muscle or adipocyte complementary models.

Yes. GLUT12 rescue experiments require attention to its dual intracellular/surface trafficking biology: • Construct design: use a codon-modified SLC2A12 sequence with a small C-terminal tag (FLAG, HA). GLUT12 has 12 transmembrane domains in the canonical GLUT family architecture — both N- and C-terminal cytoplasmic tags are tolerated, though small epitope tags are preferred over large fusions. • Trafficking-mutant rescue: GLUT12 contains dileucine-based and tyrosine-based sorting motifs in its N-terminal cytoplasmic region — specific mutations in these motifs disrupt intracellular retention and enable trafficking mechanism studies. • Transport-deficient rescue: substrate-binding pocket mutations (analogous to GLUT4 transport-deficient mutations) enable structure-function studies separating transport activity from trafficking functions. • Functional readout: rescue should restore ³H-2-deoxyglucose uptake activity; for trafficking studies, surface biotinylation or imaging-based quantification of plasma membrane GLUT12 pools. HEK293 transduces efficiently with lentivirus and is well-suited for GLUT12 biochemistry and trafficking studies in a heterologous expression context.