disease:Defects in SLC2A4 may be a cause of noninsulin-dependent diabetes mellitus (NIDDM) [MIM:125853]. Defects in SLC2A4 may be a cause of certain post-receptor defects in NIDDM. The variant in position Ile-383 is found in a small number of NIDDM patients, but seems not to be found in nondiabetic subjects.,function:Insulin-regulated facilitative glucose transporter.,miscellaneous:Insulin-stimulated phosphorylation of TBC1D4 is required for GLUT4 translocation.,online information:GLUT4 entry,PTM:Sumoylated.,similarity:Belongs to the major facilitator superfamily. Sugar transporter (TC 2.A.1.1) family. Glucose transporter subfamily.,subcellular location:Localizes primarily to the perinuclear region, undergoing continued recycling to the plasma membrane where it is rapidly reinternalized. The dileucine internalization motif is critical for intracellular sequestration.,subunit:Binds to DAXX. Interacts via its N-terminus with SRFBP1.,tissue specificity:Skeletal and cardiac muscles; brown and white fat.,
Cell membrane ; Multi-pass membrane protein . Endomembrane system ; Multi-pass membrane protein . Cytoplasm, perinuclear region . Localizes primarily to the perinuclear region, undergoing continued recycling to the plasma membrane where it is rapidly reinternalized (PubMed:8300557). The dileucine internalization motif is critical for intracellular sequestration (PubMed:8300557). Insulin stimulation induces translocation to the cell membrane (By similarity). .
Skeletal and cardiac muscles; brown and white fat.
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