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The GLUT family transporters (glucose transporters, members of the SLC2A gene family) are integral membrane proteins essential for the uptake and distribution of glucose and other sugars in mammalian cells, primarily by facilitating their diffusion across plasma membranes in accordance with concentration gradients[2][4][6]. Fourteen human isoforms are known, each with unique tissue distributions, substrate specificities, and kinetic properties[2][1]. The best-characterized are GLUT1 (basal glucose uptake), GLUT2 (bidirectional transport, important in liver/pancreas), GLUT3 (neuronal transport), and GLUT4 (insulin-responsive transporter in muscle and adipose tissue)[2][3][4]. Mutations or changes in GLUT activities are implicated in a range of diseases from cancer and diabetes to gout and neurological disorders[2][4][5][1]. The family is structurally related to the major facilitator superfamily, sharing a core architecture of 12 transmembrane helices[6][7]. Drugs targeting individual GLUTs may act by competitive or allosteric inhibition at sugar or urate binding sites, thereby modulating metabolism, cell proliferation, or signaling relevant to the associated disease[4][5].
Competitive inhibition of glucose binding sites (cytochalasin B, forskolin); Allosteric inhibition of urate transport (benzbromarone, losartan for GLUT9)
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