PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18506424-2 2008 In contrast, myo-inositol uptake is inhibited at low concentrations, reflecting that it occurs both by the high-affinity Na(+)-dependent myo-inositol transporter (SMIT) and the lower-affinity H(+)-dependent inositol transporter (HMIT). Inositol 13-25 solute carrier family 5 member 3 Homo sapiens 163-167 16420717-1 2007 Recent in-vitro data indicate that depletion of neural cells of myo-inositol by virtue of down-regulation of the high-affinity sodium-myo-inositol co-transporter (SMIT) may be a common mechanism of action of the mood stabilizers lithium, valproate and carbamazepine. Inositol 64-76 solute carrier family 5 member 3 Homo sapiens 163-167 18020950-3 2007 HaCaT cells osmo-dependently express mRNA specific for transport proteins for betaine (BGT-1), myo-inositol (SMIT) and taurine (TAUT). Inositol 95-107 solute carrier family 5 member 3 Homo sapiens 109-113 11956339-7 2002 In the absence of compatible osmolytes, increased mRNA levels and corresponding activities of betaine/gamma-aminobutyric acid transporter (BGT1) and sodium/myo-inositol transporter (SMIT) induced by hypertonicity remained high after 72 h incubation, whereas they were down regulated in the presence of betaine and myo-inositol. Inositol 156-168 solute carrier family 5 member 3 Homo sapiens 182-186 15613375-2 2005 Although their transport stoichiometries have not been directly determined, significant cooperativities in the Na+ activation of SMIT1 and SMIT2 suggest that more than one Na+ ion drives the transport of each myo-inositol. Inositol 209-221 solute carrier family 5 member 3 Homo sapiens 129-134 10362595-1 1999 myo-Inositol is a ubiquitous intracellular organic osmolyte and phosphoinositide precursor maintained at millimolar intracellular concentrations through the action of membrane-associated Na+-myo-inositol cotransporters (SMIT). Inositol 0-12 solute carrier family 5 member 3 Homo sapiens 220-224 10393611-1 1999 The Na+/myo-inositol cotransporter (SLC5A3) gene, located on the long arm of human chromosome 21, may play a key role in osmoregulation including the regulation of levels of the "idiogenic osmole," myo-inositol, in brain cells. Inositol 8-20 solute carrier family 5 member 3 Homo sapiens 36-42 11252649-2 2000 This article examines the potential relevance of an alternative mechanism for inositol depletion: inhibition of myo-inositol uptake that proceeds via the sodium/myo-inositol cotransport (SMIT). Inositol 78-86 solute carrier family 5 member 3 Homo sapiens 154-185 11252649-2 2000 This article examines the potential relevance of an alternative mechanism for inositol depletion: inhibition of myo-inositol uptake that proceeds via the sodium/myo-inositol cotransport (SMIT). Inositol 78-86 solute carrier family 5 member 3 Homo sapiens 187-191 11252649-2 2000 This article examines the potential relevance of an alternative mechanism for inositol depletion: inhibition of myo-inositol uptake that proceeds via the sodium/myo-inositol cotransport (SMIT). Inositol 112-124 solute carrier family 5 member 3 Homo sapiens 154-185 11252649-2 2000 This article examines the potential relevance of an alternative mechanism for inositol depletion: inhibition of myo-inositol uptake that proceeds via the sodium/myo-inositol cotransport (SMIT). Inositol 112-124 solute carrier family 5 member 3 Homo sapiens 187-191 9882452-4 1999 In these studies we show that TNFalpha causes a concentration- and time-dependent decrease in Na+/myo-inositol cotransporter (SMIT) mRNA levels and myo-inositol accumulation as well as a decrease in myo-inositol incorporation into phosphoinositides. Inositol 98-110 solute carrier family 5 member 3 Homo sapiens 126-130 27217553-5 2016 We found that overexpression of the Na(+)/myo-inositol cotransporter (SMIT1) and myo-inositol supplementation enlarged intracellular PI(4,5)P2 pools, modulated several PI(4,5)P2-dependent ion channels including KCNQ2/3 channels, and attenuated the action potential firing of superior cervical ganglion neurons. Inositol 42-54 solute carrier family 5 member 3 Homo sapiens 70-75 34531253-0 2022 SLC5A3-dependent myo-inositol auxotrophy in acute myeloid leukemia. Inositol 17-29 solute carrier family 5 member 3 Homo sapiens 0-6 34531253-3 2022 We demonstrate that SLC5A3 is essential to support a myo-inositol auxotrophy in AML. Inositol 53-65 solute carrier family 5 member 3 Homo sapiens 20-26 34531253-5 2022 We use gain- and loss-of-function experiments to reveal a synthetic lethal genetic interaction between ISYNA1 and SLC5A3 in AML, which function redundantly to sustain intracellular myo-inositol. Inositol 181-193 solute carrier family 5 member 3 Homo sapiens 114-120 28128227-7 2017 In contrast, myo-inositol (transported through SMIT1) reproduced the toxic effects of HG. Inositol 13-25 solute carrier family 5 member 3 Homo sapiens 47-52 9820807-2 1998 Treating 3T3-L1 adipocytes with TNF-alpha decreases Na+/myo-inositol co-transporter (SMIT) mRNA levels and myo-inositol accumulation in a concentration-and time-dependent manner. Inositol 56-68 solute carrier family 5 member 3 Homo sapiens 85-89 9820807-6 1998 Hyperosmolarity increases SMIT gene expression as evidenced by the inhibition of hyperosmotic induction of SMIT mRNA levels by actinomycin D, and of myo-inositol accumulation by actinomycin D and cycloheximide. Inositol 149-161 solute carrier family 5 member 3 Homo sapiens 26-30 28793216-9 2017 We conclude that, independent of its transport activity and indirect regulatory mechanisms involving inositol-derived increases in PIP2, SMIT1, and likely other related sodium-dependent solute transporters, regulates KCNQ channel ion selectivity, gating, and pharmacology by direct physical interaction with the pore module. Inositol 101-109 solute carrier family 5 member 3 Homo sapiens 137-142 28283543-3 2017 Here, we discovered that KCNQ2/3 channels isoform-specifically colocalize with SMIT1 and SMIT2 at sciatic nerve nodes of Ranvier and in axon initial segments, and form channel-transporter complexes in vitro and in vivo KCNQ2/3 coexpression protected SMIT1 activity from the otherwise inhibitory effects of cellular depolarization imposed by elevating extracellular [K+], and KCNQ2 was required for potentiation of SMIT activity by myo-inositol preincubation. Inositol 431-443 solute carrier family 5 member 3 Homo sapiens 79-84 28283543-3 2017 Here, we discovered that KCNQ2/3 channels isoform-specifically colocalize with SMIT1 and SMIT2 at sciatic nerve nodes of Ranvier and in axon initial segments, and form channel-transporter complexes in vitro and in vivo KCNQ2/3 coexpression protected SMIT1 activity from the otherwise inhibitory effects of cellular depolarization imposed by elevating extracellular [K+], and KCNQ2 was required for potentiation of SMIT activity by myo-inositol preincubation. Inositol 431-443 solute carrier family 5 member 3 Homo sapiens 250-255 28283543-4 2017 Cytoskeletal disruption, which speeds PIP2 dispersion, attenuated potentiation of KCNQ2/3 currents by SMIT1-mediated myo-inositol uptake, suggesting close channel-transporter juxtaposition ensures KCNQ2/3 exposure to locally high myo-inositol-derived PIP2 concentrations. Inositol 117-129 solute carrier family 5 member 3 Homo sapiens 102-107 28283543-4 2017 Cytoskeletal disruption, which speeds PIP2 dispersion, attenuated potentiation of KCNQ2/3 currents by SMIT1-mediated myo-inositol uptake, suggesting close channel-transporter juxtaposition ensures KCNQ2/3 exposure to locally high myo-inositol-derived PIP2 concentrations. Inositol 230-242 solute carrier family 5 member 3 Homo sapiens 102-107 27294516-8 2016 In contrast to TASK-1, which was not differentially expressed in lung cancer vs. normal lung tissue, we found the Na+-coupled nutrient transporters, SLC5A3, SLC5A6, and SLC38A1, transporters for myo-inositol, biotin and glutamine, respectively, to be significantly overexpressed in lung adenocarcinomas. Inositol 195-207 solute carrier family 5 member 3 Homo sapiens 149-155 25756525-2 2015 The present study explores the SLC5A3 protein as a possible transporter of myo-inositol in hyponically swollen HEK293 cells. Inositol 75-87 solute carrier family 5 member 3 Homo sapiens 31-37 26125706-2 2015 This osmolyte strategy requires the expression of specific osmolyte transporters such as betaine (BGT-1), myoinositol (SMIT), and taurine (TAUT). Inositol 106-117 solute carrier family 5 member 3 Homo sapiens 119-123 25756525-8 2015 Assuming SLC5A3 to be the major path for myo-inositol, a turnover rate of 80-800 myo-inositol molecules per second for a single transporter protein was estimated from combined volumetric and dSTORM data. Inositol 41-53 solute carrier family 5 member 3 Homo sapiens 9-15 25756525-8 2015 Assuming SLC5A3 to be the major path for myo-inositol, a turnover rate of 80-800 myo-inositol molecules per second for a single transporter protein was estimated from combined volumetric and dSTORM data. Inositol 81-93 solute carrier family 5 member 3 Homo sapiens 9-15 24884043-1 2014 Our recent DNA-microarray and proteomics studies searching for pathways affected both by chronic lithium treatment and by knockout of each of two genes (IMPA1 or Slc5a3) encoding for proteins related to inositol metabolism, indicated up-regulation of mitochondria-related genes and autophagy-related proteins in the frontal cortex. Inositol 203-211 solute carrier family 5 member 3 Homo sapiens 162-168