PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 34703915-8 2021 Sodium-dependent VC transporter 1 and 2 (SVCT1 and SVCT2) expressions were higher in ileum than in duodenum and jejunum (P < 0.05). Sodium 0-6 solute carrier family 23 member 2 Homo sapiens 51-56 15590689-9 2005 As a prerequisite for investigating 6-bromo-6-deoxy-L-ascorbic acid transported by SVCTs, SVCT2 transport activity in oocytes was enhanced 14-fold by construction and use of a vector that added a fixed poly(A) tail to the 3" end of cRNA. 6-deoxy-6-bromoascorbic acid 36-67 solute carrier family 23 member 2 Homo sapiens 90-95 15590689-10 2005 For SVCT1 and SVCT2 expressed in oocytes, similar K(m) and V(max) values were observed for ascorbic acid and 6-bromo-6-deoxy-L-ascorbic acid. Ascorbic Acid 91-104 solute carrier family 23 member 2 Homo sapiens 14-19 15590689-10 2005 For SVCT1 and SVCT2 expressed in oocytes, similar K(m) and V(max) values were observed for ascorbic acid and 6-bromo-6-deoxy-L-ascorbic acid. 6-deoxy-6-bromoascorbic acid 109-140 solute carrier family 23 member 2 Homo sapiens 14-19 34703915-12 2021 Dietary VC supplementation at 200 and 400 mg/kg increased SVCT2 expression in duodenum, but decreased GLO and SVCT1 expression in kidney and SVCT2 expression in liver (P < 0.05). Ascorbic Acid 8-10 solute carrier family 23 member 2 Homo sapiens 58-63 34703915-12 2021 Dietary VC supplementation at 200 and 400 mg/kg increased SVCT2 expression in duodenum, but decreased GLO and SVCT1 expression in kidney and SVCT2 expression in liver (P < 0.05). Ascorbic Acid 8-10 solute carrier family 23 member 2 Homo sapiens 141-146 34599650-7 2021 RESULTS: In cell culture, transporter levels and cellular location were not modified by ascorbate availability at any time up to 8h, although basal SVCT2 levels governed maximal ascorbate accumulation. Ascorbic Acid 178-187 solute carrier family 23 member 2 Homo sapiens 148-153 34673103-0 2021 Calsyntenin-3 interacts with the sodium-dependent vitamin C transporter-2 to regulate vitamin C uptake. Ascorbic Acid 86-95 solute carrier family 23 member 2 Homo sapiens 33-73 34673103-1 2021 Ascorbic acid (AA) uptake in neurons occurs via a Na+-dependent carrier-mediated process mediated by the sodium-dependent vitamin C transporter-2 (SVCT2). Ascorbic Acid 0-13 solute carrier family 23 member 2 Homo sapiens 105-145 34673103-1 2021 Ascorbic acid (AA) uptake in neurons occurs via a Na+-dependent carrier-mediated process mediated by the sodium-dependent vitamin C transporter-2 (SVCT2). Ascorbic Acid 0-13 solute carrier family 23 member 2 Homo sapiens 147-152 34403723-1 2021 Intestinal absorption of vitamin C in humans is mediated via the sodium-dependent vitamin C transporters (hSVCT1 and hSVCT2). Ascorbic Acid 25-34 solute carrier family 23 member 2 Homo sapiens 117-123 34403723-1 2021 Intestinal absorption of vitamin C in humans is mediated via the sodium-dependent vitamin C transporters (hSVCT1 and hSVCT2). Sodium 65-71 solute carrier family 23 member 2 Homo sapiens 117-123 34403723-1 2021 Intestinal absorption of vitamin C in humans is mediated via the sodium-dependent vitamin C transporters (hSVCT1 and hSVCT2). Ascorbic Acid 82-91 solute carrier family 23 member 2 Homo sapiens 117-123 34573045-0 2021 SVCT2 Overexpression and Ascorbic Acid Uptake Increase Cortical Neuron Differentiation, Which Is Dependent on Vitamin C Recycling between Neurons and Astrocytes. Ascorbic Acid 110-119 solute carrier family 23 member 2 Homo sapiens 0-5 34573045-1 2021 During brain development, sodium-vitamin C transporter (SVCT2) has been detected primarily in radial glial cells in situ, with low-to-absent expression in cerebral cortex neuroblasts. Sodium 26-32 solute carrier family 23 member 2 Homo sapiens 56-61 34573045-2 2021 However, strong SVCT2 expression is observed during the first postnatal days, resulting in increased intracellular concentration of vitamin C. Ascorbic Acid 132-141 solute carrier family 23 member 2 Homo sapiens 16-21 34573045-4 2021 Other studies have shown that vitamin C-deprived guinea pigs have reduced spatial memory, suggesting that ascorbic acid (AA) and SVCT2 have important roles in postnatal neuronal differentiation and neurite formation. Ascorbic Acid 30-39 solute carrier family 23 member 2 Homo sapiens 129-134 34439814-2 2021 Here, we examined the effect of vitamin C on human bronchial epithelium transformed with Ad12-SV40 2B (BEAS-2B) cells, and observed that sodium-dependent vitamin C transporter 2 (SVCT2) was the primary vitamin C transporter. Ascorbic Acid 202-211 solute carrier family 23 member 2 Homo sapiens 179-184 34439814-2 2021 Here, we examined the effect of vitamin C on human bronchial epithelium transformed with Ad12-SV40 2B (BEAS-2B) cells, and observed that sodium-dependent vitamin C transporter 2 (SVCT2) was the primary vitamin C transporter. Ascorbic Acid 32-41 solute carrier family 23 member 2 Homo sapiens 137-177 33677235-0 2021 Ascorbic acid analogue 6-Deoxy-6-[18F] fluoro-L-ascorbic acid as a tracer for identifying human colorectal cancer with SVCT2 overexpression. Ascorbic Acid 0-13 solute carrier family 23 member 2 Homo sapiens 119-124 34439814-2 2021 Here, we examined the effect of vitamin C on human bronchial epithelium transformed with Ad12-SV40 2B (BEAS-2B) cells, and observed that sodium-dependent vitamin C transporter 2 (SVCT2) was the primary vitamin C transporter. Ascorbic Acid 32-41 solute carrier family 23 member 2 Homo sapiens 179-184 34439814-2 2021 Here, we examined the effect of vitamin C on human bronchial epithelium transformed with Ad12-SV40 2B (BEAS-2B) cells, and observed that sodium-dependent vitamin C transporter 2 (SVCT2) was the primary vitamin C transporter. Ascorbic Acid 202-211 solute carrier family 23 member 2 Homo sapiens 137-177 34405001-1 2021 The sodium-dependent vitamin C transporter 2 (SVCT2) surface glycoprotein regulates ascorbate accumulation in the plasma, often resulting in the induction of cancer cell death. Ascorbic Acid 84-93 solute carrier family 23 member 2 Homo sapiens 4-44 34405001-1 2021 The sodium-dependent vitamin C transporter 2 (SVCT2) surface glycoprotein regulates ascorbate accumulation in the plasma, often resulting in the induction of cancer cell death. Ascorbic Acid 84-93 solute carrier family 23 member 2 Homo sapiens 46-51 32008465-6 2021 In non-cancer cells, Vit C, at a pharmacological concentration, increased SVCT2 and decreased GLUT1, while the opposite effect was noted in cancer cells. Ascorbic Acid 21-26 solute carrier family 23 member 2 Homo sapiens 74-79 34285658-1 2021 Vitamin C (ascorbic acid: AA) uptake in neurons occurs via the sodium-dependent vitamin C transporter-2 (SVCT2), which is highly expressed in the central nervous system (CNS). Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 63-103 34285658-1 2021 Vitamin C (ascorbic acid: AA) uptake in neurons occurs via the sodium-dependent vitamin C transporter-2 (SVCT2), which is highly expressed in the central nervous system (CNS). Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 105-110 34285658-1 2021 Vitamin C (ascorbic acid: AA) uptake in neurons occurs via the sodium-dependent vitamin C transporter-2 (SVCT2), which is highly expressed in the central nervous system (CNS). Ascorbic Acid 11-24 solute carrier family 23 member 2 Homo sapiens 63-103 34285658-1 2021 Vitamin C (ascorbic acid: AA) uptake in neurons occurs via the sodium-dependent vitamin C transporter-2 (SVCT2), which is highly expressed in the central nervous system (CNS). Ascorbic Acid 11-24 solute carrier family 23 member 2 Homo sapiens 105-110 34285658-10 2021 Further, the inhibitory effect of LPS on a minimal SLC23A2 promoter was attenuated when either the binding site for the transcription factor Sp1 was mutated or cells were treated with the NF-kappaB inhibitor, celastrol. celastrol 209-218 solute carrier family 23 member 2 Homo sapiens 51-58 33677235-0 2021 Ascorbic acid analogue 6-Deoxy-6-[18F] fluoro-L-ascorbic acid as a tracer for identifying human colorectal cancer with SVCT2 overexpression. 6-deoxy-6-fluoroascorbic acid 23-61 solute carrier family 23 member 2 Homo sapiens 119-124 32580031-0 2020 SVCT2-DEPENDENT PLASMA AND MITOCHONDRIAL MEMBRANE TRANSPORT OF ASCORBIC ACID IN DIFFERENTIATING MYOBLASTS. Ascorbic Acid 63-76 solute carrier family 23 member 2 Homo sapiens 0-5 33484802-0 2021 New insights into Vitamin C function: Vitamin C induces JAK2 activation through its receptor-like transporter SVCT2. Ascorbic Acid 18-27 solute carrier family 23 member 2 Homo sapiens 110-115 33484802-0 2021 New insights into Vitamin C function: Vitamin C induces JAK2 activation through its receptor-like transporter SVCT2. Ascorbic Acid 38-47 solute carrier family 23 member 2 Homo sapiens 110-115 33484802-4 2021 Here, we propose that VitC is also a bio-signaling molecule based on the finding that sodium-dependent VitC transporter (SVCT) 2 is a novel receptor-like transporter of VitC that possesses dual activities in mediating VitC uptake and Janus kinase (JAK) 2/signal transducer and activator of transcription (STAT) 2 signaling pathway. Ascorbic Acid 22-26 solute carrier family 23 member 2 Homo sapiens 86-128 33484802-5 2021 Through interaction, SVCT2 induces JAK2 phosphorylation while transporting VitC into cells. Ascorbic Acid 75-79 solute carrier family 23 member 2 Homo sapiens 21-26 33580460-1 2021 SVCT2, Sodium-dependent Vitamin C Transporter 2, uniquely transports ascorbic acid (also known as vitamin C and ascorbate) into all types of cells. Ascorbic Acid 69-82 solute carrier family 23 member 2 Homo sapiens 0-5 33580460-1 2021 SVCT2, Sodium-dependent Vitamin C Transporter 2, uniquely transports ascorbic acid (also known as vitamin C and ascorbate) into all types of cells. Ascorbic Acid 69-82 solute carrier family 23 member 2 Homo sapiens 7-47 33580460-1 2021 SVCT2, Sodium-dependent Vitamin C Transporter 2, uniquely transports ascorbic acid (also known as vitamin C and ascorbate) into all types of cells. Ascorbic Acid 98-107 solute carrier family 23 member 2 Homo sapiens 0-5 33580460-1 2021 SVCT2, Sodium-dependent Vitamin C Transporter 2, uniquely transports ascorbic acid (also known as vitamin C and ascorbate) into all types of cells. Ascorbic Acid 98-107 solute carrier family 23 member 2 Homo sapiens 7-47 33580460-1 2021 SVCT2, Sodium-dependent Vitamin C Transporter 2, uniquely transports ascorbic acid (also known as vitamin C and ascorbate) into all types of cells. Ascorbic Acid 112-121 solute carrier family 23 member 2 Homo sapiens 0-5 33580460-1 2021 SVCT2, Sodium-dependent Vitamin C Transporter 2, uniquely transports ascorbic acid (also known as vitamin C and ascorbate) into all types of cells. Ascorbic Acid 112-121 solute carrier family 23 member 2 Homo sapiens 7-47 33580460-7 2021 Overall, our data suggests that p53 is a potent transcriptional repressor of SVCT2, a critical transporter of diet-derived ascorbic acid, across the plasma membranes of numerous essential tissue cell types. Ascorbic Acid 123-136 solute carrier family 23 member 2 Homo sapiens 77-82 33307167-2 2021 The antioxidant ascorbate (the reduced form of vitamin C) is concentrated in CNS neurons through a sodium-dependent transporter named SVCT2 and participates in several CNS processes, for instance, the regulation of glutamate receptors functioning and the synthesis of neuromodulators. Ascorbic Acid 16-25 solute carrier family 23 member 2 Homo sapiens 134-139 33307167-2 2021 The antioxidant ascorbate (the reduced form of vitamin C) is concentrated in CNS neurons through a sodium-dependent transporter named SVCT2 and participates in several CNS processes, for instance, the regulation of glutamate receptors functioning and the synthesis of neuromodulators. Ascorbic Acid 47-56 solute carrier family 23 member 2 Homo sapiens 134-139 33307167-2 2021 The antioxidant ascorbate (the reduced form of vitamin C) is concentrated in CNS neurons through a sodium-dependent transporter named SVCT2 and participates in several CNS processes, for instance, the regulation of glutamate receptors functioning and the synthesis of neuromodulators. Sodium 99-105 solute carrier family 23 member 2 Homo sapiens 134-139 33307167-2 2021 The antioxidant ascorbate (the reduced form of vitamin C) is concentrated in CNS neurons through a sodium-dependent transporter named SVCT2 and participates in several CNS processes, for instance, the regulation of glutamate receptors functioning and the synthesis of neuromodulators. Glutamic Acid 215-224 solute carrier family 23 member 2 Homo sapiens 134-139 33307167-6 2021 The activation of A3 receptors increased ascorbate release in an SVCT2-dependent manner, which largely altered the neuronal redox status without interfering with cell death, glycolytic metabolism, and bioenergetics. Ascorbic Acid 41-50 solute carrier family 23 member 2 Homo sapiens 65-70 32580031-3 2020 In addition, the mitochondrial expression of SVCT2 appeared particularly elevated and, consistently, a brief pre-exposure to low concentrations of Ascorbic Acid (AA) abolished mitochondrial superoxide formation selectively induced by the cocktail arsenite/ATP. Ascorbic Acid 147-160 solute carrier family 23 member 2 Homo sapiens 45-50 32580031-3 2020 In addition, the mitochondrial expression of SVCT2 appeared particularly elevated and, consistently, a brief pre-exposure to low concentrations of Ascorbic Acid (AA) abolished mitochondrial superoxide formation selectively induced by the cocktail arsenite/ATP. Superoxides 190-200 solute carrier family 23 member 2 Homo sapiens 45-50 32580031-3 2020 In addition, the mitochondrial expression of SVCT2 appeared particularly elevated and, consistently, a brief pre-exposure to low concentrations of Ascorbic Acid (AA) abolished mitochondrial superoxide formation selectively induced by the cocktail arsenite/ATP. arsenite 247-255 solute carrier family 23 member 2 Homo sapiens 45-50 32580031-3 2020 In addition, the mitochondrial expression of SVCT2 appeared particularly elevated and, consistently, a brief pre-exposure to low concentrations of Ascorbic Acid (AA) abolished mitochondrial superoxide formation selectively induced by the cocktail arsenite/ATP. Adenosine Triphosphate 256-259 solute carrier family 23 member 2 Homo sapiens 45-50 32080778-5 2020 In addition, RSV could induce several AsA or DHA transport-related and intracellular DHA reduction-related genes including SVCT2, GLUT3, TXNRD2, and TXNRD3, necessary for AsA transport, DHA transport, and DHA reduction/regeneration, respectively. Resveratrol 13-16 solute carrier family 23 member 2 Homo sapiens 123-128 32751086-5 2020 Moreover, serum vitamin C level also is dependent on genetic factors, such as SLC23A1 and SLC23A2 genes, encoding sodium-dependent vitamin C transporters and GSTM1, GSTP1 and GSTT1 genes which encode glutathione S-transferases. Ascorbic Acid 16-25 solute carrier family 23 member 2 Homo sapiens 90-97 32751086-5 2020 Moreover, serum vitamin C level also is dependent on genetic factors, such as SLC23A1 and SLC23A2 genes, encoding sodium-dependent vitamin C transporters and GSTM1, GSTP1 and GSTT1 genes which encode glutathione S-transferases. Sodium 114-120 solute carrier family 23 member 2 Homo sapiens 90-97 32080778-5 2020 In addition, RSV could induce several AsA or DHA transport-related and intracellular DHA reduction-related genes including SVCT2, GLUT3, TXNRD2, and TXNRD3, necessary for AsA transport, DHA transport, and DHA reduction/regeneration, respectively. Dehydroascorbic Acid 85-88 solute carrier family 23 member 2 Homo sapiens 123-128 32080778-5 2020 In addition, RSV could induce several AsA or DHA transport-related and intracellular DHA reduction-related genes including SVCT2, GLUT3, TXNRD2, and TXNRD3, necessary for AsA transport, DHA transport, and DHA reduction/regeneration, respectively. Dehydroascorbic Acid 45-48 solute carrier family 23 member 2 Homo sapiens 123-128 32080778-5 2020 In addition, RSV could induce several AsA or DHA transport-related and intracellular DHA reduction-related genes including SVCT2, GLUT3, TXNRD2, and TXNRD3, necessary for AsA transport, DHA transport, and DHA reduction/regeneration, respectively. Ascorbic Acid 171-174 solute carrier family 23 member 2 Homo sapiens 123-128 31607868-7 2019 Besides, the data also represented that 250 mg/Kg AA or SVCT2 overexpression facilitated NSPCs migration via promoting F-actin assembling in the manner of up-regulating CDC42 expression using oxygen-glucose deprivation in vitro. Oxygen 192-206 solute carrier family 23 member 2 Homo sapiens 56-61 32080778-5 2020 In addition, RSV could induce several AsA or DHA transport-related and intracellular DHA reduction-related genes including SVCT2, GLUT3, TXNRD2, and TXNRD3, necessary for AsA transport, DHA transport, and DHA reduction/regeneration, respectively. Dehydroascorbic Acid 85-88 solute carrier family 23 member 2 Homo sapiens 123-128 32080778-5 2020 In addition, RSV could induce several AsA or DHA transport-related and intracellular DHA reduction-related genes including SVCT2, GLUT3, TXNRD2, and TXNRD3, necessary for AsA transport, DHA transport, and DHA reduction/regeneration, respectively. Dehydroascorbic Acid 85-88 solute carrier family 23 member 2 Homo sapiens 123-128 32080778-6 2020 On the other hand, the both protein expression levels and the localizations of sodium-dependent vitamin C transporters 2 (SVCT2) and glucose transporter 3(GLUT3) were scarcely affected by RSV treatment. Resveratrol 188-191 solute carrier family 23 member 2 Homo sapiens 79-120 32080778-6 2020 On the other hand, the both protein expression levels and the localizations of sodium-dependent vitamin C transporters 2 (SVCT2) and glucose transporter 3(GLUT3) were scarcely affected by RSV treatment. Resveratrol 188-191 solute carrier family 23 member 2 Homo sapiens 122-127 31901552-0 2020 Enhanced Anticancer Effect of Adding Magnesium to Vitamin C Therapy: Inhibition of Hormetic Response by SVCT-2 Activation. Magnesium 37-46 solute carrier family 23 member 2 Homo sapiens 104-110 31901552-0 2020 Enhanced Anticancer Effect of Adding Magnesium to Vitamin C Therapy: Inhibition of Hormetic Response by SVCT-2 Activation. Ascorbic Acid 50-59 solute carrier family 23 member 2 Homo sapiens 104-110 31901552-5 2020 Magnesium ions, which are known to activate SVCT-2, could increase the Vmax value of SVCT-2, so we investigated whether providing magnesium supplements to cancer cells with low SVCT-2 expression that had shown a hormetic response to AA would elevate the Vmax value of SVCT-2, allowing more AA to accumulate. Magnesium 0-9 solute carrier family 23 member 2 Homo sapiens 44-50 31901552-5 2020 Magnesium ions, which are known to activate SVCT-2, could increase the Vmax value of SVCT-2, so we investigated whether providing magnesium supplements to cancer cells with low SVCT-2 expression that had shown a hormetic response to AA would elevate the Vmax value of SVCT-2, allowing more AA to accumulate. Magnesium 0-9 solute carrier family 23 member 2 Homo sapiens 85-91 31901552-5 2020 Magnesium ions, which are known to activate SVCT-2, could increase the Vmax value of SVCT-2, so we investigated whether providing magnesium supplements to cancer cells with low SVCT-2 expression that had shown a hormetic response to AA would elevate the Vmax value of SVCT-2, allowing more AA to accumulate. Magnesium 0-9 solute carrier family 23 member 2 Homo sapiens 85-91 31901552-5 2020 Magnesium ions, which are known to activate SVCT-2, could increase the Vmax value of SVCT-2, so we investigated whether providing magnesium supplements to cancer cells with low SVCT-2 expression that had shown a hormetic response to AA would elevate the Vmax value of SVCT-2, allowing more AA to accumulate. Magnesium 0-9 solute carrier family 23 member 2 Homo sapiens 85-91 30660746-1 2019 In this study, a novel brain targeting ascorbic acid (AA) derivative with "lock-in" function was designed and synthesized as a liposome ligand to prepare novel liposomes to achieve the effective delivery of drug formulations to brain via glucose transporter 1 (GLUT1) and the Na+-dependent vitamin C transporter (SVCT2). Ascorbic Acid 39-52 solute carrier family 23 member 2 Homo sapiens 313-318 31594969-2 2019 While the transfer of vitamin C from the blood to the brain has been studied functionally, the vitamin C transporter, SVCT2, has not been detected in the basolateral membrane of choroid plexus cells. Ascorbic Acid 95-104 solute carrier family 23 member 2 Homo sapiens 118-123 31594969-9 2019 Finally, we observed in Guinea pig brain under scorbutic condition, that normal distribution of SVCT2 in choroid plexus may be regulated by peripheral concentrations of vitamin C. Ascorbic Acid 169-178 solute carrier family 23 member 2 Homo sapiens 96-101 30565018-9 2019 Importantly, sodium-dependent vitamin C transporter 2 (SVCT-2) siRNA was found to partially block the ability of vitamin C to promote Sirt1/SOD2 signaling. Ascorbic Acid 30-39 solute carrier family 23 member 2 Homo sapiens 55-61 31214276-8 2019 Finally, we examined the expression of sodium-dependent VC transporter-2 (SVCT-2) using western blotting and qPCR, which revealed that there was a significant increase in the expression of SVCT-2 in melanocytes following treatment with VC. Ascorbic Acid 56-58 solute carrier family 23 member 2 Homo sapiens 74-80 31143097-6 2019 There are four SVCT isoforms and SVCT2 is the major isoform controlling ascorbate transport in the CNS. Ascorbic Acid 72-81 solute carrier family 23 member 2 Homo sapiens 33-38 31143097-7 2019 Regarding ascorbate release from retinal neurons, Glutamate, by activating its ionotropic receptors leads to ascorbate release via the reversion of SVCT2. Ascorbic Acid 10-19 solute carrier family 23 member 2 Homo sapiens 148-153 31143097-7 2019 Regarding ascorbate release from retinal neurons, Glutamate, by activating its ionotropic receptors leads to ascorbate release via the reversion of SVCT2. Glutamic Acid 50-59 solute carrier family 23 member 2 Homo sapiens 148-153 31143097-7 2019 Regarding ascorbate release from retinal neurons, Glutamate, by activating its ionotropic receptors leads to ascorbate release via the reversion of SVCT2. Ascorbic Acid 109-118 solute carrier family 23 member 2 Homo sapiens 148-153 31143097-8 2019 Moreover, dopamine, via activation of D1 receptor/cyclic AMP/EPAC2 pathway, also induces ascorbate release via SVCT2 reversion. Dopamine 10-18 solute carrier family 23 member 2 Homo sapiens 111-116 31143097-8 2019 Moreover, dopamine, via activation of D1 receptor/cyclic AMP/EPAC2 pathway, also induces ascorbate release via SVCT2 reversion. Cyclic AMP 50-60 solute carrier family 23 member 2 Homo sapiens 111-116 31143097-8 2019 Moreover, dopamine, via activation of D1 receptor/cyclic AMP/EPAC2 pathway, also induces ascorbate release via SVCT2 reversion. Ascorbic Acid 89-98 solute carrier family 23 member 2 Homo sapiens 111-116 31143097-11 2019 In addition, dopamine-dependent SVCT2 reversion leading to ascorbate release occurs by activation of AMPA/Kainate receptors and downstream ERK/AKT pathways. Dopamine 13-21 solute carrier family 23 member 2 Homo sapiens 32-37 31143097-11 2019 In addition, dopamine-dependent SVCT2 reversion leading to ascorbate release occurs by activation of AMPA/Kainate receptors and downstream ERK/AKT pathways. Ascorbic Acid 59-68 solute carrier family 23 member 2 Homo sapiens 32-37 31214276-8 2019 Finally, we examined the expression of sodium-dependent VC transporter-2 (SVCT-2) using western blotting and qPCR, which revealed that there was a significant increase in the expression of SVCT-2 in melanocytes following treatment with VC. Ascorbic Acid 56-58 solute carrier family 23 member 2 Homo sapiens 189-195 31214276-9 2019 VC-mediated intracellular acidification was neutralized by phloretin (a putative SVCT-2 inhibitor) in a dose-dependent manner. Ascorbic Acid 0-2 solute carrier family 23 member 2 Homo sapiens 81-87 31214276-9 2019 VC-mediated intracellular acidification was neutralized by phloretin (a putative SVCT-2 inhibitor) in a dose-dependent manner. Phloretin 59-68 solute carrier family 23 member 2 Homo sapiens 81-87 31214276-10 2019 Taken together, these data show that VC and its derivatives suppress tyrosinase activity through cytoplasmic acidification that potentially results from enhanced VC transmembrane transport via the VC transporter SVCT-2. Ascorbic Acid 37-39 solute carrier family 23 member 2 Homo sapiens 212-218 31002656-11 2019 Consistent with these assertions, Vitamin C is known to be highly concentrated within mitochondria, by a specific transporter, namely SVCT2, in a sodium-coupled manner. Ascorbic Acid 34-43 solute carrier family 23 member 2 Homo sapiens 134-139 30902760-9 2019 This is consistent with our observations that this form of SVCT2 is completely absent from the plasma membrane and is overexpressed in mitochondria of breast cancer cells, where it mediates ascorbic acid transport. Ascorbic Acid 190-203 solute carrier family 23 member 2 Homo sapiens 59-64 31002656-11 2019 Consistent with these assertions, Vitamin C is known to be highly concentrated within mitochondria, by a specific transporter, namely SVCT2, in a sodium-coupled manner. Sodium 146-152 solute carrier family 23 member 2 Homo sapiens 134-139 28699359-2 2018 Recent Advances: Most cell types take up AA by the high-affinity sodium-dependent vitamin C transporter 2 (SVCT2) sensitive to inhibition by dehydroascorbic acid (DHA). Dehydroascorbic Acid 141-161 solute carrier family 23 member 2 Homo sapiens 65-105 30616065-1 2019 Intestinal absorption of ascorbic acid (AA) occurs via a Na+-dependent carrier-mediated process facilitated through the human sodium-dependent vitamin C transporters-1 &-2 (hSVCT1 and hSVCT2). Ascorbic Acid 25-38 solute carrier family 23 member 2 Homo sapiens 184-190 30285481-2 2019 Humans obtain vitamin C from dietary sources via intestinal absorption, a process that involves the sodium-dependent vitamin C transporters-1 and -2 (SVCT1 and SVCT2). Ascorbic Acid 14-23 solute carrier family 23 member 2 Homo sapiens 160-165 30285481-2 2019 Humans obtain vitamin C from dietary sources via intestinal absorption, a process that involves the sodium-dependent vitamin C transporters-1 and -2 (SVCT1 and SVCT2). Sodium 100-106 solute carrier family 23 member 2 Homo sapiens 160-165 30285481-10 2019 Together, these data demonstrate that ETEC infection impairs intestinal AA uptake through a cAMP-dependent NF-kappaB-mediated pathway that regulates both SLC23A1 and SLC23A2 transcription. Cyclic AMP 92-96 solute carrier family 23 member 2 Homo sapiens 166-173 30285481-12 2019 This effect is mediated through transcriptional repression of SLC23A1 (SVCT1) and SLC23A2 (SVCT2) via a cAMP-dependent NF-kappaB signaling pathway. Cyclic AMP 104-108 solute carrier family 23 member 2 Homo sapiens 82-89 28699359-2 2018 Recent Advances: Most cell types take up AA by the high-affinity sodium-dependent vitamin C transporter 2 (SVCT2) sensitive to inhibition by dehydroascorbic acid (DHA). Dehydroascorbic Acid 141-161 solute carrier family 23 member 2 Homo sapiens 107-112 28699359-2 2018 Recent Advances: Most cell types take up AA by the high-affinity sodium-dependent vitamin C transporter 2 (SVCT2) sensitive to inhibition by dehydroascorbic acid (DHA). Dehydroascorbic Acid 163-166 solute carrier family 23 member 2 Homo sapiens 65-105 28699359-2 2018 Recent Advances: Most cell types take up AA by the high-affinity sodium-dependent vitamin C transporter 2 (SVCT2) sensitive to inhibition by dehydroascorbic acid (DHA). Dehydroascorbic Acid 163-166 solute carrier family 23 member 2 Homo sapiens 107-112 28699359-7 2018 Mitochondrial SVCT2 is susceptible to inhibition by DHA and transports AA with a low affinity as a consequence of the restrictive ionic conditions. Dehydroascorbic Acid 52-55 solute carrier family 23 member 2 Homo sapiens 14-19 30054560-3 2018 In this study, we demonstrate that L-ascorbic acid treatment showed efficient anti-cancer activity in cell lines with high expression levels of SVCT-2 for a gradient concentration of L-ascorbic acid from 10 muM -2 mM. Ascorbic Acid 183-198 solute carrier family 23 member 2 Homo sapiens 144-150 29476450-2 2018 In the CNS, the plasma membrane transporter sodium vitamin C co-transporter 2 (SVCT2) is responsible for ascorbate transport in neurons. Ascorbic Acid 105-114 solute carrier family 23 member 2 Homo sapiens 79-84 30054560-0 2018 Hormetic dose response to L-ascorbic acid as an anti-cancer drug in colorectal cancer cell lines according to SVCT-2 expression. Ascorbic Acid 26-41 solute carrier family 23 member 2 Homo sapiens 110-116 30054560-4 2018 However, in low SVCT-2 expressing cell lines, high-dose L-ascorbic acid (>1 mM) showed anti-cancer effects but low-dose (<10 muM) treatment induced cell proliferation. Ascorbic Acid 56-71 solute carrier family 23 member 2 Homo sapiens 16-22 30054560-2 2018 The anti-cancer effects of L-ascorbic acid are determined by sodium-dependent vitamin C transporter 2 (SVCT-2), a transporter of L-ascorbic acid. Ascorbic Acid 27-42 solute carrier family 23 member 2 Homo sapiens 61-101 30054560-2 2018 The anti-cancer effects of L-ascorbic acid are determined by sodium-dependent vitamin C transporter 2 (SVCT-2), a transporter of L-ascorbic acid. Ascorbic Acid 27-42 solute carrier family 23 member 2 Homo sapiens 103-109 30054560-6 2018 A hormetic dose response to low-dose L-ascorbic acid was also observed in high SVCT-2 expressing cell lines in the presence of a SVCT family inhibitor. Ascorbic Acid 37-52 solute carrier family 23 member 2 Homo sapiens 79-85 30054560-2 2018 The anti-cancer effects of L-ascorbic acid are determined by sodium-dependent vitamin C transporter 2 (SVCT-2), a transporter of L-ascorbic acid. Ascorbic Acid 129-144 solute carrier family 23 member 2 Homo sapiens 61-101 30054560-2 2018 The anti-cancer effects of L-ascorbic acid are determined by sodium-dependent vitamin C transporter 2 (SVCT-2), a transporter of L-ascorbic acid. Ascorbic Acid 129-144 solute carrier family 23 member 2 Homo sapiens 103-109 30054560-7 2018 Insufficient uptake of L-ascorbic acid in low SVCT-2 expressing cancer cell lines cannot generate sufficient ROS to kill cancer cells, resulting in the hormetic response. Ascorbic Acid 23-38 solute carrier family 23 member 2 Homo sapiens 46-52 30054560-3 2018 In this study, we demonstrate that L-ascorbic acid treatment showed efficient anti-cancer activity in cell lines with high expression levels of SVCT-2 for a gradient concentration of L-ascorbic acid from 10 muM -2 mM. Ascorbic Acid 35-50 solute carrier family 23 member 2 Homo sapiens 144-150 28385602-0 2017 SVCT-2 determines the sensitivity to ascorbate-induced cell death in cholangiocarcinoma cell lines and patient derived xenografts. Ascorbic Acid 37-46 solute carrier family 23 member 2 Homo sapiens 0-6 29545069-0 2018 Ascorbic acid increases SVCT2 localization at the plasma membrane by accelerating its trafficking from early secretory compartments and through the endocytic-recycling pathway. Ascorbic Acid 0-13 solute carrier family 23 member 2 Homo sapiens 24-29 29545069-6 2018 We defined that the post-acute response was dependent on SVCT2 located in early secretory compartments, and its trafficking was abolished with Tunicamycin and Brefeldin A treatment. Tunicamycin 143-154 solute carrier family 23 member 2 Homo sapiens 57-62 29545069-6 2018 We defined that the post-acute response was dependent on SVCT2 located in early secretory compartments, and its trafficking was abolished with Tunicamycin and Brefeldin A treatment. Brefeldin A 159-170 solute carrier family 23 member 2 Homo sapiens 57-62 29030247-1 2018 Ascorbic acid (AA) accumulation in intestinal epithelial cells is an active transport process mainly mediated by two sodium-dependent vitamin C transporters (SVCT-1 and SVCT-2). Ascorbic Acid 0-13 solute carrier family 23 member 2 Homo sapiens 169-175 29872720-0 2018 Vitamin C preferentially kills cancer stem cells in hepatocellular carcinoma via SVCT-2. Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 81-87 29872720-6 2018 Mechanistically, VC uptake via SVCT-2 increased intracellular ROS, and subsequently caused DNA damage and ATP depletion, leading to cell cycle arrest and apoptosis. Vinyl Chloride 17-19 solute carrier family 23 member 2 Homo sapiens 31-37 29872720-6 2018 Mechanistically, VC uptake via SVCT-2 increased intracellular ROS, and subsequently caused DNA damage and ATP depletion, leading to cell cycle arrest and apoptosis. ros 62-65 solute carrier family 23 member 2 Homo sapiens 31-37 29872720-6 2018 Mechanistically, VC uptake via SVCT-2 increased intracellular ROS, and subsequently caused DNA damage and ATP depletion, leading to cell cycle arrest and apoptosis. Adenosine Triphosphate 106-109 solute carrier family 23 member 2 Homo sapiens 31-37 27596508-2 2017 Different cells transport the reduced form of vitamin C, ascorbic acid (AA), using sodium-dependent ascorbic acid cotransporters (SVCT1 or SVCT2). Ascorbic Acid 46-55 solute carrier family 23 member 2 Homo sapiens 139-144 27596508-2 2017 Different cells transport the reduced form of vitamin C, ascorbic acid (AA), using sodium-dependent ascorbic acid cotransporters (SVCT1 or SVCT2). Ascorbic Acid 57-70 solute carrier family 23 member 2 Homo sapiens 139-144 27596508-3 2017 SVCT2 is mainly expressed in the nervous system (CNS); however, its localization in the central nervous system during embryonic development along with the mechanism by which RG take up vitamin C and its intracellular effects is unknown. Ascorbic Acid 185-194 solute carrier family 23 member 2 Homo sapiens 0-5 28385602-7 2017 Knockdown of SVCT-2 dramatically alleviated DNA damage, ATP depletion, and inhibition of mTOR pathway induced by AA. Adenosine Triphosphate 56-59 solute carrier family 23 member 2 Homo sapiens 13-19 27932501-10 2017 These findings show, for the first time, that SVCT-1 and SVCT-2 are differentially expressed along the intestinal tract and that this pattern of expression is, at least in part, mediated via transcriptional/epigenetic mechanisms.NEW & NOTEWORTHY Our findings show, for the first time, that transporters of the water-soluble vitamin ascorbic acid (i.e., the vitamin C transporters SVCT-1 and SVCT-2) are differentially expressed along the length of the intestinal tract and that the pattern of expression is mediated, at least in part, by transcriptional and epigenetic mechanism(s) affecting both Slc23a1 and Slc23a2 genes. Adenosine Monophosphate 234-237 solute carrier family 23 member 2 Homo sapiens 57-63 27932501-10 2017 These findings show, for the first time, that SVCT-1 and SVCT-2 are differentially expressed along the intestinal tract and that this pattern of expression is, at least in part, mediated via transcriptional/epigenetic mechanisms.NEW & NOTEWORTHY Our findings show, for the first time, that transporters of the water-soluble vitamin ascorbic acid (i.e., the vitamin C transporters SVCT-1 and SVCT-2) are differentially expressed along the length of the intestinal tract and that the pattern of expression is mediated, at least in part, by transcriptional and epigenetic mechanism(s) affecting both Slc23a1 and Slc23a2 genes. Water 314-319 solute carrier family 23 member 2 Homo sapiens 57-63 27932501-1 2017 Mammalian cells utilize two transporters for the uptake of ascorbic acid (AA), Na+-dependent vitamin C transporter SVCT-1 and SVCT-2. Ascorbic Acid 59-72 solute carrier family 23 member 2 Homo sapiens 126-132 27932501-10 2017 These findings show, for the first time, that SVCT-1 and SVCT-2 are differentially expressed along the intestinal tract and that this pattern of expression is, at least in part, mediated via transcriptional/epigenetic mechanisms.NEW & NOTEWORTHY Our findings show, for the first time, that transporters of the water-soluble vitamin ascorbic acid (i.e., the vitamin C transporters SVCT-1 and SVCT-2) are differentially expressed along the length of the intestinal tract and that the pattern of expression is mediated, at least in part, by transcriptional and epigenetic mechanism(s) affecting both Slc23a1 and Slc23a2 genes. Ascorbic Acid 328-349 solute carrier family 23 member 2 Homo sapiens 57-63 26838684-3 2017 METHODS: Fruit/vegetable/vitamin C consumption from food frequency questionnaires and six low-penetrance genetic susceptibility polymorphisms in vitamin C transporter gene SLC23A2 (rs1715364, rs6133175, rs1776948, rs6139587, rs369270 and rs6052937) were examined in 434 CLL cases and 1257 randomly selected controls from primary care centres with genetic data of whom 275 cases and 1094 controls having both diet and genetic information. Ascorbic Acid 145-154 solute carrier family 23 member 2 Homo sapiens 172-179 28351945-2 2017 The plasma membrane sodium-vitamin C cotransporter 2 (SVCT2) is the primary mediator of vitamin C uptake in neurons. Ascorbic Acid 27-36 solute carrier family 23 member 2 Homo sapiens 54-59 28351945-3 2017 SVCT2 specifically transports ascorbate, the reduced form of vitamin C, which acts as a reducing agent. Ascorbic Acid 30-39 solute carrier family 23 member 2 Homo sapiens 0-5 28351945-3 2017 SVCT2 specifically transports ascorbate, the reduced form of vitamin C, which acts as a reducing agent. Ascorbic Acid 61-70 solute carrier family 23 member 2 Homo sapiens 0-5 28351945-4 2017 We demonstrated that ascorbate uptake through SVCT2 was critical for the homeostasis of microglia, the resident myeloid cells of the CNS that are essential for proper functioning of the nervous tissue. Ascorbic Acid 21-30 solute carrier family 23 member 2 Homo sapiens 46-51 27012422-4 2016 In this study, we demonstrate that L-ascorbic acid partners with cetuximab to induce killing effects, which are influenced by sodium-dependent vitamin C transporter 2 (SVCT-2) in human colon cancer cells with a mutant KRAS. Ascorbic Acid 35-50 solute carrier family 23 member 2 Homo sapiens 126-166 27476024-0 2016 Corrigendum to "L-Ascorbic acid can abrogate SVCT-2-dependent cetuximab resistance mediated by mutant KRAS in human colon cancer cells": [Free Radic. Ascorbic Acid 15-31 solute carrier family 23 member 2 Homo sapiens 45-51 27382510-0 2016 Vitamin C is taken up by human T cells via sodium-dependent vitamin C transporter 2 (SVCT2) and exerts inhibitory effects on the activation of these cells in vitro. Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 43-83 27382510-0 2016 Vitamin C is taken up by human T cells via sodium-dependent vitamin C transporter 2 (SVCT2) and exerts inhibitory effects on the activation of these cells in vitro. Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 85-90 27012422-0 2016 L-Ascorbic acid can abrogate SVCT-2-dependent cetuximab resistance mediated by mutant KRAS in human colon cancer cells. Ascorbic Acid 0-15 solute carrier family 23 member 2 Homo sapiens 29-35 27012422-4 2016 In this study, we demonstrate that L-ascorbic acid partners with cetuximab to induce killing effects, which are influenced by sodium-dependent vitamin C transporter 2 (SVCT-2) in human colon cancer cells with a mutant KRAS. Ascorbic Acid 35-50 solute carrier family 23 member 2 Homo sapiens 168-174 27012422-5 2016 L-Ascorbic acid treatment of human colon cancer cells that express a mutant KRAS differentially and synergistically induced cell death with cetuximab in a SVCT-2-dependent manner. Ascorbic Acid 0-15 solute carrier family 23 member 2 Homo sapiens 155-161 27012422-6 2016 The ectopic expression of SVCT-2 induced sensitivity to L-ascorbic acid treatment in human colon cancer cells that do not express SVCT-2, whereas the knockdown of endogenous SVCT-2 induced resistance to L-ascorbic acid treatment in SVCT-2-positive cells. Ascorbic Acid 56-71 solute carrier family 23 member 2 Homo sapiens 26-32 27012422-10 2016 Taken together, these results suggest that resistance to cetuximab in human colon cancer patients with a mutant KRAS can be bypassed by L-ascorbic acid in an SVCT-2-dependent manner. Ascorbic Acid 136-151 solute carrier family 23 member 2 Homo sapiens 158-164 27012422-11 2016 Furthermore, SVCT-2 in mutant KRAS colon cancer may act as a potent marker for potentiating L-ascorbic acid co-treatment with cetuximab. Ascorbic Acid 92-107 solute carrier family 23 member 2 Homo sapiens 13-19 26779027-4 2015 The distribution and the concentration of vitamin C in the organs depend on the ascorbate requirements of each and on the tissue distribution of sodium-dependent vitamin C transporter 1 and 2 (SVCT1 and SVCT2). Ascorbic Acid 42-51 solute carrier family 23 member 2 Homo sapiens 203-208 26340060-12 2015 Further, ascorbate efflux is opposed by re-uptake of ascorbate on the SVCT2, providing a potential regulatory mechanism. Ascorbic Acid 53-62 solute carrier family 23 member 2 Homo sapiens 70-75 26188149-0 2015 Intracellular dehydroascorbic acid inhibits SVCT2-dependent transport of ascorbic acid in mitochondria. Dehydroascorbic Acid 14-34 solute carrier family 23 member 2 Homo sapiens 44-49 26340060-1 2015 Microvascular pericytes take up ascorbic acid on the ascorbate transporter SVCT2. Ascorbic Acid 32-45 solute carrier family 23 member 2 Homo sapiens 75-80 26340060-5 2015 Ascorbate re-uptake occurred on the SVCT2, since its blockade by replacing medium sodium with choline, by the SVCT2 inhibitor sulfinpyrazone, or by extracellular ascorbate accelerated ascorbate loss from the cells. Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 36-41 26340060-5 2015 Ascorbate re-uptake occurred on the SVCT2, since its blockade by replacing medium sodium with choline, by the SVCT2 inhibitor sulfinpyrazone, or by extracellular ascorbate accelerated ascorbate loss from the cells. Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 110-115 26340060-5 2015 Ascorbate re-uptake occurred on the SVCT2, since its blockade by replacing medium sodium with choline, by the SVCT2 inhibitor sulfinpyrazone, or by extracellular ascorbate accelerated ascorbate loss from the cells. Sulfinpyrazone 126-140 solute carrier family 23 member 2 Homo sapiens 36-41 26340060-5 2015 Ascorbate re-uptake occurred on the SVCT2, since its blockade by replacing medium sodium with choline, by the SVCT2 inhibitor sulfinpyrazone, or by extracellular ascorbate accelerated ascorbate loss from the cells. Ascorbic Acid 162-171 solute carrier family 23 member 2 Homo sapiens 36-41 26340060-6 2015 This was supported by finding that net efflux of radiolabeled ascorbate was increased by unlabeled extracellular ascorbate with a half-maximal effect in the range of the high affinity Km of the SVCT2. Ascorbic Acid 62-71 solute carrier family 23 member 2 Homo sapiens 194-199 26340060-6 2015 This was supported by finding that net efflux of radiolabeled ascorbate was increased by unlabeled extracellular ascorbate with a half-maximal effect in the range of the high affinity Km of the SVCT2. Ascorbic Acid 113-122 solute carrier family 23 member 2 Homo sapiens 194-199 26340060-9 2015 These potently inhibited ascorbate transport into cells on the SVCT2, but not its efflux. Ascorbic Acid 25-34 solute carrier family 23 member 2 Homo sapiens 63-68 26340060-12 2015 Further, ascorbate efflux is opposed by re-uptake of ascorbate on the SVCT2, providing a potential regulatory mechanism. Ascorbic Acid 9-18 solute carrier family 23 member 2 Homo sapiens 70-75 26188149-0 2015 Intracellular dehydroascorbic acid inhibits SVCT2-dependent transport of ascorbic acid in mitochondria. Ascorbic Acid 21-34 solute carrier family 23 member 2 Homo sapiens 44-49 26210298-0 2015 The crucial role of vitamin C and its transporter (SVCT2) in bone marrow stromal cell autophagy and apoptosis. Ascorbic Acid 20-29 solute carrier family 23 member 2 Homo sapiens 51-56 26210298-2 2015 Previously, we reported that vitamin C is transported into bone marrow stromal cells (BMSCs) through the sodium dependent Vitamin C Transporter 2 (SVCT2) and this transporter plays an important role in osteogenic differentiation. Ascorbic Acid 29-38 solute carrier family 23 member 2 Homo sapiens 105-145 26210298-2 2015 Previously, we reported that vitamin C is transported into bone marrow stromal cells (BMSCs) through the sodium dependent Vitamin C Transporter 2 (SVCT2) and this transporter plays an important role in osteogenic differentiation. Ascorbic Acid 29-38 solute carrier family 23 member 2 Homo sapiens 147-152 26210298-4 2015 To date, however, the exact role of vitamin C and its transporter (SVCT2) in ROS regulated autophagy and apoptosis in BMSCs is poorly understood. Ascorbic Acid 36-45 solute carrier family 23 member 2 Homo sapiens 67-72 26210298-4 2015 To date, however, the exact role of vitamin C and its transporter (SVCT2) in ROS regulated autophagy and apoptosis in BMSCs is poorly understood. ros 77-80 solute carrier family 23 member 2 Homo sapiens 67-72 25014399-1 2015 PURPOSE: The main goal of this study is to investigate the existence of sodium-dependent vitamin C transport system (SVCT2) and to define time-dependent uptake mechanism and intracellular regulation of ascorbic acid (AA) in human corneal epithelial (HCEC) and human retinal pigment epithelial (D407) cells. Sodium 72-78 solute carrier family 23 member 2 Homo sapiens 117-122 26403401-4 2015 PLA2 acts increasing the synthesis of Prostaglandin E2 (PGE2), which promotes osteogenesis by raising the cellular L-ascorbic acid uptake through the membrane carrier sodium vitamin C transporter-2 (SVCT-2). Dinoprostone 38-54 solute carrier family 23 member 2 Homo sapiens 199-205 26403401-4 2015 PLA2 acts increasing the synthesis of Prostaglandin E2 (PGE2), which promotes osteogenesis by raising the cellular L-ascorbic acid uptake through the membrane carrier sodium vitamin C transporter-2 (SVCT-2). Dinoprostone 56-60 solute carrier family 23 member 2 Homo sapiens 199-205 26403401-4 2015 PLA2 acts increasing the synthesis of Prostaglandin E2 (PGE2), which promotes osteogenesis by raising the cellular L-ascorbic acid uptake through the membrane carrier sodium vitamin C transporter-2 (SVCT-2). Ascorbic Acid 115-130 solute carrier family 23 member 2 Homo sapiens 199-205 25014399-1 2015 PURPOSE: The main goal of this study is to investigate the existence of sodium-dependent vitamin C transport system (SVCT2) and to define time-dependent uptake mechanism and intracellular regulation of ascorbic acid (AA) in human corneal epithelial (HCEC) and human retinal pigment epithelial (D407) cells. Ascorbic Acid 89-98 solute carrier family 23 member 2 Homo sapiens 117-122 25014399-10 2015 CONCLUSION: This research article reports regarding the ascorbic acid uptake mechanism, kinetics and regulation by sodium dependent vitamin C transporter (SVCT2) in HCEC and D407 cells. Ascorbic Acid 56-69 solute carrier family 23 member 2 Homo sapiens 155-160 25451960-2 2015 The reduced form of the vitamin, l-ascorbic acid, is imported by an active mechanism requiring two sodium-dependent vitamin C transporters (SVCT1 and SVCT2). Ascorbic Acid 33-48 solute carrier family 23 member 2 Homo sapiens 150-155 25854967-10 2015 SVCT2 and GLUT2 were present in the apical bronchial epithelium, where SVCT2 staining was predominately localised to goblet cells and inversely related to RTLF vitamin C concentrations. Ascorbic Acid 160-169 solute carrier family 23 member 2 Homo sapiens 71-76 25854967-12 2015 A negative correlation between SVCT2-positive goblet cells and bronchial RTLF vitamin C concentrations suggests a possible role for goblet cells in regulating the extracellular vitamin C pool. Ascorbic Acid 78-87 solute carrier family 23 member 2 Homo sapiens 31-36 25854967-12 2015 A negative correlation between SVCT2-positive goblet cells and bronchial RTLF vitamin C concentrations suggests a possible role for goblet cells in regulating the extracellular vitamin C pool. Ascorbic Acid 177-186 solute carrier family 23 member 2 Homo sapiens 31-36 25645015-3 2015 Measuring intracellular ascorbate, we found that pericytes display a linear uptake over 30 min and an apparent transport Km of 21 muM, both of which are consistent with activity of the Sodium-dependent Vitamin C Transporter 2 (SVCT2). Ascorbic Acid 24-33 solute carrier family 23 member 2 Homo sapiens 185-225 25645015-4 2015 Uptake of both radiolabeled and unlabeled ascorbate was prevented by inhibiting SVCT2 activity, but not by inhibiting the activity of GLUT-type glucose transporters, which import dehydroascorbate to also generate intracellular ascorbate. Ascorbic Acid 42-51 solute carrier family 23 member 2 Homo sapiens 80-85 25645015-7 2015 Together, these data clarify previous inconsistencies in the literature, implicate SVCT2 as the pericyte ascorbate transporter, and show that pericytes are capable of concentrating intracellular ascorbate against a gradient in an energy- and sodium-dependent fashion. Ascorbic Acid 105-114 solute carrier family 23 member 2 Homo sapiens 83-88 25102111-0 2014 Molecular expression and functional activity of vitamin C specific transport system (SVCT2) in human breast cancer cells. Ascorbic Acid 48-57 solute carrier family 23 member 2 Homo sapiens 85-90 25242204-0 2014 High-dose vitamin C supplementation increases skeletal muscle vitamin C concentration and SVCT2 transporter expression but does not alter redox status in healthy males. Ascorbic Acid 10-19 solute carrier family 23 member 2 Homo sapiens 90-95 25242204-9 2014 VC supplementation significantly increased skeletal muscle SVCT2 protein expression (main treatment effect p=0.006) but did not alter skeletal muscle redox measures or citrate synthase activity. Ascorbic Acid 0-2 solute carrier family 23 member 2 Homo sapiens 59-64 25102111-1 2014 The main goal of this study is to investigate the expression of sodium dependent vitamin C transport system (SVCT2). Sodium 64-70 solute carrier family 23 member 2 Homo sapiens 109-114 25102111-1 2014 The main goal of this study is to investigate the expression of sodium dependent vitamin C transport system (SVCT2). Ascorbic Acid 81-90 solute carrier family 23 member 2 Homo sapiens 109-114 24594434-5 2014 Immunoblotting of proteins extracted from highly purified mitochondrial fractions confirmed that SVCT2 protein was associated with mitochondria, and transport analysis revealed a sigmoidal ascorbic acid concentration curve with an apparent ascorbic acid transport Km of 0.6mM. Ascorbic Acid 189-202 solute carrier family 23 member 2 Homo sapiens 97-102 24798334-10 2014 A similar formation of AGEs was observed in UVA-irradiated lenses from human IDO/human sodium-dependent vitamin C transporter-2 mice, which contain high levels of kynurenines and ASC. Kynurenine 163-174 solute carrier family 23 member 2 Homo sapiens 87-127 24798334-10 2014 A similar formation of AGEs was observed in UVA-irradiated lenses from human IDO/human sodium-dependent vitamin C transporter-2 mice, which contain high levels of kynurenines and ASC. Ascorbic Acid 179-182 solute carrier family 23 member 2 Homo sapiens 87-127 24594434-10 2014 Overall, our data indicate that intracellular SVCT2 is localized in mitochondria, is sensitive to an intracellular microenvironment low in sodium and high in potassium, and functions as a low-affinity ascorbic acid transporter. Potassium 158-167 solute carrier family 23 member 2 Homo sapiens 46-51 24927052-1 2014 A novel brain targeting l-ascorbic acid derivatives with "lock-in" function were designed and synthesized as prodrugs to achieve the effective delivery of ibuprofen to brain by glucose transporter 1 (GLUT1) and the Na(+)-dependent vitamin C transporter SVCT2. Ascorbic Acid 24-39 solute carrier family 23 member 2 Homo sapiens 253-258 24927052-1 2014 A novel brain targeting l-ascorbic acid derivatives with "lock-in" function were designed and synthesized as prodrugs to achieve the effective delivery of ibuprofen to brain by glucose transporter 1 (GLUT1) and the Na(+)-dependent vitamin C transporter SVCT2. Ibuprofen 155-164 solute carrier family 23 member 2 Homo sapiens 253-258 24594434-5 2014 Immunoblotting of proteins extracted from highly purified mitochondrial fractions confirmed that SVCT2 protein was associated with mitochondria, and transport analysis revealed a sigmoidal ascorbic acid concentration curve with an apparent ascorbic acid transport Km of 0.6mM. Ascorbic Acid 240-253 solute carrier family 23 member 2 Homo sapiens 97-102 24594434-8 2014 Further studies using HEK-293 cells overexpressing SVCT2 at the plasma membrane revealed that the altered kinetic properties of mitochondrial SVCT2 are due to the ionic intracellular microenvironment (low in sodium and high in potassium), with potassium acting as a concentration-dependent inhibitor of SVCT2. Potassium 227-236 solute carrier family 23 member 2 Homo sapiens 51-56 24594434-8 2014 Further studies using HEK-293 cells overexpressing SVCT2 at the plasma membrane revealed that the altered kinetic properties of mitochondrial SVCT2 are due to the ionic intracellular microenvironment (low in sodium and high in potassium), with potassium acting as a concentration-dependent inhibitor of SVCT2. Potassium 227-236 solute carrier family 23 member 2 Homo sapiens 142-147 24594434-8 2014 Further studies using HEK-293 cells overexpressing SVCT2 at the plasma membrane revealed that the altered kinetic properties of mitochondrial SVCT2 are due to the ionic intracellular microenvironment (low in sodium and high in potassium), with potassium acting as a concentration-dependent inhibitor of SVCT2. Potassium 227-236 solute carrier family 23 member 2 Homo sapiens 142-147 24594434-10 2014 Overall, our data indicate that intracellular SVCT2 is localized in mitochondria, is sensitive to an intracellular microenvironment low in sodium and high in potassium, and functions as a low-affinity ascorbic acid transporter. Sodium 139-145 solute carrier family 23 member 2 Homo sapiens 46-51 24578608-0 2014 Genetic polymorphisms in SLC23A2 as predictive biomarkers of severe acute toxicities after treatment with a definitive 5-fluorouracil/cisplatin-based chemoradiotherapy in Japanese patients with esophageal squamous cell carcinoma. Fluorouracil 119-133 solute carrier family 23 member 2 Homo sapiens 25-32 24365600-4 2014 In this study, we knocked-down the sodium-dependent vitamin C transporter, SVCT2, the only known transporter of vitamin C in BMSCs, and performed cell adhesion, migration, in-vitro scratch wound healing and F-actin re-arrangement studies. Sodium 35-41 solute carrier family 23 member 2 Homo sapiens 75-80 24365600-4 2014 In this study, we knocked-down the sodium-dependent vitamin C transporter, SVCT2, the only known transporter of vitamin C in BMSCs, and performed cell adhesion, migration, in-vitro scratch wound healing and F-actin re-arrangement studies. Ascorbic Acid 52-61 solute carrier family 23 member 2 Homo sapiens 75-80 24578608-0 2014 Genetic polymorphisms in SLC23A2 as predictive biomarkers of severe acute toxicities after treatment with a definitive 5-fluorouracil/cisplatin-based chemoradiotherapy in Japanese patients with esophageal squamous cell carcinoma. Cisplatin 134-143 solute carrier family 23 member 2 Homo sapiens 25-32 24578608-2 2014 In the present study, single nucleotide polymorphisms (SNPs) in SLC23A2 gene were retrospectively evaluated in 49 Japanese patients with ESCC who were treated with a definitive 5-FU/CDDP-based CRT, and the predictive values for the clinical response, severe acute toxicities, and long-term survival were assessed. Fluorouracil 177-181 solute carrier family 23 member 2 Homo sapiens 64-71 24578608-2 2014 In the present study, single nucleotide polymorphisms (SNPs) in SLC23A2 gene were retrospectively evaluated in 49 Japanese patients with ESCC who were treated with a definitive 5-FU/CDDP-based CRT, and the predictive values for the clinical response, severe acute toxicities, and long-term survival were assessed. Cisplatin 182-186 solute carrier family 23 member 2 Homo sapiens 64-71 23647458-1 2013 In vitro and in vivo studies suggest that the basolateral membrane of choroid plexus cells, which is in contact with blood vessels, is involved in the uptake of the reduced form of vitamin C, ascorbic acid (AA), through the sodium-vitamin C cotransporter, (SVCT2). Ascorbic Acid 181-190 solute carrier family 23 member 2 Homo sapiens 257-262 23708151-2 2014 The bioavailability of this vitamin depends upon the nutritional intake and its uptake by cells, mainly through the sodium-dependent transporters SVCT1/Svct1 and SVCT2/Svct2 (human/rat). Sodium 116-122 solute carrier family 23 member 2 Homo sapiens 162-167 23708151-2 2014 The bioavailability of this vitamin depends upon the nutritional intake and its uptake by cells, mainly through the sodium-dependent transporters SVCT1/Svct1 and SVCT2/Svct2 (human/rat). Sodium 116-122 solute carrier family 23 member 2 Homo sapiens 168-173 23737080-5 2013 Four SNPs were predictors of plasma vitamin C levels (SLC23A1 rs11950646 and rs33972313; SLC23A2 rs6053005 and rs6133175) in multivariable linear regression models. Ascorbic Acid 36-45 solute carrier family 23 member 2 Homo sapiens 89-96 23737080-6 2013 One SNP (SLC23A2 rs6116569) was associated with GC risk, in particular non-cardia GC (OR = 1.63, 95 % CI = 1.11-2.39, based on 178 non-cardia cases), but this association was attenuated when plasma vitamin C was included in the logistic regression model. Ascorbic Acid 198-207 solute carrier family 23 member 2 Homo sapiens 9-16 23737080-9 2013 Common variants in SLC23A1 and SLC23A2 may influence plasma vitamin C concentration independent of dietary intake, and variation in SLC23A2 may influence GC risk. Ascorbic Acid 60-69 solute carrier family 23 member 2 Homo sapiens 31-38 23647458-1 2013 In vitro and in vivo studies suggest that the basolateral membrane of choroid plexus cells, which is in contact with blood vessels, is involved in the uptake of the reduced form of vitamin C, ascorbic acid (AA), through the sodium-vitamin C cotransporter, (SVCT2). Ascorbic Acid 192-205 solute carrier family 23 member 2 Homo sapiens 257-262 23647458-4 2013 In this study, the contribution of SVCT2 and GLUT1 to vitamin C uptake in human choroid plexus papilloma (HCPP) cells in culture was examined. Ascorbic Acid 54-63 solute carrier family 23 member 2 Homo sapiens 35-40 23647458-5 2013 Both the functional activity and the kinetic parameters of GLUT1 and SVCT2 in cells isolated from HCPP were observed. hcpp 98-102 solute carrier family 23 member 2 Homo sapiens 69-74 23647458-8 2013 Thus, vitamin C can be incorporated by epithelial choroid plexus papilloma cells using the basolateral polarization of SVCT2 and GLUT1. Ascorbic Acid 6-15 solute carrier family 23 member 2 Homo sapiens 119-124 23506882-4 2013 The SVCT1 and SVCT2 transporters are rather specific for ascorbic acid, which is an important antioxidant and plays a crucial role in a many metal-containing enzymes. Ascorbic Acid 57-70 solute carrier family 23 member 2 Homo sapiens 14-19 23916956-0 2013 Expression and/or activity of the SVCT2 ascorbate transporter may be decreased in many aggressive cancers, suggesting potential utility for sodium bicarbonate and dehydroascorbic acid in cancer therapy. Sodium Bicarbonate 140-158 solute carrier family 23 member 2 Homo sapiens 34-39 23916956-0 2013 Expression and/or activity of the SVCT2 ascorbate transporter may be decreased in many aggressive cancers, suggesting potential utility for sodium bicarbonate and dehydroascorbic acid in cancer therapy. Dehydroascorbic Acid 163-183 solute carrier family 23 member 2 Homo sapiens 34-39 23916956-7 2013 Unfortunately, since SVCT2 has a high affinity for ascorbate, and its activity is nearly saturated at normal healthy serum levels of this vitamin, increased oral administration of ascorbate would be unlikely to have much impact on the intracellular ascorbate content of tumors. Ascorbic Acid 51-60 solute carrier family 23 member 2 Homo sapiens 21-26 24400138-0 2013 The human sodium-dependent ascorbic acid transporters SLC23A1 and SLC23A2 do not mediate ascorbic acid release in the proximal renal epithelial cell. Ascorbic Acid 27-40 solute carrier family 23 member 2 Homo sapiens 66-73 24400138-1 2013 Sodium-dependent ascorbic acid membrane transporters SLC23A1 and SLC23A2 mediate ascorbic acid (vitamin C) transport into cells. Sodium 0-6 solute carrier family 23 member 2 Homo sapiens 65-72 24400138-1 2013 Sodium-dependent ascorbic acid membrane transporters SLC23A1 and SLC23A2 mediate ascorbic acid (vitamin C) transport into cells. Ascorbic Acid 17-30 solute carrier family 23 member 2 Homo sapiens 65-72 24400138-1 2013 Sodium-dependent ascorbic acid membrane transporters SLC23A1 and SLC23A2 mediate ascorbic acid (vitamin C) transport into cells. Ascorbic Acid 96-105 solute carrier family 23 member 2 Homo sapiens 65-72 24400138-3 2013 We hypothesized that SLC23A1 and SLC23A2 could serve a dual role, mediating ascorbic acid cellular efflux as well as uptake. Ascorbic Acid 76-89 solute carrier family 23 member 2 Homo sapiens 33-40 24121217-5 2013 The reduced form, L-ascorbic acid is imported by an active mechanism, requiring two sodium-dependent vitamin C transporters (SVCT1 and SVCT2). Ascorbic Acid 18-33 solute carrier family 23 member 2 Homo sapiens 135-140 23990905-2 2013 The sodium-dependent vitamin C transporter 2 is responsible for the transport of vitamin C into various cells and malfunction of this protein leads to reduced vitamin C in tissue, including the arterial wall. Ascorbic Acid 81-90 solute carrier family 23 member 2 Homo sapiens 4-44 23964197-10 2013 Both cell types expressed functional SVCT2 in vitro, and ascorbic acid (AA) induced their neural differentiation, increased betaIII-tubulin and SVCT2 expression, and amplified vitamin C uptake. Ascorbic Acid 57-70 solute carrier family 23 member 2 Homo sapiens 144-149 23506882-4 2013 The SVCT1 and SVCT2 transporters are rather specific for ascorbic acid, which is an important antioxidant and plays a crucial role in a many metal-containing enzymes. Metals 141-146 solute carrier family 23 member 2 Homo sapiens 14-19 23506882-7 2013 The expression of SVCT2 is relatively widespread, where it serves to either deliver ascorbic acid to tissues with high demand of the vitamin for enzymatic reactions or to protect metabolically highly active cells or specialized tissues from oxidative stress. Ascorbic Acid 84-97 solute carrier family 23 member 2 Homo sapiens 18-23 23420099-9 2013 In conclusion, mRNA levels of SLC22A2, SLC23A2, ABCB1, ABCC2, Rad51, MSH2 and DPYD were confirmed to be strongly correlated with IC50 values for 5-FU, and mRNA levels of ABCC2, MSH2 and DPYD were confirmed to be strongly correlated with IC(50) values for CDDP. Fluorouracil 145-149 solute carrier family 23 member 2 Homo sapiens 39-46 22665050-0 2013 SVCT-2 in breast cancer acts as an indicator for L-ascorbate treatment. Ascorbic Acid 49-60 solute carrier family 23 member 2 Homo sapiens 0-6 22665050-3 2013 Here, we demonstrate that L-ascorbate has a selective killing effect, which is influenced by sodium-dependent vitamin C transporter 2 (SVCT-2) in human breast cancer cells. Ascorbic Acid 26-37 solute carrier family 23 member 2 Homo sapiens 93-133 22665050-3 2013 Here, we demonstrate that L-ascorbate has a selective killing effect, which is influenced by sodium-dependent vitamin C transporter 2 (SVCT-2) in human breast cancer cells. Ascorbic Acid 26-37 solute carrier family 23 member 2 Homo sapiens 135-141 22665050-4 2013 Treatment of human breast cancer cells with L-ascorbate differentially induced cell death, dependent on the SVCT-2 protein level. Ascorbic Acid 44-55 solute carrier family 23 member 2 Homo sapiens 108-114 22665050-5 2013 Moreover, knockdown of endogenous SVCT-2 via RNA interference in breast cancer cells expressing high levels of the protein induced resistance to L-ascorbate treatment, whereas transfection with SVCT-2 expression plasmids led to enhanced L-ascorbate chemosensitivity. Ascorbic Acid 145-156 solute carrier family 23 member 2 Homo sapiens 34-40 22665050-5 2013 Moreover, knockdown of endogenous SVCT-2 via RNA interference in breast cancer cells expressing high levels of the protein induced resistance to L-ascorbate treatment, whereas transfection with SVCT-2 expression plasmids led to enhanced L-ascorbate chemosensitivity. Ascorbic Acid 237-248 solute carrier family 23 member 2 Homo sapiens 34-40 22665050-5 2013 Moreover, knockdown of endogenous SVCT-2 via RNA interference in breast cancer cells expressing high levels of the protein induced resistance to L-ascorbate treatment, whereas transfection with SVCT-2 expression plasmids led to enhanced L-ascorbate chemosensitivity. Ascorbic Acid 237-248 solute carrier family 23 member 2 Homo sapiens 194-200 22665050-9 2013 In addition, treatment with N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger, suppressed the induction of beclin-1 and LC3 II, implying that the differential SVCT-2 protein-dependent L-ascorbate uptake was attributable to intracellular ROS induced by L-ascorbate, subsequently leading to autophagy. Acetylcysteine 28-47 solute carrier family 23 member 2 Homo sapiens 172-178 22665050-9 2013 In addition, treatment with N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger, suppressed the induction of beclin-1 and LC3 II, implying that the differential SVCT-2 protein-dependent L-ascorbate uptake was attributable to intracellular ROS induced by L-ascorbate, subsequently leading to autophagy. Reactive Oxygen Species 51-74 solute carrier family 23 member 2 Homo sapiens 172-178 22665050-9 2013 In addition, treatment with N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger, suppressed the induction of beclin-1 and LC3 II, implying that the differential SVCT-2 protein-dependent L-ascorbate uptake was attributable to intracellular ROS induced by L-ascorbate, subsequently leading to autophagy. Reactive Oxygen Species 76-79 solute carrier family 23 member 2 Homo sapiens 172-178 22665050-9 2013 In addition, treatment with N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger, suppressed the induction of beclin-1 and LC3 II, implying that the differential SVCT-2 protein-dependent L-ascorbate uptake was attributable to intracellular ROS induced by L-ascorbate, subsequently leading to autophagy. Ascorbic Acid 197-208 solute carrier family 23 member 2 Homo sapiens 172-178 22665050-9 2013 In addition, treatment with N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger, suppressed the induction of beclin-1 and LC3 II, implying that the differential SVCT-2 protein-dependent L-ascorbate uptake was attributable to intracellular ROS induced by L-ascorbate, subsequently leading to autophagy. Reactive Oxygen Species 250-253 solute carrier family 23 member 2 Homo sapiens 172-178 22665050-9 2013 In addition, treatment with N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger, suppressed the induction of beclin-1 and LC3 II, implying that the differential SVCT-2 protein-dependent L-ascorbate uptake was attributable to intracellular ROS induced by L-ascorbate, subsequently leading to autophagy. Ascorbic Acid 265-276 solute carrier family 23 member 2 Homo sapiens 172-178 22665050-10 2013 These results suggest that functional SVCT-2 sensitizes breast cancer cells to autophagic damage by increasing the L-ascorbate concentration and intracellular ROS production and furthermore, SVCT-2 in breast cancer may act as an indicator for commencing L-ascorbate treatment. Ascorbic Acid 115-126 solute carrier family 23 member 2 Homo sapiens 38-44 22665050-10 2013 These results suggest that functional SVCT-2 sensitizes breast cancer cells to autophagic damage by increasing the L-ascorbate concentration and intracellular ROS production and furthermore, SVCT-2 in breast cancer may act as an indicator for commencing L-ascorbate treatment. Reactive Oxygen Species 159-162 solute carrier family 23 member 2 Homo sapiens 38-44 22665050-10 2013 These results suggest that functional SVCT-2 sensitizes breast cancer cells to autophagic damage by increasing the L-ascorbate concentration and intracellular ROS production and furthermore, SVCT-2 in breast cancer may act as an indicator for commencing L-ascorbate treatment. Ascorbic Acid 254-265 solute carrier family 23 member 2 Homo sapiens 38-44 22665050-10 2013 These results suggest that functional SVCT-2 sensitizes breast cancer cells to autophagic damage by increasing the L-ascorbate concentration and intracellular ROS production and furthermore, SVCT-2 in breast cancer may act as an indicator for commencing L-ascorbate treatment. Ascorbic Acid 254-265 solute carrier family 23 member 2 Homo sapiens 191-197 22990596-10 2013 In addition, kinetic analysis suggested that an ascorbate-dependent mechanism accounts for targeted SVCT2 expression in the developing kidney during medullary epithelial cell differentiation. Ascorbic Acid 48-57 solute carrier family 23 member 2 Homo sapiens 100-105 23228664-0 2013 Ascorbic acid enhances the expression of type 1 and type 4 collagen and SVCT2 in cultured human skin fibroblasts. Ascorbic Acid 0-13 solute carrier family 23 member 2 Homo sapiens 72-77 21770893-1 2011 SVCT2 (sodium-vitamin C co-transporter 2) is the major transporter mediating vitamin C uptake in most organs. Ascorbic Acid 14-23 solute carrier family 23 member 2 Homo sapiens 0-5 22041898-0 2012 Nitric oxide modulates sodium vitamin C transporter 2 (SVCT-2) protein expression via protein kinase G (PKG) and nuclear factor-kappaB (NF-kappaB). Nitric Oxide 0-12 solute carrier family 23 member 2 Homo sapiens 55-61 22041898-9 2012 NO also modulates the expression of SVCT-2, an effect mediated by cGMP and PKG. Cyclic GMP 66-70 solute carrier family 23 member 2 Homo sapiens 36-42 23177992-6 2012 In fact, the SVCT1 and SVCT2 transporters are rather specific for ascorbic acid. Ascorbic Acid 66-79 solute carrier family 23 member 2 Homo sapiens 23-28 23177992-7 2012 SVCT1 is expressed in epithelial tissues such as intestine, where it contributes to the maintenance of whole-body ascorbic acid levels, whereas the expression of SVCT2 is relatively widespread either to protect metabolically active cells and specialized tissues from oxidative stress or to deliver ascorbic acid to tissues that are in high demand of the vitamin for enzymatic reactions. Ascorbic Acid 298-311 solute carrier family 23 member 2 Homo sapiens 162-167 22116696-3 2012 These high ascorbate cellular concentrations are thought to be generated and maintained by the SVCT2 (Slc23a2), a specific transporter for ascorbate. Ascorbic Acid 11-20 solute carrier family 23 member 2 Homo sapiens 95-100 22116696-3 2012 These high ascorbate cellular concentrations are thought to be generated and maintained by the SVCT2 (Slc23a2), a specific transporter for ascorbate. Ascorbic Acid 11-20 solute carrier family 23 member 2 Homo sapiens 102-109 22116696-3 2012 These high ascorbate cellular concentrations are thought to be generated and maintained by the SVCT2 (Slc23a2), a specific transporter for ascorbate. Ascorbic Acid 139-148 solute carrier family 23 member 2 Homo sapiens 95-100 22116696-3 2012 These high ascorbate cellular concentrations are thought to be generated and maintained by the SVCT2 (Slc23a2), a specific transporter for ascorbate. Ascorbic Acid 139-148 solute carrier family 23 member 2 Homo sapiens 102-109 22116696-9 2012 The aim of this review is to assess the role of the SVCT2 in regulating neuronal ascorbate homeostasis and the extent to which ascorbate affects brain function and antioxidant defenses in the CNS. Ascorbic Acid 81-90 solute carrier family 23 member 2 Homo sapiens 52-57 21897744-0 2011 Topical application of L-arginine blocks advanced glycation by ascorbic acid in the lens of hSVCT2 transgenic mice. Arginine 23-33 solute carrier family 23 member 2 Homo sapiens 92-98 22171153-12 2011 Moreover, we consistently detected a significant association between the rs1279386 SNP in SLC23A2 and plasma vitamin C concentrations: GG subjects had significantly lower plasma vitamin C concentrations than the other genotypes (9.0+-1.4 microg/ml versus 10.5+-1.6 microg/ml, p<0.001 in POAG cases and 10.9+-1.6 microg/ml versus 12.1+-1.8 microg/ml, p<0.001 in controls). Ascorbic Acid 109-118 solute carrier family 23 member 2 Homo sapiens 90-97 22513420-7 2011 Sodium ascorbic acid co-transporters (SVCTs), SVCT1 and SVCT2 transport the reduced form of vitamin C (ascorbic acid). Ascorbic Acid 92-101 solute carrier family 23 member 2 Homo sapiens 56-61 21897744-0 2011 Topical application of L-arginine blocks advanced glycation by ascorbic acid in the lens of hSVCT2 transgenic mice. Ascorbic Acid 63-76 solute carrier family 23 member 2 Homo sapiens 92-98 22171153-12 2011 Moreover, we consistently detected a significant association between the rs1279386 SNP in SLC23A2 and plasma vitamin C concentrations: GG subjects had significantly lower plasma vitamin C concentrations than the other genotypes (9.0+-1.4 microg/ml versus 10.5+-1.6 microg/ml, p<0.001 in POAG cases and 10.9+-1.6 microg/ml versus 12.1+-1.8 microg/ml, p<0.001 in controls). Ascorbic Acid 178-187 solute carrier family 23 member 2 Homo sapiens 90-97 22171153-15 2011 CONCLUSIONS: The rs1279683 SNP in SLC23A2 was significantly associated with lower plasma concentrations of vitamin C and with higher risk of POAG in GG subjects. Ascorbic Acid 107-116 solute carrier family 23 member 2 Homo sapiens 34-41 21897744-6 2011 RESULTS: In hSVCT2 mice, L-arginine decreased 335/385 and 370/440 nm fluorescence by 40% (p<0.001), CML, CEL, and glucosepane crystallin crosslinks by 35% (p<0.05), 30% (p<0.05), and 37% (p<0.05), respectively, without affecting MG-H1 and G-H1. Arginine 25-35 solute carrier family 23 member 2 Homo sapiens 12-18 19232538-1 2009 To determine whether macrophage differentiation involves increased uptake of vitamin C, or ascorbic acid, we assessed the expression and function of its transporter SVCT2 during phorbol ester-induced differentiation of human-derived THP-1 monocytes. Ascorbic Acid 77-86 solute carrier family 23 member 2 Homo sapiens 165-170 19926816-1 2010 The human sodium-dependent vitamin C transporter-2 (hSVCT2) plays an important role in cellular accumulation of ascorbic acid in liver cells. Ascorbic Acid 112-125 solute carrier family 23 member 2 Homo sapiens 10-50 19926816-1 2010 The human sodium-dependent vitamin C transporter-2 (hSVCT2) plays an important role in cellular accumulation of ascorbic acid in liver cells. Ascorbic Acid 112-125 solute carrier family 23 member 2 Homo sapiens 52-58 19926816-5 2010 Video-rate confocal imaging showed evidence of dynamic hSVCT2-YFP containing intracellular trafficking vesicles, the motility of which was impaired following disruption of microtubules using nocodazole. Nocodazole 191-201 solute carrier family 23 member 2 Homo sapiens 55-61 19254685-0 2009 Oxidized lipoprotein induces the macrophage ascorbate transporter (SVCT2): protection by intracellular ascorbate against oxidant stress and apoptosis. Ascorbic Acid 44-53 solute carrier family 23 member 2 Homo sapiens 67-72 19254685-4 2009 This was associated with increased expression of the ascorbate transporter (SVCT2), which was prevented by ascorbate and by inhibiting the NF-kappaB pathway. Ascorbic Acid 53-62 solute carrier family 23 member 2 Homo sapiens 76-81 19125272-2 2009 Ascorbate is taken up by mammalian cells through the specific sodium/ascorbate co-transporters SVCT1 and SVCT2. Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 105-110 19232538-3 2009 When ascorbate was present during PMA-induced differentiation, the increase in SVCT2 protein expression was inhibited, but differentiation was enhanced. Ascorbic Acid 5-14 solute carrier family 23 member 2 Homo sapiens 79-84 20843809-0 2010 Histidine residues in the Na+-coupled ascorbic acid transporter-2 (SVCT2) are central regulators of SVCT2 function, modulating pH sensitivity, transporter kinetics, Na+ cooperativity, conformational stability, and subcellular localization. Histidine 0-9 solute carrier family 23 member 2 Homo sapiens 67-72 20843809-0 2010 Histidine residues in the Na+-coupled ascorbic acid transporter-2 (SVCT2) are central regulators of SVCT2 function, modulating pH sensitivity, transporter kinetics, Na+ cooperativity, conformational stability, and subcellular localization. Histidine 0-9 solute carrier family 23 member 2 Homo sapiens 100-105 20843809-2 2010 SVCT2 contains six histidine residues in its primary sequence, three of which are exofacial in the transporter secondary structure model. Histidine 19-28 solute carrier family 23 member 2 Homo sapiens 0-5 20843809-3 2010 We used site-directed mutagenesis and treatment with diethylpyrocarbonate to identify histidine residues responsible for SVCT2 pH sensitivity. Diethyl Pyrocarbonate 53-73 solute carrier family 23 member 2 Homo sapiens 121-126 20843809-3 2010 We used site-directed mutagenesis and treatment with diethylpyrocarbonate to identify histidine residues responsible for SVCT2 pH sensitivity. Histidine 86-95 solute carrier family 23 member 2 Homo sapiens 121-126 20843809-4 2010 We conclude that five histidine residues, His(109), His(203), His(206), His(269), and His(413), are central regulators of SVCT2 function, participating to different degrees in modulating pH sensitivity, transporter kinetics, Na(+) cooperativity, conformational stability, and subcellular localization. Histidine 22-31 solute carrier family 23 member 2 Homo sapiens 122-127 20843809-4 2010 We conclude that five histidine residues, His(109), His(203), His(206), His(269), and His(413), are central regulators of SVCT2 function, participating to different degrees in modulating pH sensitivity, transporter kinetics, Na(+) cooperativity, conformational stability, and subcellular localization. Histidine 42-45 solute carrier family 23 member 2 Homo sapiens 122-127 20843809-4 2010 We conclude that five histidine residues, His(109), His(203), His(206), His(269), and His(413), are central regulators of SVCT2 function, participating to different degrees in modulating pH sensitivity, transporter kinetics, Na(+) cooperativity, conformational stability, and subcellular localization. Histidine 52-55 solute carrier family 23 member 2 Homo sapiens 122-127 20843809-4 2010 We conclude that five histidine residues, His(109), His(203), His(206), His(269), and His(413), are central regulators of SVCT2 function, participating to different degrees in modulating pH sensitivity, transporter kinetics, Na(+) cooperativity, conformational stability, and subcellular localization. Histidine 52-55 solute carrier family 23 member 2 Homo sapiens 122-127 20843809-4 2010 We conclude that five histidine residues, His(109), His(203), His(206), His(269), and His(413), are central regulators of SVCT2 function, participating to different degrees in modulating pH sensitivity, transporter kinetics, Na(+) cooperativity, conformational stability, and subcellular localization. Histidine 52-55 solute carrier family 23 member 2 Homo sapiens 122-127 20843809-4 2010 We conclude that five histidine residues, His(109), His(203), His(206), His(269), and His(413), are central regulators of SVCT2 function, participating to different degrees in modulating pH sensitivity, transporter kinetics, Na(+) cooperativity, conformational stability, and subcellular localization. Histidine 52-55 solute carrier family 23 member 2 Homo sapiens 122-127 20843809-6 2010 Thus, histidine residues are central regulators of SVCT2 function. Histidine 6-15 solute carrier family 23 member 2 Homo sapiens 51-56 20549544-6 2010 Although culture of the cells with ascorbate did not affect SVCT2 protein expression, the oxLDL-induced increase in SVCT2 protein expression was prevented by ascorbate. Ascorbic Acid 158-167 solute carrier family 23 member 2 Homo sapiens 116-121 20549544-7 2010 These results suggest that up-regulation of endothelial cell SVCT2 expression and function may help to maintain intracellular ascorbate during oxLDL-induced oxidative stress, and that ascorbate in turn can prevent this effect. Ascorbic Acid 126-135 solute carrier family 23 member 2 Homo sapiens 61-66 19928843-5 2009 The targeting properties of the ascorbate-decorated nanosystems were tested by fluorescence-activated cell sorting (FACS) analysis and fluorescent microscopy on a panel of tumor cell lines preliminary selected for their ability to express the SVCT2 ascorbate transporter. Ascorbic Acid 32-41 solute carrier family 23 member 2 Homo sapiens 243-248 19928843-6 2009 Cell lines had been selected on the basis of the immunological properties assessed by FACS, which showed that two glioma cell lines, C6 and F98, and fibroblasts NIH/3T3 express plasma membrane-associated SVCT2 transporter for reduced ascorbic acid. Ascorbic Acid 234-247 solute carrier family 23 member 2 Homo sapiens 204-209 19928843-7 2009 Ascorbate-decorated pharmaceutical nanocarriers were endowed with selective targeting properties toward the SVCT2 transporter expressed in glioma cell models. Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 108-113 19928843-8 2009 This study shows that SVCT2 transporter for ascorbic acid expressed both in peculiar epithelial cells of the choroid plexus responsible for the filtering of vitamin C into the central nervous system (CNS) and, in some brain tumor cell lines, can be conceivably exploited as a potential target for delivery of drug-loaded pharmaceutical nanocarriers to the brain. Ascorbic Acid 44-57 solute carrier family 23 member 2 Homo sapiens 22-27 19928843-8 2009 This study shows that SVCT2 transporter for ascorbic acid expressed both in peculiar epithelial cells of the choroid plexus responsible for the filtering of vitamin C into the central nervous system (CNS) and, in some brain tumor cell lines, can be conceivably exploited as a potential target for delivery of drug-loaded pharmaceutical nanocarriers to the brain. Ascorbic Acid 157-166 solute carrier family 23 member 2 Homo sapiens 22-27 19232538-1 2009 To determine whether macrophage differentiation involves increased uptake of vitamin C, or ascorbic acid, we assessed the expression and function of its transporter SVCT2 during phorbol ester-induced differentiation of human-derived THP-1 monocytes. Phorbol Esters 178-191 solute carrier family 23 member 2 Homo sapiens 165-170 19232538-2 2009 Induction of THP-1 monocyte differentiation by phorbol 12-myristate 13-acetate (PMA) markedly increased SVCT2 mRNA, protein, and function. Tetradecanoylphorbol Acetate 47-78 solute carrier family 23 member 2 Homo sapiens 104-109 19232538-2 2009 Induction of THP-1 monocyte differentiation by phorbol 12-myristate 13-acetate (PMA) markedly increased SVCT2 mRNA, protein, and function. Tetradecanoylphorbol Acetate 80-83 solute carrier family 23 member 2 Homo sapiens 104-109 19232538-3 2009 When ascorbate was present during PMA-induced differentiation, the increase in SVCT2 protein expression was inhibited, but differentiation was enhanced. Tetradecanoylphorbol Acetate 34-37 solute carrier family 23 member 2 Homo sapiens 79-84 19232538-4 2009 PMA-induced SVCT2 protein expression was blocked by inhibitors of protein kinase C (PKC), with most of the affect due to the PKCbetaI and betaII isoforms. Tetradecanoylphorbol Acetate 0-3 solute carrier family 23 member 2 Homo sapiens 12-17 19232538-8 2009 In conclusion, PMA-induced monocyte-macrophage differentiation is enhanced by ascorbate and associated with increased expression and function of the SVCT2 protein through a pathway involving sustained activation of PKCbetaI/II, MAP kinase, NADPH oxidase, and NF-kappaB. Tetradecanoylphorbol Acetate 15-18 solute carrier family 23 member 2 Homo sapiens 149-154 20588054-1 2009 BACKGROUND/AIMS: Vitamin C transporter proteins SVCT1 and SVCT2 are required for the absorption and transport of vitamin C in humans. Ascorbic Acid 113-122 solute carrier family 23 member 2 Homo sapiens 58-63 19162177-0 2009 Vitamin C function in the brain: vital role of the ascorbate transporter SVCT2. Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 73-78 19162177-3 2009 Ascorbate is transported into the brain and neurons via the sodium-dependent vitamin C transporter 2 (SVCT2), which causes accumulation of ascorbate within cells against a concentration gradient. Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 60-100 19162177-3 2009 Ascorbate is transported into the brain and neurons via the sodium-dependent vitamin C transporter 2 (SVCT2), which causes accumulation of ascorbate within cells against a concentration gradient. Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 102-107 19162177-3 2009 Ascorbate is transported into the brain and neurons via the sodium-dependent vitamin C transporter 2 (SVCT2), which causes accumulation of ascorbate within cells against a concentration gradient. Ascorbic Acid 139-148 solute carrier family 23 member 2 Homo sapiens 60-100 19162177-3 2009 Ascorbate is transported into the brain and neurons via the sodium-dependent vitamin C transporter 2 (SVCT2), which causes accumulation of ascorbate within cells against a concentration gradient. Ascorbic Acid 139-148 solute carrier family 23 member 2 Homo sapiens 102-107 20588054-8 2009 CONCLUSIONS: Our findings demonstrate that genetic variation in SVCT1 can influence serum ascorbic acid concentrations and that SVCT1 and SVCT2 genotypes modify the strength of the correlation between dietary vitamin C and serum ascorbic acid. Ascorbic Acid 209-218 solute carrier family 23 member 2 Homo sapiens 138-143 20588054-8 2009 CONCLUSIONS: Our findings demonstrate that genetic variation in SVCT1 can influence serum ascorbic acid concentrations and that SVCT1 and SVCT2 genotypes modify the strength of the correlation between dietary vitamin C and serum ascorbic acid. Ascorbic Acid 229-242 solute carrier family 23 member 2 Homo sapiens 138-143 18706437-7 2008 In HepG2, taurocholic acid (TCA) and UDCA up-regulated biliverdin-IX alpha reductase (BVR alpha) and the vitamin C transporter SVCT2 (not SVCT1), whereas bilirubin up-regulated both SVCT1 and SVCT2. Taurocholic Acid 10-26 solute carrier family 23 member 2 Homo sapiens 127-132 18515971-3 2009 METHODS/RESULTS: A10 cells concentrated ascorbate against a gradient in a sodium-dependent manner, most likely on the sodium-dependent vitamin C transporter type 2 (SVCT2) ascorbate transporter, which was present in immunoblots of cell extracts. Ascorbic Acid 40-49 solute carrier family 23 member 2 Homo sapiens 118-163 18515971-3 2009 METHODS/RESULTS: A10 cells concentrated ascorbate against a gradient in a sodium-dependent manner, most likely on the sodium-dependent vitamin C transporter type 2 (SVCT2) ascorbate transporter, which was present in immunoblots of cell extracts. Ascorbic Acid 40-49 solute carrier family 23 member 2 Homo sapiens 165-170 18515971-3 2009 METHODS/RESULTS: A10 cells concentrated ascorbate against a gradient in a sodium-dependent manner, most likely on the sodium-dependent vitamin C transporter type 2 (SVCT2) ascorbate transporter, which was present in immunoblots of cell extracts. Sodium 74-80 solute carrier family 23 member 2 Homo sapiens 118-163 18515971-3 2009 METHODS/RESULTS: A10 cells concentrated ascorbate against a gradient in a sodium-dependent manner, most likely on the sodium-dependent vitamin C transporter type 2 (SVCT2) ascorbate transporter, which was present in immunoblots of cell extracts. Sodium 74-80 solute carrier family 23 member 2 Homo sapiens 165-170 18515971-7 2009 CONCLUSION: These results show that the SVCT2 facilitates ascorbate uptake by vascular smooth muscle cells, which in turn increases both the synthesis and maturation of type I collagen. Ascorbic Acid 58-67 solute carrier family 23 member 2 Homo sapiens 40-45 19391462-7 2008 Ascorbic acid is transported by the SVCT family of sodium-coupled transporters, with two isoforms molecularly cloned, the transporters SVCT1 y SVCT2, that show different functional properties and differential cell and tissue expression. Ascorbic Acid 0-13 solute carrier family 23 member 2 Homo sapiens 143-148 18421088-2 2008 This process is partially explained by advanced glycation end products (AGEs) from ascorbic acid (ASA), as the authors unequivocally demonstrated in an hSVCT2 transgenic mouse. Ascorbic Acid 83-96 solute carrier family 23 member 2 Homo sapiens 152-158 18421088-2 2008 This process is partially explained by advanced glycation end products (AGEs) from ascorbic acid (ASA), as the authors unequivocally demonstrated in an hSVCT2 transgenic mouse. Ascorbic Acid 98-101 solute carrier family 23 member 2 Homo sapiens 152-158 18706437-8 2008 In JAr, TCA and UDCA up-regulated BVR alpha, SVCT1 and SVCT2, whereas bilirubin up-regulated only SVCT2. Bilirubin 70-79 solute carrier family 23 member 2 Homo sapiens 98-103 18845575-1 2008 Humans use two sodium-ascorbate cotransporters (hSVCT1 and hSVCT2) for transporting the dietary essential micronutrient ascorbic acid, the reduced and active form of vitamin C. Ascorbic Acid 120-133 solute carrier family 23 member 2 Homo sapiens 59-65 18845575-1 2008 Humans use two sodium-ascorbate cotransporters (hSVCT1 and hSVCT2) for transporting the dietary essential micronutrient ascorbic acid, the reduced and active form of vitamin C. Ascorbic Acid 166-175 solute carrier family 23 member 2 Homo sapiens 59-65 18845575-5 2008 Results using short interfering RNA suggest that in HepG2 cells, decreasing hSVCT2 message levels reduces the overall ascorbic acid uptake process more than decreasing hSVCT1 message levels. Ascorbic Acid 118-131 solute carrier family 23 member 2 Homo sapiens 76-82 18706437-7 2008 In HepG2, taurocholic acid (TCA) and UDCA up-regulated biliverdin-IX alpha reductase (BVR alpha) and the vitamin C transporter SVCT2 (not SVCT1), whereas bilirubin up-regulated both SVCT1 and SVCT2. Taurocholic Acid 10-26 solute carrier family 23 member 2 Homo sapiens 192-197 18706437-7 2008 In HepG2, taurocholic acid (TCA) and UDCA up-regulated biliverdin-IX alpha reductase (BVR alpha) and the vitamin C transporter SVCT2 (not SVCT1), whereas bilirubin up-regulated both SVCT1 and SVCT2. Taurocholic Acid 28-31 solute carrier family 23 member 2 Homo sapiens 127-132 18706437-7 2008 In HepG2, taurocholic acid (TCA) and UDCA up-regulated biliverdin-IX alpha reductase (BVR alpha) and the vitamin C transporter SVCT2 (not SVCT1), whereas bilirubin up-regulated both SVCT1 and SVCT2. Taurocholic Acid 28-31 solute carrier family 23 member 2 Homo sapiens 192-197 18619416-1 2008 The human sodium-dependent vitamin C transporters (hSVCT1 and hSVCT2) mediate cellular uptake of ascorbic acid. Ascorbic Acid 97-110 solute carrier family 23 member 2 Homo sapiens 62-68 18619416-2 2008 Both these transporters contain potential sites for N-glycosylation in their extracellular domains (Asn-138, Asn-144 [hSVCT1]; Asn-188, Asn-196 [hSVCT2]), however the role of N-glycosylation in transporter function is unexplored. Nitrogen 52-53 solute carrier family 23 member 2 Homo sapiens 145-151 18619416-4 2008 We show that removal of individual N-glycosylation sites significantly impairs protein expression and consequently ascorbic acid uptake for hSVCT1 mutants (N138Q is retained intracellularly) and for hSVCT2 mutants (all of which reach the cell surface). Nitrogen 35-36 solute carrier family 23 member 2 Homo sapiens 199-205 17291984-3 2007 Here, we showed that platelets could compensate for fluctuations in ascorbate levels by modulating the expression of the Na+-dependent transporter SVCT2. Ascorbic Acid 68-77 solute carrier family 23 member 2 Homo sapiens 147-152 18247577-1 2008 Sodium-dependent vitamin C transporters, SVCT1 and SVCT2, are the only two known proteins for the uptake of ascorbate, the active form of vitamin C. Sodium 0-6 solute carrier family 23 member 2 Homo sapiens 51-56 18247577-1 2008 Sodium-dependent vitamin C transporters, SVCT1 and SVCT2, are the only two known proteins for the uptake of ascorbate, the active form of vitamin C. Ascorbic Acid 17-26 solute carrier family 23 member 2 Homo sapiens 51-56 18247577-1 2008 Sodium-dependent vitamin C transporters, SVCT1 and SVCT2, are the only two known proteins for the uptake of ascorbate, the active form of vitamin C. Ascorbic Acid 108-117 solute carrier family 23 member 2 Homo sapiens 51-56 18247577-1 2008 Sodium-dependent vitamin C transporters, SVCT1 and SVCT2, are the only two known proteins for the uptake of ascorbate, the active form of vitamin C. Ascorbic Acid 138-147 solute carrier family 23 member 2 Homo sapiens 51-56 17901237-0 2008 Ascorbic acid transported by sodium-dependent vitamin C transporter 2 stimulates steroidogenesis in human choriocarcinoma cells. Ascorbic Acid 0-13 solute carrier family 23 member 2 Homo sapiens 29-69 17901237-6 2008 SVCT2 knockdown in JEG-3 cells significantly suppressed the AA-induced mRNA expression of placental P450 cholesterol side-chain cleavage enzyme, 3beta-hydroxysteroid dehydrogenase type 1, and aromatase. Cholesterol 105-116 solute carrier family 23 member 2 Homo sapiens 0-5 17643393-1 2007 We have previously demonstrated that skeletal muscle cells possess efficient systems for vitamin C accumulation; in particular, the SVCT2 transporter for ascorbic acid uptake seems to play a crucial role. Ascorbic Acid 89-98 solute carrier family 23 member 2 Homo sapiens 132-137 17643393-1 2007 We have previously demonstrated that skeletal muscle cells possess efficient systems for vitamin C accumulation; in particular, the SVCT2 transporter for ascorbic acid uptake seems to play a crucial role. Ascorbic Acid 154-167 solute carrier family 23 member 2 Homo sapiens 132-137 17643393-3 2007 We found that transcription of the SVCT2 gene could be positively or negatively modulated by the presence of oxidant (H(2)O(2)) or antioxidant (lipoate) compounds, respectively. dl-Thioctic acid 144-151 solute carrier family 23 member 2 Homo sapiens 35-40 17586466-5 2007 Rates of specific ascorbate transport correlated with the presence of the SVCT2. Ascorbic Acid 18-27 solute carrier family 23 member 2 Homo sapiens 74-79 17541511-0 2008 SVCT1 and SVCT2: key proteins for vitamin C uptake. Ascorbic Acid 34-43 solute carrier family 23 member 2 Homo sapiens 10-15 17541511-7 2008 Understanding the physiological role of SVCT1 and SVCT2 may lead to develop new therapeutic strategies to control intracellular vitamin C content or to promote tissue-specific delivery of vitamin C-drug conjugates. Ascorbic Acid 128-137 solute carrier family 23 member 2 Homo sapiens 50-55 17541511-7 2008 Understanding the physiological role of SVCT1 and SVCT2 may lead to develop new therapeutic strategies to control intracellular vitamin C content or to promote tissue-specific delivery of vitamin C-drug conjugates. Ascorbic Acid 188-197 solute carrier family 23 member 2 Homo sapiens 50-55 18791929-2 2008 Vitamin C transport is facilitated by membrane bound sodium-dependent transporters, SVCT1 (encoded by SLC23A1) and SVCT2 (encoded by SLC23A2). Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 115-120 18791929-2 2008 Vitamin C transport is facilitated by membrane bound sodium-dependent transporters, SVCT1 (encoded by SLC23A1) and SVCT2 (encoded by SLC23A2). Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 133-140 17689499-7 2007 Therefore, oversupplementation with AA could be deleterious in diabetic patients, because overexpression of adrenal SVCT-2 in diabetes could lead to excessive AA uptake, thus enhancing norepinephrine production and exacerbating some diabetic complications. Norepinephrine 185-199 solute carrier family 23 member 2 Homo sapiens 116-122 17012227-3 2007 The properties of SVCT2 are modulated by Ca(2+)/Mg(2+) and a reciprocal functional interaction between Na(+) and ascorbic acid that defines the substrate binding order and the transport stoichiometry. Magnesium 48-50 solute carrier family 23 member 2 Homo sapiens 18-23 17012227-3 2007 The properties of SVCT2 are modulated by Ca(2+)/Mg(2+) and a reciprocal functional interaction between Na(+) and ascorbic acid that defines the substrate binding order and the transport stoichiometry. Ascorbic Acid 113-126 solute carrier family 23 member 2 Homo sapiens 18-23 17012227-8 2007 SVCT2 showed an absolute requirement for Ca(2+)/Mg(2+) for function, with both cations switching the transporter from an inactive into an active conformation by increasing the transport V(max) without affecting the transport K(m) or the Na(+) cooperativity. magnesium ion 48-54 solute carrier family 23 member 2 Homo sapiens 0-5 17012227-9 2007 Our data indicate that SVCT2 may switch between a number of states with characteristic properties, including an inactive conformation in the absence of Ca(2+)/Mg(2+). Magnesium 159-161 solute carrier family 23 member 2 Homo sapiens 23-28 16288478-10 2006 Ascorbate is delivered to lung cells via the SVCT2 ascorbate transporter, which was found to be sensitive to nickel or cell density. Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 45-50 17075057-3 2006 To test this hypothesis, we engineered a mouse that selectively overexpresses the human vitamin C transporter SVCT2 in the lens. Ascorbic Acid 88-97 solute carrier family 23 member 2 Homo sapiens 110-115 17075057-6 2006 The hSVCT2 mouse is expected to facilitate the search for drugs that inhibit damage by vitamin C oxidation products. Ascorbic Acid 87-96 solute carrier family 23 member 2 Homo sapiens 4-10 16933033-6 2006 Incubation of cells with 6-deoxy-6-fluoro-ascorbic (F-ASA), i.e. a probe specific for the sodium-dependent Vitamin C uptake (SVCT2), revealed a 10-fold uptake suppression into mouse 17EM15 relative to human HLE-B3 and JAR choriocarcinoma cells (a control), that could be overcome by overexpressing hSVCT2 using two different promoter constructs. 6-deoxy-6-fluoro-ascorbic 25-50 solute carrier family 23 member 2 Homo sapiens 298-304 16933033-6 2006 Incubation of cells with 6-deoxy-6-fluoro-ascorbic (F-ASA), i.e. a probe specific for the sodium-dependent Vitamin C uptake (SVCT2), revealed a 10-fold uptake suppression into mouse 17EM15 relative to human HLE-B3 and JAR choriocarcinoma cells (a control), that could be overcome by overexpressing hSVCT2 using two different promoter constructs. f-asa 52-57 solute carrier family 23 member 2 Homo sapiens 298-304 16933033-6 2006 Incubation of cells with 6-deoxy-6-fluoro-ascorbic (F-ASA), i.e. a probe specific for the sodium-dependent Vitamin C uptake (SVCT2), revealed a 10-fold uptake suppression into mouse 17EM15 relative to human HLE-B3 and JAR choriocarcinoma cells (a control), that could be overcome by overexpressing hSVCT2 using two different promoter constructs. Sodium 90-96 solute carrier family 23 member 2 Homo sapiens 298-304 16933033-6 2006 Incubation of cells with 6-deoxy-6-fluoro-ascorbic (F-ASA), i.e. a probe specific for the sodium-dependent Vitamin C uptake (SVCT2), revealed a 10-fold uptake suppression into mouse 17EM15 relative to human HLE-B3 and JAR choriocarcinoma cells (a control), that could be overcome by overexpressing hSVCT2 using two different promoter constructs. Ascorbic Acid 107-116 solute carrier family 23 member 2 Homo sapiens 298-304 16288478-10 2006 Ascorbate is delivered to lung cells via the SVCT2 ascorbate transporter, which was found to be sensitive to nickel or cell density. Nickel 109-115 solute carrier family 23 member 2 Homo sapiens 45-50 16357110-2 2006 There are two sodium-dependent membrane transporters encoded by SLC23A1 and SLC23A2, which have key roles in human vitamin C metabolism and which control dietary uptake, reabsorption, and tissue distribution of vitamin C. Sodium 14-20 solute carrier family 23 member 2 Homo sapiens 76-83 16357110-2 2006 There are two sodium-dependent membrane transporters encoded by SLC23A1 and SLC23A2, which have key roles in human vitamin C metabolism and which control dietary uptake, reabsorption, and tissue distribution of vitamin C. Ascorbic Acid 115-124 solute carrier family 23 member 2 Homo sapiens 76-83 16357110-2 2006 There are two sodium-dependent membrane transporters encoded by SLC23A1 and SLC23A2, which have key roles in human vitamin C metabolism and which control dietary uptake, reabsorption, and tissue distribution of vitamin C. Ascorbic Acid 211-220 solute carrier family 23 member 2 Homo sapiens 76-83 15316768-2 2004 Sodium-dependent vitamin C transport is mediated by two transporters, SVCT 1 and SVCT 2, encoded by SLC23A1 and SLC23A2. Sodium 0-6 solute carrier family 23 member 2 Homo sapiens 81-87 15578707-1 2005 Specialized cells transport vitamin C in its reduced form using sodium-dependent cotransporters (SVCT1 and SVCT2). Ascorbic Acid 28-37 solute carrier family 23 member 2 Homo sapiens 107-112 15921655-0 2005 Chondrocyte transport and concentration of ascorbic acid is mediated by SVCT2. Ascorbic Acid 43-56 solute carrier family 23 member 2 Homo sapiens 72-77 15921655-9 2005 Thus, we provide the first evidence that SVCT2 mediates the secondary active and concentrative transport of ascorbic acid in human chondrocytes. Ascorbic Acid 108-121 solute carrier family 23 member 2 Homo sapiens 41-46 15316768-2 2004 Sodium-dependent vitamin C transport is mediated by two transporters, SVCT 1 and SVCT 2, encoded by SLC23A1 and SLC23A2. Sodium 0-6 solute carrier family 23 member 2 Homo sapiens 112-119 15316768-2 2004 Sodium-dependent vitamin C transport is mediated by two transporters, SVCT 1 and SVCT 2, encoded by SLC23A1 and SLC23A2. Ascorbic Acid 17-26 solute carrier family 23 member 2 Homo sapiens 81-87 15316768-2 2004 Sodium-dependent vitamin C transport is mediated by two transporters, SVCT 1 and SVCT 2, encoded by SLC23A1 and SLC23A2. Ascorbic Acid 17-26 solute carrier family 23 member 2 Homo sapiens 112-119 15060139-0 2004 A human sodium-dependent vitamin C transporter 2 isoform acts as a dominant-negative inhibitor of ascorbic acid transport. Ascorbic Acid 98-111 solute carrier family 23 member 2 Homo sapiens 8-48 15094391-2 2004 Our previous studies suggested that Zn-induced osteoblast differentiation and Ca2+-, PO4(3-)-stimulated osteopontin (OPN) expression might result from their up-regulation effect on SVCT2 expression and AA uptake. Zinc 36-38 solute carrier family 23 member 2 Homo sapiens 181-186 15094391-2 2004 Our previous studies suggested that Zn-induced osteoblast differentiation and Ca2+-, PO4(3-)-stimulated osteopontin (OPN) expression might result from their up-regulation effect on SVCT2 expression and AA uptake. Phosphates 85-92 solute carrier family 23 member 2 Homo sapiens 181-186 15094391-5 2004 Alkaline phosphatase activity, hydroxyproline content significantly increased in SVCT2-overexpressing cells, and the induction of OPN mRNA was through up-regulation of OPN promoter activity by SVCT2 overexpression. Hydroxyproline 31-45 solute carrier family 23 member 2 Homo sapiens 81-86 15094391-6 2004 Moreover, SVCT2-overexpressing cells exhibited more ability to promote mineralization and increase calcium deposition under the stimulation of 5 mM beta-glycerophosphate. Calcium 99-106 solute carrier family 23 member 2 Homo sapiens 10-15 15094391-6 2004 Moreover, SVCT2-overexpressing cells exhibited more ability to promote mineralization and increase calcium deposition under the stimulation of 5 mM beta-glycerophosphate. beta-glycerophosphoric acid 148-169 solute carrier family 23 member 2 Homo sapiens 10-15 15340249-9 2004 Transfection of HUVECs with the antisense oligonucleotide of SVCT-2 significantly suppressed the uptake of AA. Oligonucleotides 42-57 solute carrier family 23 member 2 Homo sapiens 61-67 12845532-3 2004 SVCT1 and SVCT2 display similar properties, including high affinity for l-ascorbic acid, but are discretely distributed. Ascorbic Acid 72-87 solute carrier family 23 member 2 Homo sapiens 10-15 14993613-8 2004 Sodium dependency and phloretin sensitivity, as well as the expression of transcripts for sodium-dependent vitamin C transporter (SVCT)-1 and SVCT2, support a model in which an apical vitamin C transporter is central for relaying the effect of vitamin C to CFTR. Ascorbic Acid 184-193 solute carrier family 23 member 2 Homo sapiens 142-147 14622981-3 2003 We examined the roles of L-ascorbic acid (AA) and its transporter, sodium-dependent vitamin C transporter (SVCT) 2, in the Zn-induced expression of osteoblastic differentiation markers. Zinc 123-125 solute carrier family 23 member 2 Homo sapiens 67-114 14622981-7 2003 These findings suggest that AA and SVCT2 mediate Zn-induced OPN and OCN expression and partly regulate Zn-induced osteoblastic differentiation. Zinc 49-51 solute carrier family 23 member 2 Homo sapiens 35-40 14622981-5 2003 Western blotting and kinetic assays showed that Zn increased functional SVCT2 protein levels and AA transport. Zinc 48-50 solute carrier family 23 member 2 Homo sapiens 72-77 14622981-7 2003 These findings suggest that AA and SVCT2 mediate Zn-induced OPN and OCN expression and partly regulate Zn-induced osteoblastic differentiation. Zinc 103-105 solute carrier family 23 member 2 Homo sapiens 35-40 10471399-1 1999 We report here on the cloning and functional characterization of human SVCT2, a sodium-dependent vitamin C (ascorbate) transporter. Ascorbic Acid 97-106 solute carrier family 23 member 2 Homo sapiens 71-76 11584081-2 2001 Vitamin C is actively transported into cells by one of two closely related sodium-dependent transporters, SVCT1 or SVCT2. Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 115-120 11446766-0 2001 Vitamin C transport in human lens epithelial cells: evidence for the presence of SVCT2. Ascorbic Acid 0-9 solute carrier family 23 member 2 Homo sapiens 81-86 11446766-12 2001 Exposure to the chemical oxidant tert-butylhydroperoxide (TBH) up-regulated SVCT2 gene expression in HLE-B3 cells. tert-Butylhydroperoxide 33-56 solute carrier family 23 member 2 Homo sapiens 76-81 11446766-12 2001 Exposure to the chemical oxidant tert-butylhydroperoxide (TBH) up-regulated SVCT2 gene expression in HLE-B3 cells. tert-Butylhydroperoxide 58-61 solute carrier family 23 member 2 Homo sapiens 76-81 11396616-4 2001 L-ascorbic acid enters cells via Na+-dependent systems, and two isoforms of these transporters (SVCT1 and SVCT2) have recently been cloned from humans and rats. Ascorbic Acid 0-15 solute carrier family 23 member 2 Homo sapiens 106-111 11396616-6 2001 SVCT2 may exhibit a higher affinity for ascorbic acid than SVCT1 but with a lower maximum velocity. Ascorbic Acid 40-53 solute carrier family 23 member 2 Homo sapiens 0-5 10556521-0 1999 Cloning and functional characterization of the human sodium-dependent vitamin C transporters hSVCT1 and hSVCT2. Sodium 53-59 solute carrier family 23 member 2 Homo sapiens 104-110 12388072-1 2002 Protein kinase C (PKC) regulation of l-ascorbic acid transport mediated by the Na+/ascorbic acid transporters, hSVCT1 and hSVCT2, expressed in COS-1 cells was studied using recombinant carboxyl-terminal V5 epitope-tagged forms of the transporters. Ascorbic Acid 37-52 solute carrier family 23 member 2 Homo sapiens 122-128 12388072-7 2002 However, for hSVCT2 there was no apparent change in transporter distribution, suggesting that the PKC-dependent modulation of L-ascorbic acid transport mediated by hSVCT2 was the result of reduced catalytic transport efficiency. Ascorbic Acid 126-141 solute carrier family 23 member 2 Homo sapiens 164-170 11806707-1 2002 To improve the entry of certain drugs into brain, ascorbic acid (AA) conjugates of these drugs were synthesized and their capacity to interact with SVCT2 ascorbate transporters was explored. Ascorbic Acid 50-63 solute carrier family 23 member 2 Homo sapiens 148-153 10841345-4 2000 In contrast, in situ hybridization experiments reveal that SVCT2 mRNA is expressed only in neurons and not in normal astrocytes or astrocytes stimulated by an intrastriatal injection of the neurotoxin quinolinic acid. Quinolinic Acid 201-216 solute carrier family 23 member 2 Homo sapiens 59-64 10841345-5 2000 We conclude that SVCT2 is neuron specific and that the majority of ascorbate storage occurs in neurons. Ascorbic Acid 67-76 solute carrier family 23 member 2 Homo sapiens 17-22 10841345-6 2000 Furthermore, we propose that the observed sodium-dependent ascorbate transport in cultured astrocytes may be due to artificial upregulation of SVCT2 during cell culturing. Sodium 42-48 solute carrier family 23 member 2 Homo sapiens 143-148 10841345-6 2000 Furthermore, we propose that the observed sodium-dependent ascorbate transport in cultured astrocytes may be due to artificial upregulation of SVCT2 during cell culturing. Ascorbic Acid 59-68 solute carrier family 23 member 2 Homo sapiens 143-148 10556521-5 1999 By Eadie-Hofstee transformation the apparent K(m) of hSVCT1 for ascorbate was 252.0 microM and of hSVCT2 for ascorbate was 21.3 microM. Ascorbic Acid 109-118 solute carrier family 23 member 2 Homo sapiens 98-104 10471399-4 1999 When functionally expressed in mammalian cells, hSVCT2 induces the transport of ascorbic acid. Ascorbic Acid 80-93 solute carrier family 23 member 2 Homo sapiens 48-54 10471399-5 1999 The transport process induced by hSVCT2 is Na(+)-dependent and is specific for ascorbate. Ascorbic Acid 79-88 solute carrier family 23 member 2 Homo sapiens 33-39 10331392-4 1999 We find that SVCT1 and SVCT2 each mediate concentrative, high-affinity L-ascorbic acid transport that is stereospecific and is driven by the Na+ electrochemical gradient. Ascorbic Acid 71-86 solute carrier family 23 member 2 Homo sapiens 23-28