PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34019094-1 2021 In the small intestine, Na:H (NHE3) and Cl:HCO3 (DRA or PAT1) exchangers present in the brush border membrane (BBM) of absorptive villus cells are primarily responsible for the coupled absorption of NaCl, the malabsorption of which causes diarrhea, a common symptom of inflammatory bowel disease (IBD). Bicarbonates 43-47 solute carrier family 26 member 3 Homo sapiens 49-52 35076190-1 2022 BACKGROUND/AIMS: NHE3 (Na+/H+ exchanger3) and SLC26A3 (Cl-/HCO3- exchanger, DRA) are the major components of the intestinal neutral NaCl absorptive process and based on the intestinal segment, contribute to HCO3- absorption and HCO3- secretion. Bicarbonates 59-63 solute carrier family 26 member 3 Homo sapiens 46-53 35076190-1 2022 BACKGROUND/AIMS: NHE3 (Na+/H+ exchanger3) and SLC26A3 (Cl-/HCO3- exchanger, DRA) are the major components of the intestinal neutral NaCl absorptive process and based on the intestinal segment, contribute to HCO3- absorption and HCO3- secretion. Bicarbonates 59-63 solute carrier family 26 member 3 Homo sapiens 76-79 35076190-1 2022 BACKGROUND/AIMS: NHE3 (Na+/H+ exchanger3) and SLC26A3 (Cl-/HCO3- exchanger, DRA) are the major components of the intestinal neutral NaCl absorptive process and based on the intestinal segment, contribute to HCO3- absorption and HCO3- secretion. Bicarbonates 207-211 solute carrier family 26 member 3 Homo sapiens 46-53 35076190-1 2022 BACKGROUND/AIMS: NHE3 (Na+/H+ exchanger3) and SLC26A3 (Cl-/HCO3- exchanger, DRA) are the major components of the intestinal neutral NaCl absorptive process and based on the intestinal segment, contribute to HCO3- absorption and HCO3- secretion. Bicarbonates 207-211 solute carrier family 26 member 3 Homo sapiens 76-79 35076190-1 2022 BACKGROUND/AIMS: NHE3 (Na+/H+ exchanger3) and SLC26A3 (Cl-/HCO3- exchanger, DRA) are the major components of the intestinal neutral NaCl absorptive process and based on the intestinal segment, contribute to HCO3- absorption and HCO3- secretion. Bicarbonates 228-232 solute carrier family 26 member 3 Homo sapiens 46-53 35076190-1 2022 BACKGROUND/AIMS: NHE3 (Na+/H+ exchanger3) and SLC26A3 (Cl-/HCO3- exchanger, DRA) are the major components of the intestinal neutral NaCl absorptive process and based on the intestinal segment, contribute to HCO3- absorption and HCO3- secretion. Bicarbonates 228-232 solute carrier family 26 member 3 Homo sapiens 76-79 33191723-8 2020 Genetic analysis demonstrated that the patient had a SLC26A3 c.269_270dupAA homozygous mutation in exon 3, leading to a frameshift from 91st amino acid Gly and alteration of the SLC26A3 transmembrane protein sequence, thus resulting in a Cl-/HCO3- exchange barrier. Bicarbonates 242-246 solute carrier family 26 member 3 Homo sapiens 53-60 32989468-2 2021 Slc26a3 (DRA), as a key chloride-bicarbonate exchanger protein in the intestinal epithelial luminal membrane, participates in the electroneutral NaCl absorption of intestine, together with Na+/H+ exchangers. Bicarbonates 33-44 solute carrier family 26 member 3 Homo sapiens 0-7 32989468-2 2021 Slc26a3 (DRA), as a key chloride-bicarbonate exchanger protein in the intestinal epithelial luminal membrane, participates in the electroneutral NaCl absorption of intestine, together with Na+/H+ exchangers. Bicarbonates 33-44 solute carrier family 26 member 3 Homo sapiens 9-12 33599438-8 2021 Genetic analysis demonstrated that the patient had a SLC26A3 c.269_270dupAA homozygous mutation in exon 3, leading to a frameshift from 91st amino acid Gly and alteration of the SLC26A3 transmembrane protein sequence, thus resulting in a Cl-/HCO3- exchange barrier. Bicarbonates 242-246 solute carrier family 26 member 3 Homo sapiens 53-60 33599438-8 2021 Genetic analysis demonstrated that the patient had a SLC26A3 c.269_270dupAA homozygous mutation in exon 3, leading to a frameshift from 91st amino acid Gly and alteration of the SLC26A3 transmembrane protein sequence, thus resulting in a Cl-/HCO3- exchange barrier. Bicarbonates 242-246 solute carrier family 26 member 3 Homo sapiens 178-185 33191723-8 2020 Genetic analysis demonstrated that the patient had a SLC26A3 c.269_270dupAA homozygous mutation in exon 3, leading to a frameshift from 91st amino acid Gly and alteration of the SLC26A3 transmembrane protein sequence, thus resulting in a Cl-/HCO3- exchange barrier. Bicarbonates 242-246 solute carrier family 26 member 3 Homo sapiens 178-185 31483700-6 2019 We and others have previously shown impaired chloride absorption in infectious diarrhea due to dysregulation of SLC26A3 [downregulated in adenoma (DRA)], the human intestinal apical membrane Cl-/HCO3- exchanger protein. Bicarbonates 195-199 solute carrier family 26 member 3 Homo sapiens 112-119 32951339-2 2020 CCD is a rare autosomal recessive disorder caused by defects in the solute carrier family 26 member 3 (SLC26A3) gene, which encodes an intestinal Cl- /HCO3- , Na+ -independent exchanger. Bicarbonates 151-156 solute carrier family 26 member 3 Homo sapiens 68-101 32951339-2 2020 CCD is a rare autosomal recessive disorder caused by defects in the solute carrier family 26 member 3 (SLC26A3) gene, which encodes an intestinal Cl- /HCO3- , Na+ -independent exchanger. Bicarbonates 151-156 solute carrier family 26 member 3 Homo sapiens 103-110 30914450-10 2019 Proteomic alterations in penetrable mucus samples included a reduction of the SLC26A3 apical membrane anion exchanger, which supplies bicarbonate required for colonic mucin barrier formation. Bicarbonates 134-145 solute carrier family 26 member 3 Homo sapiens 78-85 32850522-1 2020 Objectives and Study: Congenital chloride diarrhea (CCD) is a rare, autosomal recessive disorder caused by mutations in the SLC26A3 gene encoding a transmembrane chloride/bicarbonate ion exchanger mainly expressed in the apical brush border of the ileal and colonic epithelium. Bicarbonates 171-182 solute carrier family 26 member 3 Homo sapiens 124-131 31145360-1 2019 Congenital chloride losing diarrhea (CCLD) is a rare type of chronic watery diarrhea due to mutations in SLC26A3 gene leading to defective chloride-bicarbonate exchanges with the resultant loss of chloride and retention of bicarbonate.We aim to define pediatric Saudi CCLD patients" characteristics to achieve prompt diagnosis, management, follow up with good quality of life, and prevention of complications in these patients.We carried retrospective data review of demographic, clinical, laboratory, radiographic, and outcome of all pediatric patients fulfilling the criteria of CCLD over 10 years from 2004 to 2014 from a single center in Taif region, Saudi Arabia.Forty-nine patients fulfilled the criteria of CCLD from 21 families with more than one affected patient in the same family in 90% of them and positive consanguinity in 91% of the cohort. Bicarbonates 148-159 solute carrier family 26 member 3 Homo sapiens 105-112 31145360-1 2019 Congenital chloride losing diarrhea (CCLD) is a rare type of chronic watery diarrhea due to mutations in SLC26A3 gene leading to defective chloride-bicarbonate exchanges with the resultant loss of chloride and retention of bicarbonate.We aim to define pediatric Saudi CCLD patients" characteristics to achieve prompt diagnosis, management, follow up with good quality of life, and prevention of complications in these patients.We carried retrospective data review of demographic, clinical, laboratory, radiographic, and outcome of all pediatric patients fulfilling the criteria of CCLD over 10 years from 2004 to 2014 from a single center in Taif region, Saudi Arabia.Forty-nine patients fulfilled the criteria of CCLD from 21 families with more than one affected patient in the same family in 90% of them and positive consanguinity in 91% of the cohort. Bicarbonates 223-234 solute carrier family 26 member 3 Homo sapiens 105-112 30659943-2 2019 An area that has continued to be poorly understood is related to DRA regulation in acute adenosine 3",5"-cyclic monophosphate (cAMP)-related diarrheas, in which DRA appears to be both inhibited as part of NaCl absorption and stimulated to contribute to increased HCO3- secretion. Bicarbonates 263-267 solute carrier family 26 member 3 Homo sapiens 65-68 29305650-5 2018 Apical uptake of SCFA thus involves non-saturable diffusion of the undissociated acid (HSCFA), SCFA-/HCO3- exchange via DRA (SLC26A3) and/or SCFA--H+ symport (MCT1, SLC16A1). Bicarbonates 101-105 solute carrier family 26 member 3 Homo sapiens 125-132 30118583-2 2018 Among them, SLC26A3 acts as a chloride/bicarbonate exchanger, highly expressed in the gastrointestinal, pancreatic and renal tissues. Bicarbonates 39-50 solute carrier family 26 member 3 Homo sapiens 12-19 29079751-1 2017 Chloride absorption and bicarbonate excretion through exchange by the solute carrier family 26 member 3 (SLC26A3) and cystic fibrosis transmembrane conductance regulator (CFTR) are crucial for many tissues including sperm and epithelia of the male reproductive tract. Bicarbonates 24-35 solute carrier family 26 member 3 Homo sapiens 70-103 28823863-7 2017 DRA-mediated exchange of Cl- for HCO3- was measured by uptake of 125I. Bicarbonates 33-37 solute carrier family 26 member 3 Homo sapiens 0-3 29079751-1 2017 Chloride absorption and bicarbonate excretion through exchange by the solute carrier family 26 member 3 (SLC26A3) and cystic fibrosis transmembrane conductance regulator (CFTR) are crucial for many tissues including sperm and epithelia of the male reproductive tract. Bicarbonates 24-35 solute carrier family 26 member 3 Homo sapiens 105-112 29079751-7 2017 Functional studies showed that while SLC26A3 is a strong activator of CFTR-dependent anion transport, SLC26A3-p.Asp688His mutant retains normal Cl-/HCO3- exchange activity but suppresses CFTR, despite unaffected domain binding and expression. Bicarbonates 148-152 solute carrier family 26 member 3 Homo sapiens 102-109 24115633-1 2014 The solute carrier 26 (SLC26) family emerges as a distinct class of anion transporters with its members SLC26A3 (Slc26a3) and SLC26A6 (Slc26a6) reported to be electrogenic Cl(-)/HCO3(-) exchangers. Bicarbonates 178-182 solute carrier family 26 member 3 Homo sapiens 104-111 25907791-0 2015 Bicarbonate exchangers SLC26A3 and SLC26A6 are localized at the apical membrane of porcine vas deferens epithelium. Bicarbonates 0-11 solute carrier family 26 member 3 Homo sapiens 23-30 24868584-0 2014 HCO3- secretion by SLC26A3 and mucosal defence in the colon. Bicarbonates 0-4 solute carrier family 26 member 3 Homo sapiens 19-26 27346053-0 2016 Involvement of Cl(-)/HCO3(-) exchanger SLC26A3 and SLC26A6 in preimplantation embryo cleavage. Bicarbonates 21-25 solute carrier family 26 member 3 Homo sapiens 39-46 27346053-6 2016 We further showed that Cl(-)/HCO3(-) exchanger solute carrier family 26 (SLC26) A3 and A6 were expressed at 2-cell through blastocyst stage. Bicarbonates 29-33 solute carrier family 26 member 3 Homo sapiens 47-82 27346053-8 2016 These results indicate the involvement of SLC26A3 and A6 in transporting HCO3(-) essential for embryo cleavage, possibly working in concert with CFTR through a Cl(-) recycling pathway. Bicarbonates 73-77 solute carrier family 26 member 3 Homo sapiens 42-49 25711268-2 2015 Life-long secretory diarrhea is caused by mutations in solute carrier family 26, member 3, (SLC26A3), which disrupt epithelial Cl(-) /HCO3 (-) transport in the ileum and colon. Bicarbonates 134-138 solute carrier family 26 member 3 Homo sapiens 55-89 25711268-2 2015 Life-long secretory diarrhea is caused by mutations in solute carrier family 26, member 3, (SLC26A3), which disrupt epithelial Cl(-) /HCO3 (-) transport in the ileum and colon. Bicarbonates 134-138 solute carrier family 26 member 3 Homo sapiens 92-99 24115633-1 2014 The solute carrier 26 (SLC26) family emerges as a distinct class of anion transporters with its members SLC26A3 (Slc26a3) and SLC26A6 (Slc26a6) reported to be electrogenic Cl(-)/HCO3(-) exchangers. Bicarbonates 178-182 solute carrier family 26 member 3 Homo sapiens 113-120 24115633-4 2014 We also summarise recent work on Slc26a3 and Slc26a6 in uterine epithelial cells and sperm, revealing their functional role in working closely with the cystic fibrosis transmembrane conductance regulator (CFTR) for HCO3(-) transport in these cells. Bicarbonates 215-219 solute carrier family 26 member 3 Homo sapiens 33-40 22779076-2 2012 Mutations in the solute carrier family 26, member 3 (SLC26A3) gene, which encodes a coupled Cl(-)/HCO(3)(-) exchanger in the ileum and colon, are known to cause CLD. Bicarbonates 98-103 solute carrier family 26 member 3 Homo sapiens 17-51 23274434-1 2013 UNLABELLED: Congenital chloride diarrhea (CLD, OMIM#214700) is an autosomal recessive disorder caused by mutations in the solute carrier family 26 member 3 (SLC26A3) gene, which encodes an intestinal chloride/bicarbonate exchanger. Bicarbonates 209-220 solute carrier family 26 member 3 Homo sapiens 122-155 23274434-1 2013 UNLABELLED: Congenital chloride diarrhea (CLD, OMIM#214700) is an autosomal recessive disorder caused by mutations in the solute carrier family 26 member 3 (SLC26A3) gene, which encodes an intestinal chloride/bicarbonate exchanger. Bicarbonates 209-220 solute carrier family 26 member 3 Homo sapiens 157-164 22779076-2 2012 Mutations in the solute carrier family 26, member 3 (SLC26A3) gene, which encodes a coupled Cl(-)/HCO(3)(-) exchanger in the ileum and colon, are known to cause CLD. Bicarbonates 98-103 solute carrier family 26 member 3 Homo sapiens 53-60 18827800-1 2008 Congenital chloride diarrhea is due to mutations in the intestinal Cl(-)/HCO(3)(-) exchange (SLC26A3) which results in sodium chloride and fluid depletion leading to hypochloremic and hypokalemic metabolic alkalosis. Bicarbonates 73-82 solute carrier family 26 member 3 Homo sapiens 93-100 22159277-4 2012 In this regard, we have recently shown that short-term treatment by lysophosphatidic acid (LPA), an important bioactive phospholipid, stimulates Cl(-)/HCO(3)(-)(OH(-)) exchange activity via an increase in DRA surface levels in human intestinal epithelial cells. Bicarbonates 151-158 solute carrier family 26 member 3 Homo sapiens 205-208 19321737-15 2009 These results suggest that Cl(-)/HCO(3)(-) exchange mode of human SLC26A3 is controlled by a pH-sensitive intracellular modifier site, which is likely in the transmembrane domain. Bicarbonates 33-39 solute carrier family 26 member 3 Homo sapiens 66-73 21805424-4 2011 The defective gene is SLC26A3, which encodes a Na-independent CL/HCO3 exchanger that is expressed primarily in the apical brush border membrane of ileal enterocytes and colonic epithelium. Bicarbonates 65-69 solute carrier family 26 member 3 Homo sapiens 22-29 20884887-13 2010 Our results demonstrate that NPY modulates Cl-/HCO3-(OH-) exchange activity by enhancing the association of DRA with lipid rafts, thereby resulting in an increase in Cl-/HCO3-(OH-) exchange activity. Bicarbonates 47-51 solute carrier family 26 member 3 Homo sapiens 108-111 20884887-13 2010 Our results demonstrate that NPY modulates Cl-/HCO3-(OH-) exchange activity by enhancing the association of DRA with lipid rafts, thereby resulting in an increase in Cl-/HCO3-(OH-) exchange activity. Bicarbonates 170-174 solute carrier family 26 member 3 Homo sapiens 108-111 19447883-5 2009 DRA-mediated Cl/HCO(3) exchange was measured as intracellular pH changes. Bicarbonates 16-22 solute carrier family 26 member 3 Homo sapiens 0-3 19015189-7 2009 Slc26a3 and Slc26a6 function as coupled electrogenic Cl-/HCO(3)- exchangers or as bona fide anion channels. Bicarbonates 57-63 solute carrier family 26 member 3 Homo sapiens 0-7 19538314-2 2009 DRA (downregulated in adenoma) is an intestinal chloride/bicarbonate exchanger that is functionally coupled to CFTR (cystic fibrosis transmembrane regulator) in the upper gastrointestinal tract to mediate chloride and bicarbonate secretion and to NHE3 (Na/H exchanger- isoform 3) in the lower gastrointestinal tract to mediate electroneutral NaCl absorption. Bicarbonates 57-68 solute carrier family 26 member 3 Homo sapiens 0-3 19538314-2 2009 DRA (downregulated in adenoma) is an intestinal chloride/bicarbonate exchanger that is functionally coupled to CFTR (cystic fibrosis transmembrane regulator) in the upper gastrointestinal tract to mediate chloride and bicarbonate secretion and to NHE3 (Na/H exchanger- isoform 3) in the lower gastrointestinal tract to mediate electroneutral NaCl absorption. Bicarbonates 218-229 solute carrier family 26 member 3 Homo sapiens 0-3 15480750-6 2005 DRA mediated electroneutral Cl-/HCO3- exchange but OH- was not transported and SO4(2-)/HCO3- exchange was minimal. Bicarbonates 32-36 solute carrier family 26 member 3 Homo sapiens 0-3 17700966-3 2007 Members of the SLC26 family are known to mediate Cl(-)-HCO3(-) exchange across the apical membrane of other epithelia and both SLC26A6 and SLC26A3 have been detected in pancreatic ducts. Bicarbonates 55-62 solute carrier family 26 member 3 Homo sapiens 139-146 16715296-0 2006 Chloride and bicarbonate have similar affinities to the intestinal anion exchanger DRA (down regulated in adenoma). Bicarbonates 13-24 solute carrier family 26 member 3 Homo sapiens 83-86 16715296-0 2006 Chloride and bicarbonate have similar affinities to the intestinal anion exchanger DRA (down regulated in adenoma). Bicarbonates 13-24 solute carrier family 26 member 3 Homo sapiens 88-113 16715296-1 2006 DRA (down regulated in adenoma, SLC26A3) is an anion exchanger that mediates electroneutral NaCl absorption in the ileum and proximal colon together with NHE3 (Na/H exchanger isoform 3), and that is involved in duodenal and possibly pancreatic bicarbonate secretion. Bicarbonates 244-255 solute carrier family 26 member 3 Homo sapiens 0-3 16715296-1 2006 DRA (down regulated in adenoma, SLC26A3) is an anion exchanger that mediates electroneutral NaCl absorption in the ileum and proximal colon together with NHE3 (Na/H exchanger isoform 3), and that is involved in duodenal and possibly pancreatic bicarbonate secretion. Bicarbonates 244-255 solute carrier family 26 member 3 Homo sapiens 5-30 16715296-1 2006 DRA (down regulated in adenoma, SLC26A3) is an anion exchanger that mediates electroneutral NaCl absorption in the ileum and proximal colon together with NHE3 (Na/H exchanger isoform 3), and that is involved in duodenal and possibly pancreatic bicarbonate secretion. Bicarbonates 244-255 solute carrier family 26 member 3 Homo sapiens 32-39 16715296-7 2006 Cl and HCO3 compete with similar affinities for transport by DRA. Bicarbonates 7-11 solute carrier family 26 member 3 Homo sapiens 61-64 18216024-2 2008 Mutations in SLC26A3 (solute carrier 26 family member 3), which functions as a coupled Cl(-)/HCO(3)(-) exchanger, cause CLD. Bicarbonates 93-98 solute carrier family 26 member 3 Homo sapiens 13-20 18216024-2 2008 Mutations in SLC26A3 (solute carrier 26 family member 3), which functions as a coupled Cl(-)/HCO(3)(-) exchanger, cause CLD. Bicarbonates 93-98 solute carrier family 26 member 3 Homo sapiens 22-55 18216024-4 2008 The STAS domain is required for SLC26A3 Cl(-)/HCO(3)(-) exchange function and for the activation of cystic fibrosis transmembrane conductance regulator by SLC26A3. Bicarbonates 46-52 solute carrier family 26 member 3 Homo sapiens 32-39 18216024-4 2008 The STAS domain is required for SLC26A3 Cl(-)/HCO(3)(-) exchange function and for the activation of cystic fibrosis transmembrane conductance regulator by SLC26A3. Bicarbonates 46-52 solute carrier family 26 member 3 Homo sapiens 155-162 16606687-0 2006 Coupling modes and stoichiometry of Cl-/HCO3- exchange by slc26a3 and slc26a6. Bicarbonates 40-44 solute carrier family 26 member 3 Homo sapiens 58-65 16606687-5 2006 The membrane potential modulated the apparent affinity for extracellular Cl- of Cl-/HCO3- exchange by slc26a3. Bicarbonates 84-88 solute carrier family 26 member 3 Homo sapiens 102-109 16606687-7 2006 An apparent uncoupled current was also developed during the incubation of slc26a3-expressing oocytes in HCO3--buffered Cl--free media. Bicarbonates 104-109 solute carrier family 26 member 3 Homo sapiens 74-81 16606687-8 2006 These findings were used to develop a turnover cycle for Cl- and HCO3- transport by slc26a3. Bicarbonates 65-69 solute carrier family 26 member 3 Homo sapiens 84-91 16606687-12 2006 The significance of isoform-specific Cl- and HCO3- transport stoichiometry by slc26a3 and slc26a6 is discussed in the context of diseases of epithelial Cl- absorption and HCO3- secretion. Bicarbonates 45-49 solute carrier family 26 member 3 Homo sapiens 78-85 16641574-1 2006 OBJECTIVES: Congenital chloride diarrhea (CLD) is a rare, autosomal recessive disorder of intestinal Cl/HCO3 exchange caused by mutations in the SLC26A3 gene and characterized by persistent Cl rich diarrhea from birth. Bicarbonates 104-108 solute carrier family 26 member 3 Homo sapiens 145-152 17120762-1 2006 Congenital chloride diarrhoea (CLD, OMIM214700) is a rare genetic disease caused by mutations in a plasma membrane protein, the solute-linked carrier family 26 member A3 (SLC26A3) protein, which encodes for an epithelial anion exchanger for Cl- and HCO3-. Bicarbonates 249-253 solute carrier family 26 member 3 Homo sapiens 128-169 17120762-1 2006 Congenital chloride diarrhoea (CLD, OMIM214700) is a rare genetic disease caused by mutations in a plasma membrane protein, the solute-linked carrier family 26 member A3 (SLC26A3) protein, which encodes for an epithelial anion exchanger for Cl- and HCO3-. Bicarbonates 249-253 solute carrier family 26 member 3 Homo sapiens 171-178 15766278-0 2005 The CFTR associated protein CAP70 interacts with the apical Cl-/HCO3- exchanger DRA in rabbit small intestinal mucosa. Bicarbonates 64-68 solute carrier family 26 member 3 Homo sapiens 80-83 15480750-6 2005 DRA mediated electroneutral Cl-/HCO3- exchange but OH- was not transported and SO4(2-)/HCO3- exchange was minimal. Bicarbonates 87-91 solute carrier family 26 member 3 Homo sapiens 0-3 15480750-7 2005 In the presence of 5% CO2/HCO3- the apparent affinity of DRA for Cl- in transfected HEK cells was 23-36 mM, which is lower than that reported for rabbit ileal brush border membrane vesicles and for oocytes injected with human DRA. Bicarbonates 26-30 solute carrier family 26 member 3 Homo sapiens 57-60 15480750-8 2005 DRA was inhibited by 4 mM DIDS (45+/-11%), by 50 microM tenidap (71+/-8%) and by 100 microM glibenclamide (59+/-22% inhibition of HCO3- transport and 79+/-3% inhibition of Cl- transport). Bicarbonates 130-134 solute carrier family 26 member 3 Homo sapiens 0-3 15499994-7 2004 All examined bicarbonate transport proteins, except the DRA (SLC26A3) Cl-/HCO3(-) exchange protein, have a consensus CAII binding site in their cytoplasmic C-terminus. Bicarbonates 13-24 solute carrier family 26 member 3 Homo sapiens 56-59 15498800-10 2004 HCO3(-) fluxes were similar for cells expressing AE3fl, SLC26A6 or Slc26a3, suggesting that they have similar transport activity. Bicarbonates 0-4 solute carrier family 26 member 3 Homo sapiens 67-74 15499994-7 2004 All examined bicarbonate transport proteins, except the DRA (SLC26A3) Cl-/HCO3(-) exchange protein, have a consensus CAII binding site in their cytoplasmic C-terminus. Bicarbonates 13-24 solute carrier family 26 member 3 Homo sapiens 61-68 15499994-7 2004 All examined bicarbonate transport proteins, except the DRA (SLC26A3) Cl-/HCO3(-) exchange protein, have a consensus CAII binding site in their cytoplasmic C-terminus. Bicarbonates 74-78 solute carrier family 26 member 3 Homo sapiens 56-59 11875004-2 2002 The recently discovered dra (down-regulated in adenoma) gene encodes a transport protein (DRA) for SO4(2-), Cl-, and HCO3-. Bicarbonates 117-121 solute carrier family 26 member 3 Homo sapiens 24-27 12651923-2 2003 hDRA expressed in Xenopus oocytes mediated bidirectional Cl--Cl- and Cl--HCO3- exchange. Bicarbonates 73-77 solute carrier family 26 member 3 Homo sapiens 0-4 12651923-9 2003 cAMP-insensitive Cl--HCO3- exchange mediated by hDRA gained modest cAMP sensitivity when co-expressed with cystic fibrosis transmembrane conductance regulator (CFTR). Bicarbonates 21-25 solute carrier family 26 member 3 Homo sapiens 48-52 12442266-3 2002 CLD is caused by mutations in the solute carrier family 26, member 3 gene (SLC26A3, alias CLD or DRA), which encodes a Na+-independent Cl-/HCO3- (or OH-) exchanger. Bicarbonates 139-143 solute carrier family 26 member 3 Homo sapiens 34-68 12442266-3 2002 CLD is caused by mutations in the solute carrier family 26, member 3 gene (SLC26A3, alias CLD or DRA), which encodes a Na+-independent Cl-/HCO3- (or OH-) exchanger. Bicarbonates 139-143 solute carrier family 26 member 3 Homo sapiens 75-82 12442266-3 2002 CLD is caused by mutations in the solute carrier family 26, member 3 gene (SLC26A3, alias CLD or DRA), which encodes a Na+-independent Cl-/HCO3- (or OH-) exchanger. Bicarbonates 139-143 solute carrier family 26 member 3 Homo sapiens 97-100 12372813-3 2002 DRA-mediated bicarbonate transport activity of 18 +/- 1 mM H+ equivalents/min was inhibited 53 +/- 2% by 100 mM of the CAII inhibitor, acetazolamide, but was unaffected by the membrane-impermeant carbonic anhydrase inhibitor, 1-[5-sulfamoyl-1,3,4-thiadiazol-2-yl-(aminosulfonyl-4-phenyl)]-2,6-dimethyl-4-phenyl-pyridinium perchlorate. Bicarbonates 13-24 solute carrier family 26 member 3 Homo sapiens 0-3 12372813-6 2002 We conclude that cytosolic CAII is required for full DRA-mediated bicarbonate transport. Bicarbonates 66-77 solute carrier family 26 member 3 Homo sapiens 53-56 12372813-7 2002 However, DRA differs from other bicarbonate transport proteins because its transport activity is not stimulated by direct interaction with CAII. Bicarbonates 32-43 solute carrier family 26 member 3 Homo sapiens 9-12 12369822-0 2002 The down regulated in adenoma (dra) gene product binds to the second PDZ domain of the NHE3 kinase A regulatory protein (E3KARP), potentially linking intestinal Cl-/HCO3- exchange to Na+/H+ exchange. Bicarbonates 165-169 solute carrier family 26 member 3 Homo sapiens 4-35 11875004-2 2002 The recently discovered dra (down-regulated in adenoma) gene encodes a transport protein (DRA) for SO4(2-), Cl-, and HCO3-. Bicarbonates 117-121 solute carrier family 26 member 3 Homo sapiens 90-93 11875004-3 2002 The aim of this study was to investigate whether DRA may be the duodenal apical Cl-/HCO3- exchanger. Bicarbonates 84-88 solute carrier family 26 member 3 Homo sapiens 49-52 11875004-10 2002 The strong predominance of DRA over NHE3 and NHE2 expression in duodenum was paralleled by much higher Cl-/HCO3- than Na+/H+ exchange rates in brush border membrane vesicles and likely explains the high duodenal HCO3- secretory rates. Bicarbonates 107-111 solute carrier family 26 member 3 Homo sapiens 27-30 11875004-10 2002 The strong predominance of DRA over NHE3 and NHE2 expression in duodenum was paralleled by much higher Cl-/HCO3- than Na+/H+ exchange rates in brush border membrane vesicles and likely explains the high duodenal HCO3- secretory rates. Bicarbonates 212-216 solute carrier family 26 member 3 Homo sapiens 27-30 11875004-11 2002 CONCLUSIONS: These data suggest that DRA is the major apical anion exchanger in the duodenum as well as the colon and the likely transport protein for duodenal electroneutral HCO3- secretion. Bicarbonates 175-179 solute carrier family 26 member 3 Homo sapiens 37-40 11087667-3 2000 Three human transporter proteins have been functionally characterized: SLC26A2 (DTDST), SLC26A3 (CLD or DRA), and SLC26A4 (PDS) can transport with different specificities the chloride, iodine, bicarbonate, oxalate, and hydroxyl anions, whereas SLC26A5 (prestin) was suggested to act as the motor protein of the cochlear outer hair cell. Bicarbonates 193-204 solute carrier family 26 member 3 Homo sapiens 88-95 11826292-6 2002 The metabolic alkalosis of congenital chloride-losing diarrhea is caused by mutations in the DRA Cl(-)/HCO3(-) exchanger of the ileocolonic apical membrane. Bicarbonates 103-107 solute carrier family 26 member 3 Homo sapiens 93-96 11087667-3 2000 Three human transporter proteins have been functionally characterized: SLC26A2 (DTDST), SLC26A3 (CLD or DRA), and SLC26A4 (PDS) can transport with different specificities the chloride, iodine, bicarbonate, oxalate, and hydroxyl anions, whereas SLC26A5 (prestin) was suggested to act as the motor protein of the cochlear outer hair cell. Bicarbonates 193-204 solute carrier family 26 member 3 Homo sapiens 104-107 10428871-1 1999 Mutations in human DRA cause congenital chloride diarrhea, thereby raising the possibility that it functions as a Cl(-)/HCO(3)(-) exchanger. Bicarbonates 120-125 solute carrier family 26 member 3 Homo sapiens 19-22 10898717-12 2000 We propose that the tracheal HCO(3)(-) secretion defect in patients with CF is partly due to the downregulation of the apical Cl(-)/HCO(3)(-) exchange activity mediated by DRA. Bicarbonates 29-35 solute carrier family 26 member 3 Homo sapiens 172-175 10898717-12 2000 We propose that the tracheal HCO(3)(-) secretion defect in patients with CF is partly due to the downregulation of the apical Cl(-)/HCO(3)(-) exchange activity mediated by DRA. Bicarbonates 29-34 solute carrier family 26 member 3 Homo sapiens 172-175