PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
20375274-4	2010	Pendrin knockout (KO) mice display significantly acidic urine at baseline [pH 5.20 in KO vs. 6.01 in wild type (WT); P < 0.0001] along with elevated serum HCO(3)(-) concentration (27.4 vs. 24 meq/l in KO vs. WT, respectively; P < 0.02), consistent with decreased bicarbonate secretion in vivo.	7 alpha-hydroxy-4-cholesten-3-one	158-161	solute carrier family 26, member 4	Mus musculus	0-7
20511491-8	2010	Injection of a cyp27a1(-/-) mouse with (2)H(7)-labeled 7alpha-hydroxy-4-cholesten-3-one resulted in a significant incorporation of (2)H(7)-cholestanol in the brain.	7 alpha-hydroxy-4-cholesten-3-one	55-87	cytochrome P450, family 27, subfamily a, polypeptide 1	Mus musculus	15-22
20511491-9	2010	The results are consistent with a concentration-dependent flux of 7alpha-hydroxy-4-cholesten-3-one across the blood-brain barrier in cyp27a1(-/-) mice and subsequent formation of cholestanol.	7 alpha-hydroxy-4-cholesten-3-one	66-98	cytochrome P450, family 27, subfamily a, polypeptide 1	Mus musculus	133-140
20371151-8	2010	The activation efficiencies of PMS by SO(4)(2-) and NO(3)(-) are negligible, whereas remarkable by HCO(3)(-), HPO(4)(2-), Cl(-) and CO(3)(2-).	7 alpha-hydroxy-4-cholesten-3-one	99-102	proline rich protein BstNI subfamily 1	Homo sapiens	31-34
20721884-3	2010	An intact interplay of hepatocellular and cholangiocellular adenosine triphosphate (ATP) secretion, ATP/P2Y- and bile salt/TGR5-mediated Cl(-)/ HCO(3)(-) exchange and HCO(3)(-) secretion, and alkaline phosphatase-mediated ATP breakdown may guarantee a stable biliary HCO(3)(-) umbrella under physiological conditions.	7 alpha-hydroxy-4-cholesten-3-one	144-147	G protein-coupled bile acid receptor 1	Homo sapiens	123-127
20566632-8	2010	In conclusion, the data suggest that slc4a10 expressed in mammalian cells encodes a Na(+)-dependent Cl(-)/HCO(3)(-) exchanger in which four specific charged amino acids seem necessary for ion transport.	7 alpha-hydroxy-4-cholesten-3-one	106-109	solute carrier family 4 member 10	Homo sapiens	37-44
20375274-10	2010	We conclude that Slc26a4 (pendrin) deletion impairs the secretion of bicarbonate in vivo and reduces apical Cl(-)/HCO(3)(-) exchanger activity in B-IC and non-A, non-B-IC cells in CCD.	7 alpha-hydroxy-4-cholesten-3-one	114-117	solute carrier family 26 member 4	Homo sapiens	17-24
20375274-10	2010	We conclude that Slc26a4 (pendrin) deletion impairs the secretion of bicarbonate in vivo and reduces apical Cl(-)/HCO(3)(-) exchanger activity in B-IC and non-A, non-B-IC cells in CCD.	7 alpha-hydroxy-4-cholesten-3-one	114-117	solute carrier family 26, member 4	Mus musculus	26-33
20375274-7	2010	The apical Cl(-)/HCO(3)(-) exchanger activity in B-IC and non-A, non-B-IC cells, as assessed by intracellular pH monitoring, was significantly reduced in pendrin-null mice.	7 alpha-hydroxy-4-cholesten-3-one	17-20	solute carrier family 26, member 4	Mus musculus	154-161
20406739-7	2010	Mouse embryo development from 2-cell to morula or blastocyst stage was significantly inhibited in the absence of HCO(3)(-) or when co-cultured with HCO(3)(-) secretion-deficient CFTR mutant cells as compared with the wild-type.	7 alpha-hydroxy-4-cholesten-3-one	148-151	cystic fibrosis transmembrane conductance regulator	Mus musculus	178-182
20147654-1	2010	The sodium-bicarbonate cotransporter NBCn1 (SLC4A7) is an acid-base transporter that normally moves Na(+) and HCO(3)(-) into the cell.	7 alpha-hydroxy-4-cholesten-3-one	110-113	solute carrier family 4 member 7	Rattus norvegicus	37-42
20147654-1	2010	The sodium-bicarbonate cotransporter NBCn1 (SLC4A7) is an acid-base transporter that normally moves Na(+) and HCO(3)(-) into the cell.	7 alpha-hydroxy-4-cholesten-3-one	110-113	solute carrier family 4 member 7	Rattus norvegicus	44-50
20110461-3	2010	However, additional evidence suggests that the AE2 Cl(-)/HCO(3)(-) exchanger, when coupled with the NHE1 Na(+)/H(+) exchanger or a Na(+)-HCO(3)(-) cotransporter (NBC), contributes to HCO(3)(-) and/or Cl(-) uptake.	7 alpha-hydroxy-4-cholesten-3-one	57-60	solute carrier family 4 (anion exchanger), member 2	Mus musculus	47-50
20150244-12	2010	Measurement of Cl(-)/HCO(3)(-) exchange in the presence of Gly-Sar revealed an increased rate of Cl(-)(OUT)/HCO(3)(-)(IN) exchange that was both Pat-1 dependent and CA dependent.	7 alpha-hydroxy-4-cholesten-3-one	21-24	solute carrier family 26, member 6	Mus musculus	145-150
20150244-12	2010	Measurement of Cl(-)/HCO(3)(-) exchange in the presence of Gly-Sar revealed an increased rate of Cl(-)(OUT)/HCO(3)(-)(IN) exchange that was both Pat-1 dependent and CA dependent.	7 alpha-hydroxy-4-cholesten-3-one	108-111	solute carrier family 26, member 6	Mus musculus	145-150
20150244-13	2010	In conclusion, Pat-1 Cl(-)/HCO(3)(-) exchange contributes to pH(i) regulation in the villous epithelium during H(+)-dipeptide absorption, possibly by providing a HCO(3)(-) import pathway.	7 alpha-hydroxy-4-cholesten-3-one	27-30	solute carrier family 26, member 6	Mus musculus	15-20
20150244-13	2010	In conclusion, Pat-1 Cl(-)/HCO(3)(-) exchange contributes to pH(i) regulation in the villous epithelium during H(+)-dipeptide absorption, possibly by providing a HCO(3)(-) import pathway.	7 alpha-hydroxy-4-cholesten-3-one	162-165	solute carrier family 26, member 6	Mus musculus	15-20
20110461-3	2010	However, additional evidence suggests that the AE2 Cl(-)/HCO(3)(-) exchanger, when coupled with the NHE1 Na(+)/H(+) exchanger or a Na(+)-HCO(3)(-) cotransporter (NBC), contributes to HCO(3)(-) and/or Cl(-) uptake.	7 alpha-hydroxy-4-cholesten-3-one	57-60	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	100-104
20062076-1	2010	Anion exchanger-1 (AE1), an erythroid-specific membrane protein, mediates the Cl(-)/HCO(-)(3) exchange across the plasma membrane and regulates intracellular pH.	7 alpha-hydroxy-4-cholesten-3-one	84-87	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	0-17
20062076-1	2010	Anion exchanger-1 (AE1), an erythroid-specific membrane protein, mediates the Cl(-)/HCO(-)(3) exchange across the plasma membrane and regulates intracellular pH.	7 alpha-hydroxy-4-cholesten-3-one	84-87	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	19-22
20093562-10	2010	In NAFLD patients with HOMA score <2.5, the postprandial increase in plasma FGF19 was accompanied by a lowering of plasma levels of 7alpha-hydroxy-4-cholesten-3-one (-30%, P = 0.015).	7 alpha-hydroxy-4-cholesten-3-one	135-167	fibroblast growth factor 19	Homo sapiens	79-84
20231443-10	2010	A second Cl(-) transporter, the Cl(-)/HCO(3)(-) exchanger SLC4A1, is expressed in the cilia and may support Cl(-) accumulation.	7 alpha-hydroxy-4-cholesten-3-one	38-41	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	58-64
19808031-8	2010	The mean plasma concentration of 7alpha-hydroxy-4-cholesten-3-one in untreated CTX-affected patients (n=6) was 107-fold that in unaffected subjects (n=9), with the lowest concentration in affected patients >10-fold the highest concentration in unaffected subjects.	7 alpha-hydroxy-4-cholesten-3-one	33-65	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	79-82
20041402-5	2010	Cl(-) withdrawal by isethionate-based perfusions showed that Ae2(a,b) (+/+) but not Ae2(a,b) (-/-) mouse cholangiocytes can display Cl(-)/HCO(3) (-) exchange, which is therefore entirely mediated by Ae2.	7 alpha-hydroxy-4-cholesten-3-one	138-141	solute carrier family 4 (anion exchanger), member 2	Mus musculus	61-64
20041402-10	2010	Whereas Ae2-mediated Cl(-)/HCO(3) (-) exchange in Ae2(a,b) (+/+) mouse cholangiocytes is stimulated by cyclic adenosine monophosphate (cAMP) and acetylcholine, the NBC activity is down-regulated by cAMP and adenosine triphosphate (ATP) in Ae2(a,b) (-/-) mouse cholangiocytes.	7 alpha-hydroxy-4-cholesten-3-one	27-30	solute carrier family 4 (anion exchanger), member 2	Mus musculus	8-11
20041402-10	2010	Whereas Ae2-mediated Cl(-)/HCO(3) (-) exchange in Ae2(a,b) (+/+) mouse cholangiocytes is stimulated by cyclic adenosine monophosphate (cAMP) and acetylcholine, the NBC activity is down-regulated by cAMP and adenosine triphosphate (ATP) in Ae2(a,b) (-/-) mouse cholangiocytes.	7 alpha-hydroxy-4-cholesten-3-one	27-30	solute carrier family 4 (anion exchanger), member 2	Mus musculus	50-53
19907019-3	2010	The mutant polypeptide exhibited, in parallel, strong GPA dependence of DIDS-sensitive (36)Cl(-) influx, trans-anion-dependent (36)Cl(-) efflux, and Cl(-)/HCO(3)(-) exchange activities at near wild-type levels.	7 alpha-hydroxy-4-cholesten-3-one	155-158	glycophorin A (MNS blood group)	Homo sapiens	54-57
20007010-3	2010	The down-regulation of KCC2 is expected to cause a reduction in Cl(-) extrusion capacity in dorsal horn neurons, which, together with the depolarizing efflux of HCO(3)(-) anions via GABA(A) channels, would result in a decrease in the efficacy of GABA(A)-mediated inhibition.	7 alpha-hydroxy-4-cholesten-3-one	161-164	solute carrier family 12 member 5	Homo sapiens	23-27
20041402-10	2010	Whereas Ae2-mediated Cl(-)/HCO(3) (-) exchange in Ae2(a,b) (+/+) mouse cholangiocytes is stimulated by cyclic adenosine monophosphate (cAMP) and acetylcholine, the NBC activity is down-regulated by cAMP and adenosine triphosphate (ATP) in Ae2(a,b) (-/-) mouse cholangiocytes.	7 alpha-hydroxy-4-cholesten-3-one	27-30	solute carrier family 4 (anion exchanger), member 2	Mus musculus	50-53
20041402-12	2010	CONCLUSION: Bicarbonate secretion in mouse cholangiocytes involves two differentially regulated activities: Ae2-mediated Cl(-)/HCO(3) (-) exchange and Na(+)-HCO(3) (-) cotransport.	7 alpha-hydroxy-4-cholesten-3-one	127-130	solute carrier family 4 (anion exchanger), member 2	Mus musculus	108-111
19940027-1	2010	Two members of the SLC26 gene family, SLC26A3 or DRA (downregulated in adenoma) and SLC26A6 (putative anion transporter 1, PAT1), are known to play a major role in apical Cl(-)/OH(-) (HCO(3)(-)) exchange process in the human intestine.	7 alpha-hydroxy-4-cholesten-3-one	184-187	solute carrier family 26 member 3	Homo sapiens	38-45
19940027-1	2010	Two members of the SLC26 gene family, SLC26A3 or DRA (downregulated in adenoma) and SLC26A6 (putative anion transporter 1, PAT1), are known to play a major role in apical Cl(-)/OH(-) (HCO(3)(-)) exchange process in the human intestine.	7 alpha-hydroxy-4-cholesten-3-one	184-187	solute carrier family 26 member 3	Homo sapiens	49-52
19940027-1	2010	Two members of the SLC26 gene family, SLC26A3 or DRA (downregulated in adenoma) and SLC26A6 (putative anion transporter 1, PAT1), are known to play a major role in apical Cl(-)/OH(-) (HCO(3)(-)) exchange process in the human intestine.	7 alpha-hydroxy-4-cholesten-3-one	184-187	solute carrier family 26 member 6	Homo sapiens	84-91
19940027-1	2010	Two members of the SLC26 gene family, SLC26A3 or DRA (downregulated in adenoma) and SLC26A6 (putative anion transporter 1, PAT1), are known to play a major role in apical Cl(-)/OH(-) (HCO(3)(-)) exchange process in the human intestine.	7 alpha-hydroxy-4-cholesten-3-one	184-187	solute carrier family 36 member 1	Homo sapiens	123-127
19808031-9	2010	CONCLUSION: Quantification of the bile acid precursor 7alpha-hydroxy-4-cholesten-3-one with LC-ESI-MS/MS is a novel approach to improved diagnostic testing of plasma for CTX, amenable to high-throughput analysis and automated sample handling.	7 alpha-hydroxy-4-cholesten-3-one	54-86	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	170-173
19641131-1	2009	Experiments were performed to test the hypothesis that three members of the SLC26 anion transporter gene family (SLC26a3, A4, and A6; hereafter termed za3, za4, and za6) mediate branchial Cl(-)/HCO(3)(-) exchange in adult zebrafish (Danio rerio).	7 alpha-hydroxy-4-cholesten-3-one	194-197	solute carrier family 26 member 3	Danio rerio	113-120
19823673-7	2009	A GFP-tagged form of the HCO(3)(-)/Cl(-) exchanger isoform Ae2 (Slc4a2) was strongly expressed at the GV oocyte plasma membrane, but membrane localization decreased markedly during meiotic progression.	7 alpha-hydroxy-4-cholesten-3-one	25-28	solute carrier family 4 (anion exchanger), member 2	Mus musculus	59-62
19823673-7	2009	A GFP-tagged form of the HCO(3)(-)/Cl(-) exchanger isoform Ae2 (Slc4a2) was strongly expressed at the GV oocyte plasma membrane, but membrane localization decreased markedly during meiotic progression.	7 alpha-hydroxy-4-cholesten-3-one	25-28	solute carrier family 4 (anion exchanger), member 2	Mus musculus	64-70
19643730-5	2009	When Slc26a9 and (R)CFTR fragments are co-expressed in Xenopus oocytes, both Slc26a9-mediated nCl(-)-HCO(3)(-) exchange and Cl(-) currents are almost fully inhibited.	7 alpha-hydroxy-4-cholesten-3-one	101-105	cystic fibrosis transmembrane conductance regulator L homeolog	Xenopus laevis	20-24
19643730-5	2009	When Slc26a9 and (R)CFTR fragments are co-expressed in Xenopus oocytes, both Slc26a9-mediated nCl(-)-HCO(3)(-) exchange and Cl(-) currents are almost fully inhibited.	7 alpha-hydroxy-4-cholesten-3-one	101-105	nucleolin S homeolog	Xenopus laevis	94-97
19330352-1	2009	PURPOSE: Anion exchanger 1 (AE1) is a transmembrane glycoprotein which is abundantly expressed in erythrocyte plasma membrane and mediates the electroneutral exchange of Cl(-) and HCO(3) (-).	7 alpha-hydroxy-4-cholesten-3-one	180-183	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	9-26
19645628-1	2009	CONTEXT: Enlargement of the vestibular aqueduct (EVA) is a commonly detected inner ear anomaly related to hearing loss and often associated with mutations of SLC26A4 encoding pendrin, a transmembrane exchanger of Cl(-), I(-), and HCO(3)(-).	7 alpha-hydroxy-4-cholesten-3-one	230-233	solute carrier family 26 member 4 gene 3 S homeolog	Xenopus laevis	158-165
19645628-1	2009	CONTEXT: Enlargement of the vestibular aqueduct (EVA) is a commonly detected inner ear anomaly related to hearing loss and often associated with mutations of SLC26A4 encoding pendrin, a transmembrane exchanger of Cl(-), I(-), and HCO(3)(-).	7 alpha-hydroxy-4-cholesten-3-one	230-233	solute carrier family 26 member 4 gene 3 S homeolog	Xenopus laevis	175-182
19645628-4	2009	We characterized the ability of p.V138L and p.P542R pendrin products to traffic to the plasma membrane in COS-7 cells and to transport Cl(-), I(-), and HCO(3)(-) in Xenopus oocytes.	7 alpha-hydroxy-4-cholesten-3-one	152-155	solute carrier family 26 member 4 gene 3 S homeolog	Xenopus laevis	52-59
19330352-1	2009	PURPOSE: Anion exchanger 1 (AE1) is a transmembrane glycoprotein which is abundantly expressed in erythrocyte plasma membrane and mediates the electroneutral exchange of Cl(-) and HCO(3) (-).	7 alpha-hydroxy-4-cholesten-3-one	180-183	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	28-31
21468181-1	2009	Pendrin (SLC26A4) is a Na(+)-independent Cl(-)/HCO(3) (-) exchanger which is expressed in the apical membranes of type B and non-A, non-B intercalated cells within the distal convoluted tubule, the connecting tubule, and the cortical collecting duct.	7 alpha-hydroxy-4-cholesten-3-one	47-50	solute carrier family 26 member 4	Homo sapiens	0-7
19522522-1	2009	Quantum yields, Phi, for the production of the formyl radical, HCO, in the photolysis of glyoxal were determined at 85 wavelengths, lambda, in the range of 290-420 nm at pressures between 50 and 550 Torr (N(2)) at 298 K using pulsed-laser photolysis combined with cavity ring-down spectroscopy detection of HCO.	7 alpha-hydroxy-4-cholesten-3-one	63-66	glucose-6-phosphate isomerase	Homo sapiens	16-19
19342507-5	2009	Intracellular pH recovery upon luminal Cl(-) restoration (nominal Cl(-)/HCO(3)(-) exchange) in cAMP-stimulated ducts was largely inhibited by luminal dihydro-DIDS (H(2)DIDS), accelerated by luminal CFTR inhibitor inh-172 (CFTRinh-172), and was insensitive to elevated bath K(+) concentration.	7 alpha-hydroxy-4-cholesten-3-one	72-75	ATP-binding cassette sub-family C member 7	Cavia porcellus	198-202
19342507-10	2009	Thus Cl(-)-dependent apical HCO(3)(-) secretion in pancreatic duct is mediated predominantly by an Slc26a6-like Cl(-)/HCO(3)(-) exchanger and is accelerated by inhibition of CFTR.	7 alpha-hydroxy-4-cholesten-3-one	28-32	solute carrier family 26 member 6	Cavia porcellus	99-106
19342507-10	2009	Thus Cl(-)-dependent apical HCO(3)(-) secretion in pancreatic duct is mediated predominantly by an Slc26a6-like Cl(-)/HCO(3)(-) exchanger and is accelerated by inhibition of CFTR.	7 alpha-hydroxy-4-cholesten-3-one	28-31	solute carrier family 26 member 6	Cavia porcellus	99-106
19321737-9	2009	We monitored the transport activity of SLC26A3 by reverse mode of Cl(-)/HCO(3)(-) and Cl(-)/NO(3)(-) exchange.	7 alpha-hydroxy-4-cholesten-3-one	72-75	solute carrier family 26 member 3	Homo sapiens	39-46
21468181-1	2009	Pendrin (SLC26A4) is a Na(+)-independent Cl(-)/HCO(3) (-) exchanger which is expressed in the apical membranes of type B and non-A, non-B intercalated cells within the distal convoluted tubule, the connecting tubule, and the cortical collecting duct.	7 alpha-hydroxy-4-cholesten-3-one	47-50	solute carrier family 26 member 4	Homo sapiens	9-16
19279262-3	2009	Yet evidence from others has suggested that CA4 acts in a complex with anion exchangers (AEs) to facilitate Cl(-)-HCO(3)(-) exchange in cotransfected cells.	7 alpha-hydroxy-4-cholesten-3-one	114-117	carbonic anhydrase 4	Mus musculus	44-47
19287372-2	2009	PDS is caused by mutations of the SLC26A4 gene encoding pendrin, a transmembrane exchanger of Cl(-), I(-) and HCO(3)(-), which is expressed in the thyroid and inner ear.	7 alpha-hydroxy-4-cholesten-3-one	110-113	solute carrier family 26 member 4	Homo sapiens	34-41
19287372-2	2009	PDS is caused by mutations of the SLC26A4 gene encoding pendrin, a transmembrane exchanger of Cl(-), I(-) and HCO(3)(-), which is expressed in the thyroid and inner ear.	7 alpha-hydroxy-4-cholesten-3-one	110-113	solute carrier family 26 member 4	Homo sapiens	56-63
19279262-12	2009	Our results indicate that CA4 and CA14 both play important roles in the regulation of intracellular pH in hippocampal neurons, by facilitating AE3-mediated Cl(-)-HCO(3)(-) exchange.	7 alpha-hydroxy-4-cholesten-3-one	162-165	carbonic anhydrase 4	Mus musculus	26-29
19279262-12	2009	Our results indicate that CA4 and CA14 both play important roles in the regulation of intracellular pH in hippocampal neurons, by facilitating AE3-mediated Cl(-)-HCO(3)(-) exchange.	7 alpha-hydroxy-4-cholesten-3-one	162-165	carbonic anhydrase 14	Mus musculus	34-38
19279262-12	2009	Our results indicate that CA4 and CA14 both play important roles in the regulation of intracellular pH in hippocampal neurons, by facilitating AE3-mediated Cl(-)-HCO(3)(-) exchange.	7 alpha-hydroxy-4-cholesten-3-one	162-165	solute carrier family 4 (anion exchanger), member 3	Mus musculus	143-146
19157624-1	2009	BACKGROUND/AIMS: Cl(-)/HCO(3)(-) anion exchanger 2 (AE2) is involved in intracellular pH (pH(i)) regulation and transepithelial acid-base transport, including secretin-stimulated biliary bicarbonate excretion.	7 alpha-hydroxy-4-cholesten-3-one	23-26	solute carrier family 4 (anion exchanger), member 2	Mus musculus	33-50
19121635-10	2009	Microfluorimetry of villi demonstrated that Dra is the dominant Cl(-)/HCO(3)(-) exchanger in the lower villous epithelium.	7 alpha-hydroxy-4-cholesten-3-one	70-73	solute carrier family 26, member 3	Mus musculus	44-47
19019741-1	2009	BACKGROUND: CFTR contributes to HCO(3)(-) transport in epithelial cells both directly (by HCO(3)(-) permeation through the channel) and indirectly (by regulating Cl(-)/HCO(3)(-) exchange proteins).	7 alpha-hydroxy-4-cholesten-3-one	32-35	CF transmembrane conductance regulator	Homo sapiens	12-16
19157624-1	2009	BACKGROUND/AIMS: Cl(-)/HCO(3)(-) anion exchanger 2 (AE2) is involved in intracellular pH (pH(i)) regulation and transepithelial acid-base transport, including secretin-stimulated biliary bicarbonate excretion.	7 alpha-hydroxy-4-cholesten-3-one	23-26	solute carrier family 4 (anion exchanger), member 2	Mus musculus	52-55
19164575-4	2009	Along with intracellular production of H(+) and HCO(3)(-) by carbonic anhydrase II, the H(+)-ATPases and ClC-7 exchangers seems prerequisite for bone resorption, because genetic disruption of either of these proteins leads to osteopetrosis.	7 alpha-hydroxy-4-cholesten-3-one	48-51	carbonic anhydrase 2	Mus musculus	61-82
19028925-8	2009	These results indicate that, in the experimental conditions used, pHi is regulated by the action of an Na(+)-driven HCO(3)(-)/Cl(-) exchanger and an Na(+)/HCO(3)(-) co-transporter and also by the action of the Na(+)/H(+) exchanger.	7 alpha-hydroxy-4-cholesten-3-one	116-119	glucose-6-phosphate isomerase	Homo sapiens	66-69
19028925-10	2009	Finally, pHi was shown to be sensitive to the removal of external Cl(-), but not of Na(+) or K(+), evidencing the presence of a membrane Cl(-)-dependent base extruder, namely the Na(+)-independent HCO(3)(-)/Cl(-) exchanger, and its role on pHi maintenance on these cells.	7 alpha-hydroxy-4-cholesten-3-one	197-201	glucose-6-phosphate isomerase	Homo sapiens	9-12
18655181-1	2008	SLC26A6 (putative anion transporter 1, PAT1) has been shown to play an important role in mediating the luminal Cl(-)/OH(-)(HCO(3)(-)) exchange process in the intestine.	7 alpha-hydroxy-4-cholesten-3-one	123-126	solute carrier family 26 member 6	Homo sapiens	0-7
20224218-2	2009	HCO(3)(-) transport across the apical membrane is thought to be mediated by both SLC26A6 Cl(-)-HCO(3)(-) exchange and CFTR HCO(3)(-) conductance.	7 alpha-hydroxy-4-cholesten-3-one	0-3	solute carrier family 26, member 6	Mus musculus	81-88
20224218-2	2009	HCO(3)(-) transport across the apical membrane is thought to be mediated by both SLC26A6 Cl(-)-HCO(3)(-) exchange and CFTR HCO(3)(-) conductance.	7 alpha-hydroxy-4-cholesten-3-one	0-3	cystic fibrosis transmembrane conductance regulator	Mus musculus	118-122
20224218-11	2009	This suggests that HCO(3)(-) conductance of CFTR mediates a significant portion of apical HCO(3)(-) secretion with high HCO(3)(-) in the lumen.	7 alpha-hydroxy-4-cholesten-3-one	19-22	cystic fibrosis transmembrane conductance regulator	Mus musculus	44-48
19004773-7	2008	Expression studies indicated that Slc26a9 can function as a chloride conductive pathway in oocytes as well as a Cl(-)/HCO(3)(-) exchanger in cultured cells, and localization studies in parietal cells detected its presence in tubulovesicles.	7 alpha-hydroxy-4-cholesten-3-one	118-121	solute carrier family 26, member 9	Mus musculus	34-41
19536486-3	2009	Because CO(2)/HCO(3) mediates depolarization in chemoreceptors, we hypothesized that sAC mRNA would be expressed in the CB, and its expression and function would be regulated by CO(2)/HCO(3).Sprague-Dawley rats at postnatal days 16-17 were used to compare sAC mRNA gene expression between CB and non-chemosensitive tissues: superior cervical (SCG), petrosal (PG) and nodose ganglia (NG) by quantitative real time-PCR.	7 alpha-hydroxy-4-cholesten-3-one	14-17	adenylate cyclase 10	Rattus norvegicus	85-88
19075558-1	2008	The 5beta-reductases (AKR1D1-3) are unique enzymes able to catalyze efficiently and in a stereospecific manner the 5beta-reduction of the C4-C5 double bond found in Delta4-3-ketosteroids, including steroid hormones and bile acids precursors such as 7alpha-hydroxy-4-cholesten-3-one and 7alpha,12alpha-dihydroxy-4-cholesten-3-one.	7 alpha-hydroxy-4-cholesten-3-one	249-281	aldo-keto reductase family 1 member D1	Homo sapiens	22-30
18655181-1	2008	SLC26A6 (putative anion transporter 1, PAT1) has been shown to play an important role in mediating the luminal Cl(-)/OH(-)(HCO(3)(-)) exchange process in the intestine.	7 alpha-hydroxy-4-cholesten-3-one	123-126	solute carrier family 36 member 1	Homo sapiens	39-43
18582481-2	2008	Plasma levels of 7alpha-hydroxy-4-cholesten-3-one have been reported to reflect bile acid synthesis and the expression or activity of the limiting enzyme of the main biosynthetic pathway, cholesterol 7alpha-hydroxylase.	7 alpha-hydroxy-4-cholesten-3-one	17-49	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	188-218
18660503-1	2008	In the medullary thick ascending limb, inhibiting the basolateral NHE1 Na(+)/H(+) exchanger with nerve growth factor (NGF) induces actin cytoskeleton remodeling that secondarily inhibits apical NHE3 and transepithelial HCO(3)(-) absorption.	7 alpha-hydroxy-4-cholesten-3-one	219-222	solute carrier family 9 member A1	Homo sapiens	66-70
18660503-1	2008	In the medullary thick ascending limb, inhibiting the basolateral NHE1 Na(+)/H(+) exchanger with nerve growth factor (NGF) induces actin cytoskeleton remodeling that secondarily inhibits apical NHE3 and transepithelial HCO(3)(-) absorption.	7 alpha-hydroxy-4-cholesten-3-one	219-222	nerve growth factor	Homo sapiens	97-116
18660503-1	2008	In the medullary thick ascending limb, inhibiting the basolateral NHE1 Na(+)/H(+) exchanger with nerve growth factor (NGF) induces actin cytoskeleton remodeling that secondarily inhibits apical NHE3 and transepithelial HCO(3)(-) absorption.	7 alpha-hydroxy-4-cholesten-3-one	219-222	nerve growth factor	Homo sapiens	118-121
18407247-9	2008	It is concluded that SHR PTE cells, which overexpress the Slc26a6 protein, are endowed with an enhanced activity of the Cl(-)/HCO(3)(-) exchanger.	7 alpha-hydroxy-4-cholesten-3-one	126-129	solute carrier family 26 member 6	Rattus norvegicus	58-65
18565999-5	2008	In the duct, Slc26a4 is expressed in the luminal membrane and mainly mediates I(-) secretion with minimal role in luminal HCO(3)(-) transport.	7 alpha-hydroxy-4-cholesten-3-one	122-125	solute carrier family 26, member 4	Mus musculus	13-20
18501404-7	2008	The competitive effects of these ions on As(V) removal were in the order of PO(4)(3-), SiO(3)(2-), HA, HCO(3)(-), and Cl(-).	7 alpha-hydroxy-4-cholesten-3-one	103-106	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	41-46
18391104-2	2008	The exposure of cells to Ang II increased Cl(-)/HCO(3)(-) exchanger activity with EC(50)s of 0.10 and 12.2 nmol/L in SHR and WKY PTE cells, respectively.	7 alpha-hydroxy-4-cholesten-3-one	48-51	angiotensinogen	Rattus norvegicus	25-31
18319254-7	2008	In agreement with others we found that NCBE mediates the 4,4"-diisothiocyanato-stilbene-2,2"-disulfonic acid-sensitive, Na(+)-dependent transport of HCO(3)(-).	7 alpha-hydroxy-4-cholesten-3-one	149-152	solute carrier family 4 member 10	Homo sapiens	39-43
18319254-10	2008	Moreover we found that that the (36)Cl efflux from NCBE-expressing oocytes, interpreted by others to be coupled to the influx of Na(+) and HCO(3)(-), actually represents a CO(2)/HCO(3)(-)-stimulated Cl(-) self-exchange not coupled to either Na(+) or net HCO(3)(-) transport.	7 alpha-hydroxy-4-cholesten-3-one	139-142	solute carrier family 4 member 10	Homo sapiens	51-55
17881426-11	2008	RESULTS: The father and all four children had RTA with blood HCO(-)(3) levels of 11-14 meq/l and urine pH of 5.3-5.4.	7 alpha-hydroxy-4-cholesten-3-one	61-64	RNA binding fox-1 homolog 2	Homo sapiens	46-49
17947343-5	2008	Endogenously, ZIP8 is a Mn(2+)/HCO(3)(-)symporter that may also contribute to Cd damage in the kidney.	7 alpha-hydroxy-4-cholesten-3-one	31-35	solute carrier family 39 (metal ion transporter), member 8	Mus musculus	14-18
17409310-7	2007	Thus, the slc4a1-/- mouse is the first genetic model of complete dRTA and demonstrates that the AE1/slc4a1 Cl(-)/HCO(3)(-) exchanger is required for maintenance of normal acid-base homeostasis by distal renal regeneration of bicarbonate in the mouse as well as in humans.	7 alpha-hydroxy-4-cholesten-3-one	113-116	solute carrier family 4 (anion exchanger), member 1	Mus musculus	10-16
17662298-7	2007	Arsenic adsorption in the filter from As-spiked tap water was relatively lower than that from artificial As solution because high HCO(-)(3) concentration restrained siderite dissolution and thus suppressed production of the fresh Fe oxides on the siderite grains.	7 alpha-hydroxy-4-cholesten-3-one	130-133	nuclear RNA export factor 1	Homo sapiens	48-51
17652430-3	2007	We examined in transfected HEK293 cells the functional and physical interactions between CAIX and the parietal cell Cl(-)/HCO(3)(-) exchanger AE2 or the putative Cl(-)/HCO(3)(-) exchanger SLC26A7.	7 alpha-hydroxy-4-cholesten-3-one	122-125	carbonic anhydrase 9	Homo sapiens	89-93
17455918-9	2007	We have also proposed that a new HCO formation pathway via QOOH isomerization to HOQO species and OH + CH3OCH2O2 --> HO2 + CH3OCH2O are to be considered, to account for the fast and slow HO2 formations, as well as the total yield.	7 alpha-hydroxy-4-cholesten-3-one	33-36	heme oxygenase 2	Homo sapiens	120-123
17455918-9	2007	We have also proposed that a new HCO formation pathway via QOOH isomerization to HOQO species and OH + CH3OCH2O2 --> HO2 + CH3OCH2O are to be considered, to account for the fast and slow HO2 formations, as well as the total yield.	7 alpha-hydroxy-4-cholesten-3-one	33-36	heme oxygenase 2	Homo sapiens	190-193
17455918-11	2007	It was revealed that the HO2 formation mechanism changes at 500 K, i.e., HCO + O2 via HCHO + OH and the above proposed direct HCO formation dominates over 500 K, while a series of reactions following CH3OCH2O2 self-reaction and OH + CH3OCH2O2 reaction mainly contribute below 500 K. The pressure dependent rate constant of the CH3OCH2 thermal decomposition reaction has been separately measured since it has large negative sensitivity for HO2 formation and is essential to eliminate the ambiguity in the CH3OCH2 + O2 mechanism at higher temperature.	7 alpha-hydroxy-4-cholesten-3-one	73-76	heme oxygenase 2	Homo sapiens	25-28
17455918-11	2007	It was revealed that the HO2 formation mechanism changes at 500 K, i.e., HCO + O2 via HCHO + OH and the above proposed direct HCO formation dominates over 500 K, while a series of reactions following CH3OCH2O2 self-reaction and OH + CH3OCH2O2 reaction mainly contribute below 500 K. The pressure dependent rate constant of the CH3OCH2 thermal decomposition reaction has been separately measured since it has large negative sensitivity for HO2 formation and is essential to eliminate the ambiguity in the CH3OCH2 + O2 mechanism at higher temperature.	7 alpha-hydroxy-4-cholesten-3-one	73-76	heme oxygenase 2	Homo sapiens	439-442
17455918-11	2007	It was revealed that the HO2 formation mechanism changes at 500 K, i.e., HCO + O2 via HCHO + OH and the above proposed direct HCO formation dominates over 500 K, while a series of reactions following CH3OCH2O2 self-reaction and OH + CH3OCH2O2 reaction mainly contribute below 500 K. The pressure dependent rate constant of the CH3OCH2 thermal decomposition reaction has been separately measured since it has large negative sensitivity for HO2 formation and is essential to eliminate the ambiguity in the CH3OCH2 + O2 mechanism at higher temperature.	7 alpha-hydroxy-4-cholesten-3-one	126-129	heme oxygenase 2	Homo sapiens	25-28
18165320-2	2008	Here we report that disrupting the Slc4a10 gene, which encodes the Na(+)-coupled Cl(-)-HCO(3)(-) exchanger Slc4a10 (NCBE), drastically reduces brain ventricle volume and protects against fatal epileptic seizures in mice.	7 alpha-hydroxy-4-cholesten-3-one	87-90	solute carrier family 4, sodium bicarbonate cotransporter-like, member 10	Mus musculus	35-42
18165320-2	2008	Here we report that disrupting the Slc4a10 gene, which encodes the Na(+)-coupled Cl(-)-HCO(3)(-) exchanger Slc4a10 (NCBE), drastically reduces brain ventricle volume and protects against fatal epileptic seizures in mice.	7 alpha-hydroxy-4-cholesten-3-one	87-90	solute carrier family 4, sodium bicarbonate cotransporter-like, member 10	Mus musculus	107-114
17577636-2	2008	CHAp nanospheres were successfully synthesized by mixing an acetone solution of Ca(NO(3))(2).4H(2)O with an aqueous solution of (NH(4))(2)HPO(4) and NH(4)HCO(3).	7 alpha-hydroxy-4-cholesten-3-one	154-157	transcription factor like 5	Homo sapiens	0-4
17890222-4	2007	Conversely, Cl(-)/HCO(3)(-) exchanger activity increased nearly 4-fold in Nhe1-deficient mice, despite only minimal or any change in mRNA and protein levels of the anion exchanger Ae2.	7 alpha-hydroxy-4-cholesten-3-one	18-21	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	74-78
17890222-5	2007	Acetazolamide completely blocked the increase in Cl(-)/HCO(3)(-) exchanger activity in Nhe1-null mice suggesting that increased anion exchange required carbonic anhydrase activity.	7 alpha-hydroxy-4-cholesten-3-one	55-58	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	87-91
17890222-7	2007	Moreover, the enhanced Cl(-)/HCO(3)(-) exchange activity was accompanied by an increased abundance of Car2.Ae2 complexes in the parotid plasma membranes of Nhe1(-/-) mice.	7 alpha-hydroxy-4-cholesten-3-one	29-33	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	156-160
17634418-1	2007	Secretin stimulates ductal secretion by activation of cAMP --> PKA --> CFTR --> Cl(-)/HCO(3)(-) exchanger in cholangiocytes.	7 alpha-hydroxy-4-cholesten-3-one	95-98	CF transmembrane conductance regulator	Rattus norvegicus	77-81
17570466-6	2007	In groundwaters of the Kalikratia area with higher Eh values (272-352 mV), pH 6.7-7.5 and 6-12 mM HCO(3) alkalinity, As(V) was the main species.	7 alpha-hydroxy-4-cholesten-3-one	98-101	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	117-122
17561450-7	2007	The similarity and very high correlation between the levels in the two vessels (r=0.97) are consistent with the contention that 7alpha-hydroxy-4-cholesten-3-one is a suitable marker for the activity of the hepatic cholesterol 7alpha-hydroxylase and thus bile acid synthesis.	7 alpha-hydroxy-4-cholesten-3-one	128-160	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	214-244
17409310-7	2007	Thus, the slc4a1-/- mouse is the first genetic model of complete dRTA and demonstrates that the AE1/slc4a1 Cl(-)/HCO(3)(-) exchanger is required for maintenance of normal acid-base homeostasis by distal renal regeneration of bicarbonate in the mouse as well as in humans.	7 alpha-hydroxy-4-cholesten-3-one	113-116	solute carrier family 4 (anion exchanger), member 1	Mus musculus	96-99
17409310-7	2007	Thus, the slc4a1-/- mouse is the first genetic model of complete dRTA and demonstrates that the AE1/slc4a1 Cl(-)/HCO(3)(-) exchanger is required for maintenance of normal acid-base homeostasis by distal renal regeneration of bicarbonate in the mouse as well as in humans.	7 alpha-hydroxy-4-cholesten-3-one	113-116	solute carrier family 4 (anion exchanger), member 1	Mus musculus	100-106
17476549-7	2007	The EPR results imply that the CHL probe in the HCO membrane has quite different behavior in comparison with that of PC (phosphatidylcholine) from egg.	7 alpha-hydroxy-4-cholesten-3-one	48-51	chordin like 1	Homo sapiens	31-34
17367404-4	2007	RESULTS: The rats treated with PTH developed hypercalcaemia and exhibited metabolic alkalosis (arterial HCO: 31.1 +/- 0.8 vs. 28.1 +/- 0.8 mmol L(-1) in controls, P < 0.05, n = 6), whereas the urine pH of 6.85 +/- 0.1 was significantly decreased compared with the pH of 7.38 +/- 0.1 in controls (P < 0.05, n = 12).	7 alpha-hydroxy-4-cholesten-3-one	104-107	parathyroid hormone	Rattus norvegicus	31-34
17005605-2	2007	In Xenopus oocytes, heterologous AE2-mediated Cl(-)/Cl(-) and Cl(-)/HCO(3)(-) exchange are inhibited by acid pH(i) or extracellular pH (pH(o)).	7 alpha-hydroxy-4-cholesten-3-one	68-71	solute carrier family 4 (anion exchanger), member 2	Mus musculus	33-36
17077386-1	2007	Pendrin (Slc26a4) localizes to type B and non-A, non-B intercalated cells in the distal convoluted tubule, the connecting tubule, and the cortical collecting duct (CCD), where it mediates apical Cl(-)/HCO(3)(-) exchange.	7 alpha-hydroxy-4-cholesten-3-one	201-204	solute carrier family 26, member 4	Mus musculus	0-7
17077386-1	2007	Pendrin (Slc26a4) localizes to type B and non-A, non-B intercalated cells in the distal convoluted tubule, the connecting tubule, and the cortical collecting duct (CCD), where it mediates apical Cl(-)/HCO(3)(-) exchange.	7 alpha-hydroxy-4-cholesten-3-one	201-204	solute carrier family 26, member 4	Mus musculus	9-16
17170027-5	2007	Under basal conditions, Cl(-)/HCO(3)(-) exchange activity was reduced by 65-80% in the PAT-1(-) duodenum, 30-40% in the DRA(-) duodenum, and <5% in the AE4(-) duodenum compared with the WT duodenum.	7 alpha-hydroxy-4-cholesten-3-one	30-33	solute carrier family 26, member 6	Mus musculus	87-92
17170027-9	2007	We conclude that 1) PAT-1 is the major contributor to basal Cl(-)/HCO(3)(-) and SO(4)(2-)/HCO(3)(-) exchange across the apical membrane and 2) PAT-1 plays a role in pH(i) regulation in the upper villous epithelium of the murine duodenum.	7 alpha-hydroxy-4-cholesten-3-one	66-69	solute carrier family 26, member 6	Mus musculus	20-25
17170027-9	2007	We conclude that 1) PAT-1 is the major contributor to basal Cl(-)/HCO(3)(-) and SO(4)(2-)/HCO(3)(-) exchange across the apical membrane and 2) PAT-1 plays a role in pH(i) regulation in the upper villous epithelium of the murine duodenum.	7 alpha-hydroxy-4-cholesten-3-one	90-93	solute carrier family 26, member 6	Mus musculus	20-25
17056673-1	2007	Anion exchanger 1 (AE1; SLC4A1), the plasma membrane Cl(-)/HCO(3)(-) exchanger of erythrocytes, is also expressed in heart.	7 alpha-hydroxy-4-cholesten-3-one	59-62	solute carrier family 4 (anion exchanger), member 1	Mus musculus	0-17
17056673-1	2007	Anion exchanger 1 (AE1; SLC4A1), the plasma membrane Cl(-)/HCO(3)(-) exchanger of erythrocytes, is also expressed in heart.	7 alpha-hydroxy-4-cholesten-3-one	59-62	solute carrier family 4 (anion exchanger), member 1	Mus musculus	19-22
17056673-1	2007	Anion exchanger 1 (AE1; SLC4A1), the plasma membrane Cl(-)/HCO(3)(-) exchanger of erythrocytes, is also expressed in heart.	7 alpha-hydroxy-4-cholesten-3-one	59-62	solute carrier family 4 (anion exchanger), member 1	Mus musculus	24-30
16986849-2	2006	The rate constants for the lower barrier reaction channels producing HOCl + HCO, H atom, OCH(2)OCl, cis-HC(O)OCl and trans-HC(O)OCl have been calculated by TST and multichannel RRKM theory.	7 alpha-hydroxy-4-cholesten-3-one	76-79	thiosulfate sulfurtransferase	Homo sapiens	156-159
17213682-1	2006	At least three kinds of Cl(-)/HCO(3)(-) exchangers, SLC26A3, SLC26A6 and AE2, have been demonstrated to be expressed in the intestinal epithelial cell.	7 alpha-hydroxy-4-cholesten-3-one	30-33	solute carrier family 26, member 3	Mus musculus	52-59
17213682-1	2006	At least three kinds of Cl(-)/HCO(3)(-) exchangers, SLC26A3, SLC26A6 and AE2, have been demonstrated to be expressed in the intestinal epithelial cell.	7 alpha-hydroxy-4-cholesten-3-one	30-33	solute carrier family 26, member 6	Mus musculus	61-68
17213682-1	2006	At least three kinds of Cl(-)/HCO(3)(-) exchangers, SLC26A3, SLC26A6 and AE2, have been demonstrated to be expressed in the intestinal epithelial cell.	7 alpha-hydroxy-4-cholesten-3-one	30-33	solute carrier family 4 (anion exchanger), member 2	Mus musculus	73-76
17982256-5	2007	Shrinkage-activation of JNK1/2 was attenuated by EIPA, augmented by hNHE1 expression, and abolished in the presence of HCO(3)(-).	7 alpha-hydroxy-4-cholesten-3-one	119-123	mitogen-activated protein kinase 8	Mus musculus	24-30
17053783-3	2006	The molecular identity of the Cl(-)/HCO(3)(-) exchangers and their relationship with CFTR in determining fluid and HCO(3)(-) secretion are not known.	7 alpha-hydroxy-4-cholesten-3-one	36-39	cystic fibrosis transmembrane conductance regulator	Mus musculus	85-89
17053783-3	2006	The molecular identity of the Cl(-)/HCO(3)(-) exchangers and their relationship with CFTR in determining fluid and HCO(3)(-) secretion are not known.	7 alpha-hydroxy-4-cholesten-3-one	115-118	cystic fibrosis transmembrane conductance regulator	Mus musculus	85-89
17053783-4	2006	We show here that the Cl(-)/HCO(3)(-) exchanger slc26a6 controls CFTR activity and ductal fluid and HCO(3)(-) secretion.	7 alpha-hydroxy-4-cholesten-3-one	28-31	solute carrier family 26, member 6	Mus musculus	48-55
17053783-4	2006	We show here that the Cl(-)/HCO(3)(-) exchanger slc26a6 controls CFTR activity and ductal fluid and HCO(3)(-) secretion.	7 alpha-hydroxy-4-cholesten-3-one	28-31	cystic fibrosis transmembrane conductance regulator	Mus musculus	65-69
16707554-2	2006	Mutations in the SLC4A4 gene cause an autosomal recessive proximal renal tubular acidosis (pRTA), a disease characterized by impaired ability of the proximal tubule to reabsorb HCO(3)(-) from the glomerular filtrate.	7 alpha-hydroxy-4-cholesten-3-one	177-180	solute carrier family 4 member 4	Homo sapiens	17-23
16883319-4	2006	Functional expression studies in Xenopus oocytes demonstrated that CFEX is capable of mediating not only Cl(-)-formate exchange but also Cl(-)-oxalate exchange, Cl(-)-OH(-) exchange, and Cl(-)-HCO(3)(-) exchange.	7 alpha-hydroxy-4-cholesten-3-one	193-196	solute carrier family 26, member 6	Mus musculus	67-71
16883392-2	2006	Formyl radicals (HCO) were produced from the reaction of atomic chlorine, generated by photolysis of Cl2 at 335 nm, with formaldehyde.	7 alpha-hydroxy-4-cholesten-3-one	17-20	endogenous retrovirus group W member 5	Homo sapiens	101-104
16735752-7	2006	In whole-cell experiments (V(m) = -60 mV), removing the unique amino terminus of NBCe1-A reduced the mean HCO(3)(-)-induced NBC current 55%, whereas removing the different amino terminus of NBCe1-C increased the mean NBC current 2.7-fold.	7 alpha-hydroxy-4-cholesten-3-one	106-109	solute carrier family 4 member 4 L homeolog	Xenopus laevis	81-86
16816370-1	2006	In parietal cells, basolateral Ae2 Cl(-)/HCO(3)(-) exchanger (Slc4a2) appears to compensate for luminal H(+) pumping while providing Cl(-) for apical secretion.	7 alpha-hydroxy-4-cholesten-3-one	41-44	solute carrier family 4 (anion exchanger), member 2	Mus musculus	31-34
16816370-1	2006	In parietal cells, basolateral Ae2 Cl(-)/HCO(3)(-) exchanger (Slc4a2) appears to compensate for luminal H(+) pumping while providing Cl(-) for apical secretion.	7 alpha-hydroxy-4-cholesten-3-one	41-44	solute carrier family 4 (anion exchanger), member 2	Mus musculus	62-68
16807546-1	2006	In the proximal tubule, angiotensin II (Ang-II) regulates HCO(-)(3) reabsorption and H+ secretion by binding the type 1 Ang-II (AT1) receptor, stimulating Na(+)/HCO(-)(3) cotransport and Na(+)/H(+) exchange.	7 alpha-hydroxy-4-cholesten-3-one	58-61	angiotensinogen	Rattus norvegicus	24-38
16807546-1	2006	In the proximal tubule, angiotensin II (Ang-II) regulates HCO(-)(3) reabsorption and H+ secretion by binding the type 1 Ang-II (AT1) receptor, stimulating Na(+)/HCO(-)(3) cotransport and Na(+)/H(+) exchange.	7 alpha-hydroxy-4-cholesten-3-one	58-61	angiotensinogen	Rattus norvegicus	40-46
16807546-1	2006	In the proximal tubule, angiotensin II (Ang-II) regulates HCO(-)(3) reabsorption and H+ secretion by binding the type 1 Ang-II (AT1) receptor, stimulating Na(+)/HCO(-)(3) cotransport and Na(+)/H(+) exchange.	7 alpha-hydroxy-4-cholesten-3-one	58-61	angiotensinogen	Rattus norvegicus	120-126
16807546-1	2006	In the proximal tubule, angiotensin II (Ang-II) regulates HCO(-)(3) reabsorption and H+ secretion by binding the type 1 Ang-II (AT1) receptor, stimulating Na(+)/HCO(-)(3) cotransport and Na(+)/H(+) exchange.	7 alpha-hydroxy-4-cholesten-3-one	58-61	angiotensin II receptor, type 1a	Rattus norvegicus	128-131
16352747-1	2006	SLC26A7 is a newly identified basolateral Cl(-)/HCO(3)(-) exchanger specific to alpha-intercalated cells of the outer medullary collecting duct (OMCD).	7 alpha-hydroxy-4-cholesten-3-one	48-51	solute carrier family 26 member 7	Rattus norvegicus	0-7
16458934-0	2006	Involvement of AE3 isoform of Na(+)-independent Cl(-)/HCO(3)(-) exchanger in myocardial pH(i) recovery from intracellular alkalization.	7 alpha-hydroxy-4-cholesten-3-one	54-57	solute carrier family 4 member 3	Rattus norvegicus	15-18
16722672-11	2006	The further reactions CH3O --> CH2O + H; CH2O + OH --> HCO + H2O; HCO + O2 --> HO2 + CO; and H + O2 + M --> HO2 + M complete the sequence.	7 alpha-hydroxy-4-cholesten-3-one	61-64	heme oxygenase 2	Homo sapiens	120-123
16544968-7	2006	The mean value of urine HCO at sea level was 1.67 +/- 0.25 mmol/L, increased significantly after 6 h at all altitudes, and then returned to near baseline after 24 h at three lower altitudes (1780, 2085, and 2455 m).	7 alpha-hydroxy-4-cholesten-3-one	24-27	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	31-34
16834172-5	2005	Since CH2O is a major product in both reactions, reliable rates for the reaction CH2O + O2 --> HCO + HO2 could be derived from [OH]t and [O]t experiments over the T-range 1587-2109 K. The combined linear least-squares fit result, k = 1.34 x 10(-8) exp(-26883 K/T) cm3 molecule(-1) s(-1), and a recent VTST calculation clearly overlap within the uncertainties in both studies.	7 alpha-hydroxy-4-cholesten-3-one	98-101	EBP cholestenol delta-isomerase	Homo sapiens	81-90
16914894-6	2006	These findings are in line with the observed increase in mRNA expression of the Na(+)/HCO(3) (-)-cotransporter SLC4A4b for the uptake and the Cl(-)/HCO(3) (-)-exchanger SLC26A6 for the secretion of HCO(3) (-).	7 alpha-hydroxy-4-cholesten-3-one	86-89	solute carrier family 26 member 6	Homo sapiens	169-176
16144965-1	2005	Slc26a4 (Pds) encodes pendrin, a Cl(-)/HCO(3)(-) exchanger expressed in the apical region of type B and non-A, non-B cells, which mediates secretion of OH(-) equivalents.	7 alpha-hydroxy-4-cholesten-3-one	39-42	solute carrier family 26, member 4	Mus musculus	0-7
16144965-1	2005	Slc26a4 (Pds) encodes pendrin, a Cl(-)/HCO(3)(-) exchanger expressed in the apical region of type B and non-A, non-B cells, which mediates secretion of OH(-) equivalents.	7 alpha-hydroxy-4-cholesten-3-one	39-42	solute carrier family 26, member 4	Mus musculus	22-29
16524946-1	2006	SLC26A7 is a Cl(-)/HCO(3)(-) exchanger that is expressed on the basolateral membrane and in the cytoplasm of two distinct acid-secreting epithelial cells: The A-intercalated cells in the kidney outer medullary collecting duct and the gastric parietal cells.	7 alpha-hydroxy-4-cholesten-3-one	19-22	solute carrier family 26 member 7	Homo sapiens	0-7
16204407-1	2006	Previous authors showed that, at low doses, both basolateral and luminal ANG II increase the proximal tubule"s HCO(3)(-) reabsorption rate (J(HCO(3))).	7 alpha-hydroxy-4-cholesten-3-one	111-114	angiogenin	Oryctolagus cuniculus	73-76
16392851-5	2006	Furthermore, the 193 nm photolysis of glyoxal, (CHO)2, has been proven to be an efficient HCO source.	7 alpha-hydroxy-4-cholesten-3-one	90-93	EBP cholestenol delta-isomerase	Homo sapiens	48-53
16392851-9	2006	H atoms are transformed via reaction 4, H+(CHO)2-->H2+HCO+CO, into additional HCO radicals.	7 alpha-hydroxy-4-cholesten-3-one	57-60	EBP cholestenol delta-isomerase	Homo sapiens	43-48
19565014-1	2005	Mutations of SLC4A1 (AE1) encoding the kidney anion (Cl(-)/HCO(3) (-)) exchanger 1 (kAE1 or band 3) can result in either autosomal dominant (AD) or autosomal recessive (AR) distal renal tubular acidosis (dRTA).	7 alpha-hydroxy-4-cholesten-3-one	59-62	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	13-19
19565014-1	2005	Mutations of SLC4A1 (AE1) encoding the kidney anion (Cl(-)/HCO(3) (-)) exchanger 1 (kAE1 or band 3) can result in either autosomal dominant (AD) or autosomal recessive (AR) distal renal tubular acidosis (dRTA).	7 alpha-hydroxy-4-cholesten-3-one	59-62	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	21-24
19565014-1	2005	Mutations of SLC4A1 (AE1) encoding the kidney anion (Cl(-)/HCO(3) (-)) exchanger 1 (kAE1 or band 3) can result in either autosomal dominant (AD) or autosomal recessive (AR) distal renal tubular acidosis (dRTA).	7 alpha-hydroxy-4-cholesten-3-one	59-62	O-sialoglycoprotein endopeptidase	Homo sapiens	84-88
15958523-9	2005	In cell-attached membrane patches, 25 or 50 mM HCO(3)(-) in the bath markedly increased the product of channel number and open probability of CFTR, and this activation was attenuated by 2-HE.	7 alpha-hydroxy-4-cholesten-3-one	47-50	CF transmembrane conductance regulator	Homo sapiens	142-146
16834172-5	2005	Since CH2O is a major product in both reactions, reliable rates for the reaction CH2O + O2 --> HCO + HO2 could be derived from [OH]t and [O]t experiments over the T-range 1587-2109 K. The combined linear least-squares fit result, k = 1.34 x 10(-8) exp(-26883 K/T) cm3 molecule(-1) s(-1), and a recent VTST calculation clearly overlap within the uncertainties in both studies.	7 alpha-hydroxy-4-cholesten-3-one	98-101	heme oxygenase 2	Homo sapiens	104-107
15548570-12	2005	Collectively, reduced basolateral HCO(3)(-) permeability, basolateral-to-apical fluxes, and net HCO(3)(-) flux as a result of reduced expression of NBC1 indicate that NBC1 plays a key role in transendothelial HCO(3)(-) flux and is functional only at the basolateral membrane.	7 alpha-hydroxy-4-cholesten-3-one	34-37	solute carrier family 4 member 4	Bos taurus	148-152
15539434-5	2005	Similarly, the ACh-induced increase in [Na(+)](c) was totally blocked by bumetanide in the absence of HCO(3)(-), but only by one-half in the presence of HCO(3)(-).	7 alpha-hydroxy-4-cholesten-3-one	102-105	acyl-CoA thioesterase 12	Rattus norvegicus	15-18
15539434-5	2005	Similarly, the ACh-induced increase in [Na(+)](c) was totally blocked by bumetanide in the absence of HCO(3)(-), but only by one-half in the presence of HCO(3)(-).	7 alpha-hydroxy-4-cholesten-3-one	153-156	acyl-CoA thioesterase 12	Rattus norvegicus	15-18
15548529-4	2005	Four human SLC26A6 polypeptide variants each exhibited rates of bidirectional [(14)C]oxalate flux, Cl(-)/HCO(3)(-) exchange, and Cl(-)/OH(-) exchange nearly equivalent to those of mouse slc26a6.	7 alpha-hydroxy-4-cholesten-3-one	105-108	solute carrier family 26 member 6	Homo sapiens	11-18
15790507-7	2005	Serum levels of TGF-beta from advanced TB patients have increased values if compared with Hco (p < 0.005) and Mild-Moderate patients (p < 0.05).	7 alpha-hydroxy-4-cholesten-3-one	90-93	transforming growth factor beta 1	Homo sapiens	16-24
15795435-5	2005	Because liver biopsies were not feasible, we measured plasma levels of 7alpha-hydroxy-4-cholesten-3-one, a marker for the activity of cholesterol 7alpha-hydroxylase in the liver.	7 alpha-hydroxy-4-cholesten-3-one	71-103	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	134-164
15010471-3	2004	Simultaneous measurements of membrane potential and pH(i) and/or current in CFTRexpressing Xenopus oocytes revealed dynamic control of CFTR Cl(-)/HCO(3)(-) permeability ratio, which is regulated by external Cl(-) (Cl(-)(o)).	7 alpha-hydroxy-4-cholesten-3-one	146-149	cystic fibrosis transmembrane conductance regulator L homeolog	Xenopus laevis	76-80
15591059-4	2005	SLC26A7 is a member of the SLC26 transporter family reported to be expressed in the basolateral membrane of the cortical collecting duct and parietal cells and functions as a coupled Cl(-)/HCO(3)(-) exchanger.	7 alpha-hydroxy-4-cholesten-3-one	189-193	solute carrier family 26 member 7	Homo sapiens	0-7
15591059-6	2005	We found that when expressed in Xenopus oocytes or HEK293 cells SLC26A7 functions as a pH(i)-regulated Cl(-) channel with minimal OH(-)/HCO(3)(-) permeability.	7 alpha-hydroxy-4-cholesten-3-one	136-139	solute carrier family 26 member 7	Homo sapiens	64-71
15653539-6	2005	Reduced yields of 8:0-16:0 and cis9-18:1 fatty acids accounted for 69 and 17%, respectively, of the decrease in milk fat yield with HC vs. LC (-90 g/d), and for 26 and 33%, respectively, of the decrease with HCO vs. LCO (-400 g/d).	7 alpha-hydroxy-4-cholesten-3-one	208-211	Weaning weight-maternal milk	Bos taurus	112-116
15308466-5	2004	Basal HCO(3)(-) secretion (5.6 +/- 0.03 microeq.h(-1).cm(-2)) was abolished by removal of either lumen Cl(-) or bath HCO(3)(-); this Cl(-)-dependent HCO(3)(-) secretion was also inhibited by 100 microM DIDS (0.5 +/- 0.03 microeq.h(-1).cm(-2)) but not by 5-nitro-3-(3-phenylpropyl-amino)benzoic acid (NPPB), a Cl(-) channel blocker.	7 alpha-hydroxy-4-cholesten-3-one	6-9	natriuretic peptide B	Rattus norvegicus	300-304
15308466-6	2004	8-Bromo-cAMP induced Cl(-)-independent HCO(3)(-) secretion (and also inhibited Cl(-)-dependent HCO(3)(-) secretion), which was inhibited by NPPB and by glibenclamide, a CFTR blocker, but not by DIDS.	7 alpha-hydroxy-4-cholesten-3-one	39-42	natriuretic peptide B	Rattus norvegicus	140-144
15308466-6	2004	8-Bromo-cAMP induced Cl(-)-independent HCO(3)(-) secretion (and also inhibited Cl(-)-dependent HCO(3)(-) secretion), which was inhibited by NPPB and by glibenclamide, a CFTR blocker, but not by DIDS.	7 alpha-hydroxy-4-cholesten-3-one	39-42	CF transmembrane conductance regulator	Rattus norvegicus	169-173
15123612-5	2004	The mutation of Trp-32 by phenylalanine totally eliminated the Trp-32 radical signal generated from W32F hSOD1 treated with HCO(3)(-) and H(2)O(2).	7 alpha-hydroxy-4-cholesten-3-one	124-127	thioredoxin like 1	Homo sapiens	16-22
15123612-5	2004	The mutation of Trp-32 by phenylalanine totally eliminated the Trp-32 radical signal generated from W32F hSOD1 treated with HCO(3)(-) and H(2)O(2).	7 alpha-hydroxy-4-cholesten-3-one	124-127	superoxide dismutase 1	Homo sapiens	105-110
15544920-1	2004	Previously, we showed that oxidation of tryptophan-32 (Trp-32) residue was crucial for H(2)O(2)/bicarbonate (HCO(3)(-))-dependent covalent aggregation of human Cu,Zn SOD1 (hSOD1).	7 alpha-hydroxy-4-cholesten-3-one	109-112	superoxide dismutase 1	Homo sapiens	166-170
15544920-1	2004	Previously, we showed that oxidation of tryptophan-32 (Trp-32) residue was crucial for H(2)O(2)/bicarbonate (HCO(3)(-))-dependent covalent aggregation of human Cu,Zn SOD1 (hSOD1).	7 alpha-hydroxy-4-cholesten-3-one	109-112	superoxide dismutase 1	Homo sapiens	172-177
15010471-12	2004	These results indicate that CFTR exists in two conformations, a Cl(-) only and a Cl(-) and OH(-)/HCO(3)(-) permeable state.	7 alpha-hydroxy-4-cholesten-3-one	97-100	cystic fibrosis transmembrane conductance regulator L homeolog	Xenopus laevis	28-32
14733916-1	2004	The purpose of this study was to determine expression and localization of NH(2)-terminal variants of the electrogenic Na(+)-HCO(3)(-) co-transporter NBC1 (SLC4A4) in the rat kidney and pancreas.	7 alpha-hydroxy-4-cholesten-3-one	124-127	solute carrier family 4 member 4	Rattus norvegicus	149-153
15084132-7	2004	Some of these derivatives were also tested for their inhibitory activity against the Cl(-)/HCO(3)(-) anion exchanger AE1: two derivatives showed inhibitory activity in the low micromolar range, whereas one compound was inactive at these concentrations.	7 alpha-hydroxy-4-cholesten-3-one	91-94	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	117-120
28786676-2	2004	It has been found that the eta1-HCO species attached to a Ru atom by a single Ru-C bond is unstable, and that it will convert to more strongly bound eta2- and eta3-HCO surface species.	7 alpha-hydroxy-4-cholesten-3-one	32-35	secreted phosphoprotein 1	Homo sapiens	27-31
28786676-2	2004	It has been found that the eta1-HCO species attached to a Ru atom by a single Ru-C bond is unstable, and that it will convert to more strongly bound eta2- and eta3-HCO surface species.	7 alpha-hydroxy-4-cholesten-3-one	32-35	DNA polymerase iota	Homo sapiens	149-153
14733916-1	2004	The purpose of this study was to determine expression and localization of NH(2)-terminal variants of the electrogenic Na(+)-HCO(3)(-) co-transporter NBC1 (SLC4A4) in the rat kidney and pancreas.	7 alpha-hydroxy-4-cholesten-3-one	124-127	solute carrier family 4 member 4	Rattus norvegicus	155-161
12519749-9	2003	CFTR phosphorylation was increased 23, 150, and 32% by 20 mM HSO(3)(-), 28.5 mM HCO(3)(-), and 28.5 mM HCO(3)(-) + 20 mM HSO(3)(-), respectively.	7 alpha-hydroxy-4-cholesten-3-one	80-83	CF transmembrane conductance regulator	Bos taurus	0-4
12759755-9	2004	SLC26 Cl(-)-HCO(3)(-) and Cl(-)-OH(-) exchange is activated by the cystic fibrosis transmembrane regulator (CFTR), implicating defective regulation of these exchangers in the reduced HCO(3)(-) transport seen in cystic fibrosis and related disorders; CFTR-independent activation of these exchangers is thus an important and novel goal for the future therapy of cystic fibrosis.	7 alpha-hydroxy-4-cholesten-3-one	12-15	cystic fibrosis transmembrane conductance regulator	Mus musculus	67-106
12759755-9	2004	SLC26 Cl(-)-HCO(3)(-) and Cl(-)-OH(-) exchange is activated by the cystic fibrosis transmembrane regulator (CFTR), implicating defective regulation of these exchangers in the reduced HCO(3)(-) transport seen in cystic fibrosis and related disorders; CFTR-independent activation of these exchangers is thus an important and novel goal for the future therapy of cystic fibrosis.	7 alpha-hydroxy-4-cholesten-3-one	12-15	cystic fibrosis transmembrane conductance regulator	Mus musculus	108-112
12759755-9	2004	SLC26 Cl(-)-HCO(3)(-) and Cl(-)-OH(-) exchange is activated by the cystic fibrosis transmembrane regulator (CFTR), implicating defective regulation of these exchangers in the reduced HCO(3)(-) transport seen in cystic fibrosis and related disorders; CFTR-independent activation of these exchangers is thus an important and novel goal for the future therapy of cystic fibrosis.	7 alpha-hydroxy-4-cholesten-3-one	183-186	cystic fibrosis transmembrane conductance regulator	Mus musculus	67-106
12759755-9	2004	SLC26 Cl(-)-HCO(3)(-) and Cl(-)-OH(-) exchange is activated by the cystic fibrosis transmembrane regulator (CFTR), implicating defective regulation of these exchangers in the reduced HCO(3)(-) transport seen in cystic fibrosis and related disorders; CFTR-independent activation of these exchangers is thus an important and novel goal for the future therapy of cystic fibrosis.	7 alpha-hydroxy-4-cholesten-3-one	183-186	cystic fibrosis transmembrane conductance regulator	Mus musculus	108-112
12951370-0	2003	Assay method for mitochondrial sterol 27-hydroxylase with 7alpha-hydroxy-4-cholesten-3-one as a substrate in the rat liver.	7 alpha-hydroxy-4-cholesten-3-one	58-90	cytochrome P450, family 27, subfamily a, polypeptide 1	Rattus norvegicus	31-52
14567693-12	2003	The tethering of CAII and CAIV close to the NBC1 HCO(3)(-) transport site maximizes the transmembrane HCO(3)(-) gradient local to NBC1 and thereby activates the transport rate.	7 alpha-hydroxy-4-cholesten-3-one	49-52	carbonic anhydrase 2	Homo sapiens	17-21
14567693-12	2003	The tethering of CAII and CAIV close to the NBC1 HCO(3)(-) transport site maximizes the transmembrane HCO(3)(-) gradient local to NBC1 and thereby activates the transport rate.	7 alpha-hydroxy-4-cholesten-3-one	49-52	carbonic anhydrase 4	Homo sapiens	26-30
14567693-12	2003	The tethering of CAII and CAIV close to the NBC1 HCO(3)(-) transport site maximizes the transmembrane HCO(3)(-) gradient local to NBC1 and thereby activates the transport rate.	7 alpha-hydroxy-4-cholesten-3-one	49-52	solute carrier family 4 member 4	Homo sapiens	44-48
14567693-12	2003	The tethering of CAII and CAIV close to the NBC1 HCO(3)(-) transport site maximizes the transmembrane HCO(3)(-) gradient local to NBC1 and thereby activates the transport rate.	7 alpha-hydroxy-4-cholesten-3-one	49-52	solute carrier family 4 member 4	Homo sapiens	130-134
14681840-10	2004	In conclusion, plasma 7alpha-hydroxy-4-cholesten-3-one concentrations reflected hepatic cholesterol 7alpha-hydroxylase activities when the sterol levels were adjusted to plasma cholesterol concentrations in rabbits with hypercholesterolemia.	7 alpha-hydroxy-4-cholesten-3-one	22-54	cytochrome P450 7A1	Oryctolagus cuniculus	88-118
14572579-9	2003	Serum C-reactive protein levels correlated positively with biliary levels of 7-alpha-hydroxycholesterol (R = 0.948), 7-beta-hydroxycholesterol (R = 0.976), cholestan-3-beta,5-alpha,6-beta-triol (R = 0.823), 7-alpha-hydroxy-4-cholesten-3-one (R = 0.846,) and 7-ketocholesterol (R = 0.973).	7 alpha-hydroxy-4-cholesten-3-one	207-240	C-reactive protein	Homo sapiens	6-24
12915121-9	2003	Translocation of Bax and cytochrome c was not suppressed by the omission of HCO(3)(-), suggesting HCO(3)(-) regulation at postmitochondrial levels.	7 alpha-hydroxy-4-cholesten-3-one	98-101	BCL2 associated X, apoptosis regulator	Homo sapiens	17-20
12736153-6	2003	Immunofluorescence labeling localized this exchanger exclusively to the basolateral membrane of gastric parietal cells, and functional studies in oocytes indicated that SLC26A7 is a DIDS-sensitive Cl(-)/HCO(3)(-) exchanger that is active in both acidic and alkaline pH(i).	7 alpha-hydroxy-4-cholesten-3-one	203-206	solute carrier family 26, member 7	Mus musculus	169-176
12736153-7	2003	On the basis of its unique expression pattern and function, we propose that SLC26A7 is a basolateral Cl(-)/HCO(3)(-) exchanger in gastric parietal cells and plays a major role in gastric acid secretion.	7 alpha-hydroxy-4-cholesten-3-one	107-110	solute carrier family 26, member 7	Mus musculus	76-83
12519749-9	2003	CFTR phosphorylation was increased 23, 150, and 32% by 20 mM HSO(3)(-), 28.5 mM HCO(3)(-), and 28.5 mM HCO(3)(-) + 20 mM HSO(3)(-), respectively.	7 alpha-hydroxy-4-cholesten-3-one	103-106	CF transmembrane conductance regulator	Bos taurus	0-4
12670492-4	2003	Inhibition experiments indicated that tolterodine and 7 alpha-hydroxy-4-cholesten-3-one were selective inhibitors of the CYP2D25- and CYP27A-mediated 25-hydroxylation of vitamin D(3), respectively.	7 alpha-hydroxy-4-cholesten-3-one	54-87	cytochrome P450 family 2 subfamily D member 6	Sus scrofa	121-128
12409301-9	2003	Notably, adenoviral transfection of wild-type CFTR in CFPAC-1 cells completely restored the stimulatory effect of ATP on luminal Cl(-)/HCO(3)(-) exchange.	7 alpha-hydroxy-4-cholesten-3-one	135-138	CF transmembrane conductance regulator	Homo sapiens	46-50
12493726-7	2003	The results indicate that the basolaterally located NHE1, NHE2, and NHE4, in addition to participating in the homeostatic control of intracellular pH, may play a role in H(+) extrusion in order to achieve transepithelial HCO(3)(-) secretion.	7 alpha-hydroxy-4-cholesten-3-one	221-224	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	52-56
12388388-1	2003	Pendrin is an apical Cl(-)/OH(-)/HCO(3)(-) exchanger in beta-intercalated cells (beta-ICs) of rat and mouse cortical collecting duct (CCD).	7 alpha-hydroxy-4-cholesten-3-one	33-36	solute carrier family 26 member 4	Rattus norvegicus	0-7
12388388-12	2003	We conclude that metabolic acidosis decreases the activity of the apical Cl(-)/HCO(3)(-) exchanger in beta-ICs of the rat CCD by reducing the expression of pendrin.	7 alpha-hydroxy-4-cholesten-3-one	79-82	solute carrier family 26 member 4	Rattus norvegicus	156-163
12493726-7	2003	The results indicate that the basolaterally located NHE1, NHE2, and NHE4, in addition to participating in the homeostatic control of intracellular pH, may play a role in H(+) extrusion in order to achieve transepithelial HCO(3)(-) secretion.	7 alpha-hydroxy-4-cholesten-3-one	221-224	solute carrier family 9 (sodium/hydrogen exchanger), member 2	Mus musculus	58-62
12493726-7	2003	The results indicate that the basolaterally located NHE1, NHE2, and NHE4, in addition to participating in the homeostatic control of intracellular pH, may play a role in H(+) extrusion in order to achieve transepithelial HCO(3)(-) secretion.	7 alpha-hydroxy-4-cholesten-3-one	221-224	solute carrier family 9 (sodium/hydrogen exchanger), member 4	Mus musculus	68-72
12217875-6	2002	Measurement of intracellular pH during the removal of extracellular Cl(-) in the presence and absence of HCO indicates that Slc26a6 functions as both a Cl(-)/HCO and a Cl(-)/OH(-) exchanger; simultaneous membrane hyperpolarization during these experimental maneuvers reveals that HCO and OH(-) transport mediated by Slc26a6 is electrogenic.	7 alpha-hydroxy-4-cholesten-3-one	105-108	solute carrier family 26, member 6	Mus musculus	124-131
12403779-7	2002	In this work, we report that transient or stable expression of human NBC3 (hNBC3) in HEK cells resulted in a Na(+)-dependent, DIDS (4,4"-diisothiocyanostilbene-2,2"-disulfonic acid)- and 5-ethylisopropylamiloride-insensitive HCO(3)(-) transport.	7 alpha-hydroxy-4-cholesten-3-one	225-228	solute carrier family 4 member 8	Homo sapiens	69-73
12403779-7	2002	In this work, we report that transient or stable expression of human NBC3 (hNBC3) in HEK cells resulted in a Na(+)-dependent, DIDS (4,4"-diisothiocyanostilbene-2,2"-disulfonic acid)- and 5-ethylisopropylamiloride-insensitive HCO(3)(-) transport.	7 alpha-hydroxy-4-cholesten-3-one	225-228	solute carrier family 4 member 8	Homo sapiens	75-80
12482890-8	2002	Taken together, the results indicate that the effects of modulating PKA activity on steady-state pH(i) in rat CA1 neurons under HCO(3)(-)/CO(2)-buffered conditions reflect not only changes in Na(+)-H(+) exchange activity but also changes in Na(+)-dependent and Na(+)-independent Cl(-)-HCO(3)(-) exchange activity that, in turn, may be dependent upon the initial pH(i).	7 alpha-hydroxy-4-cholesten-3-one	128-131	carbonic anhydrase 1	Rattus norvegicus	110-113
12411484-1	2002	Aberrant HCO(3)(-) transport is a hallmark of cystic fibrosis (CF) and is associated with aberrant Cl(-)-dependent HCO(3)(-) transport by the cystic fibrosis transmembrane conductance regulator (CFTR).	7 alpha-hydroxy-4-cholesten-3-one	9-12	cystic fibrosis transmembrane conductance regulator	Mus musculus	142-193
12411484-1	2002	Aberrant HCO(3)(-) transport is a hallmark of cystic fibrosis (CF) and is associated with aberrant Cl(-)-dependent HCO(3)(-) transport by the cystic fibrosis transmembrane conductance regulator (CFTR).	7 alpha-hydroxy-4-cholesten-3-one	9-12	cystic fibrosis transmembrane conductance regulator	Mus musculus	195-199
12411484-1	2002	Aberrant HCO(3)(-) transport is a hallmark of cystic fibrosis (CF) and is associated with aberrant Cl(-)-dependent HCO(3)(-) transport by the cystic fibrosis transmembrane conductance regulator (CFTR).	7 alpha-hydroxy-4-cholesten-3-one	115-118	cystic fibrosis transmembrane conductance regulator	Mus musculus	142-193
12411484-5	2002	DRA activity occurred at a Cl(-)/HCO(3)(-) ratio > or =2.	7 alpha-hydroxy-4-cholesten-3-one	33-36	solute carrier family 26, member 3	Mus musculus	0-3
12411484-8	2002	These findings provide a molecular mechanism for epithelial HCO(3)(-) transport (one SLC26 transporter-electrogenic transport; two SLC26 transporters with opposite stoichiometry in the same membrane domain-electroneutral transport), the CF-associated aberrant HCO(3)(-) transport, and reveal a new function of CFTR with clinical implications for CF and congenital chloride diarrhea.	7 alpha-hydroxy-4-cholesten-3-one	60-63	cystic fibrosis transmembrane conductance regulator	Mus musculus	310-314
12217856-1	2002	Our laboratory has previously shown that mice lacking neuronal nitric oxide synthase (nNOS) are defective in fluid absorption (J(v)) and HCO absorption (J(HCO3)) in the proximal tubule and develop metabolic acidosis.	7 alpha-hydroxy-4-cholesten-3-one	137-140	nitric oxide synthase 1, neuronal	Mus musculus	54-84
12217856-1	2002	Our laboratory has previously shown that mice lacking neuronal nitric oxide synthase (nNOS) are defective in fluid absorption (J(v)) and HCO absorption (J(HCO3)) in the proximal tubule and develop metabolic acidosis.	7 alpha-hydroxy-4-cholesten-3-one	137-140	nitric oxide synthase 1, neuronal	Mus musculus	86-90
12217856-11	2002	These results indicated that iNOS upregulates Na(+) and HCO transport, whereas eNOS does not directly modulate Na(+) and HCO transport in the kidney proximal tubules.	7 alpha-hydroxy-4-cholesten-3-one	56-59	nitric oxide synthase 2, inducible	Mus musculus	29-33
12217875-6	2002	Measurement of intracellular pH during the removal of extracellular Cl(-) in the presence and absence of HCO indicates that Slc26a6 functions as both a Cl(-)/HCO and a Cl(-)/OH(-) exchanger; simultaneous membrane hyperpolarization during these experimental maneuvers reveals that HCO and OH(-) transport mediated by Slc26a6 is electrogenic.	7 alpha-hydroxy-4-cholesten-3-one	158-161	solute carrier family 26, member 6	Mus musculus	124-131
12217866-9	2002	Furthermore, the presence of pendrin in both the apical plasma membrane and the apical intracellular vesicles of type B and non-A-non-B intercalated cells suggests that HCO secretion may be regulated by trafficking of pendrin between the two membrane compartments.	7 alpha-hydroxy-4-cholesten-3-one	169-172	solute carrier family 26, member 4	Mus musculus	29-36
12217866-9	2002	Furthermore, the presence of pendrin in both the apical plasma membrane and the apical intracellular vesicles of type B and non-A-non-B intercalated cells suggests that HCO secretion may be regulated by trafficking of pendrin between the two membrane compartments.	7 alpha-hydroxy-4-cholesten-3-one	169-172	solute carrier family 26, member 4	Mus musculus	218-225
12217875-6	2002	Measurement of intracellular pH during the removal of extracellular Cl(-) in the presence and absence of HCO indicates that Slc26a6 functions as both a Cl(-)/HCO and a Cl(-)/OH(-) exchanger; simultaneous membrane hyperpolarization during these experimental maneuvers reveals that HCO and OH(-) transport mediated by Slc26a6 is electrogenic.	7 alpha-hydroxy-4-cholesten-3-one	158-161	solute carrier family 26, member 6	Mus musculus	124-131
11997322-5	2002	The selective MAP kinase kinase (MEK1/2) inhibitors U0126 and PD-98059 abolished the NGF-induced ERK activation and largely eliminated (> or = 60%) the effects of NGF to inhibit basolateral Na(+)/H(+) exchange activity and transepithelial HCO absorption in perfused MTALs.	7 alpha-hydroxy-4-cholesten-3-one	242-245	mitogen activated protein kinase kinase 1	Rattus norvegicus	33-39
12225984-0	2002	AE4 is a DIDS-sensitive Cl(-)/HCO(-)(3) exchanger in the basolateral membrane of the renal CCD and the SMG duct.	7 alpha-hydroxy-4-cholesten-3-one	30-33	solute carrier family 4 member 9	Rattus norvegicus	0-3
12225984-11	2002	Measurement of intracellular pH (pH(i)) revealed that AE4 indeed functions as a Cl(-)/HCO(-)(3) exchanger.	7 alpha-hydroxy-4-cholesten-3-one	86-89	solute carrier family 4 member 9	Rattus norvegicus	54-57
12225984-19	2002	In the rat and mouse AE4 functions as a Cl(-)/HCO(-)(3) exchanger in the basolateral membrane of alpha-intercalated cells and may participate in HCO(-)(3) absorption.	7 alpha-hydroxy-4-cholesten-3-one	46-49	solute carrier family 4, sodium bicarbonate cotransporter, member 9	Mus musculus	21-24
12225984-20	2002	In the rabbit AE4 may contribute to HCO(-)(3) secretion.	7 alpha-hydroxy-4-cholesten-3-one	36-39	anion exchange protein 4	Oryctolagus cuniculus	14-17
12121896-7	2002	The presence of NBCn1 at the basolateral membrane of human striated duct cells suggests that it may contribute to ductal HCO secretion.	7 alpha-hydroxy-4-cholesten-3-one	121-124	solute carrier family 4 member 7	Homo sapiens	16-21
12121896-8	2002	In contrast, the expression of NBC3 at the apical membranes of acinar and duct cells in both human and rat salivary glands indicates a possible role of this isoform in HCO salvage under resting conditions.	7 alpha-hydroxy-4-cholesten-3-one	168-171	solute carrier family 4 member 7	Homo sapiens	31-35
12107849-1	2002	Cells within the acidic extracellular environment of solid tumours maintain their intracellular pH (pHi) through the activity of membrane-based ion exchange mechanisms including the Na(+)/H(+) antiport and the Na(+)-dependent Cl(-)/HCO(3)(-) exchanger.	7 alpha-hydroxy-4-cholesten-3-one	232-235	glucose-6-phosphate isomerase 1	Mus musculus	100-103
12225967-8	2002	These results demonstrate that vas deferens epithelial cells possess the proteins necessary for the vectoral transport of HCO and that these mechanisms are maintained in primary culture.	7 alpha-hydroxy-4-cholesten-3-one	122-125	arginine vasopressin	Rattus norvegicus	31-34
11880256-14	2002	In summary, we conclude that CFTR is present in the apical membrane of bovine corneal endothelium and could contribute to transendothelial Cl(-) and HCO transport.	7 alpha-hydroxy-4-cholesten-3-one	149-152	CF transmembrane conductance regulator	Bos taurus	29-33
11698263-1	2001	The Na(+)/H(+) exchangers NHE2 and NHE3 are involved in epithelial Na(+) and HCO absorption.	7 alpha-hydroxy-4-cholesten-3-one	77-80	solute carrier family 9 member A2	Homo sapiens	26-30
11762832-13	2002	By decreasing the amount of HCO-60 and citric acid, the PA of G-CSF decreased.	7 alpha-hydroxy-4-cholesten-3-one	28-32	colony stimulating factor 3	Canis lupus familiaris	62-67
11880289-10	2002	In aggregate, these findings indicate the presence of cAMP-activated Cl(-) and HCO(-)(3) secretion across rat FDLE cells mediated via CFTR.	7 alpha-hydroxy-4-cholesten-3-one	79-82	CF transmembrane conductance regulator	Rattus norvegicus	134-138
11788449-14	2002	Consistent with the increase in NBCn1, measurements of pH transients in medullary thick ascending limb (mTAL) cells in kidney slices revealed two- to threefold increases in DIDS- sensitive, Na(+)-dependent HCO uptake in rats with CMA.	7 alpha-hydroxy-4-cholesten-3-one	206-209	solute carrier family 4 member 7	Rattus norvegicus	32-37
11788449-14	2002	Consistent with the increase in NBCn1, measurements of pH transients in medullary thick ascending limb (mTAL) cells in kidney slices revealed two- to threefold increases in DIDS- sensitive, Na(+)-dependent HCO uptake in rats with CMA.	7 alpha-hydroxy-4-cholesten-3-one	206-209	talipes	Mus musculus	104-108
11788449-16	2002	The increased abundance of NBCn1 may play a role in the reabsorption of NH in the mTAL and increased NBC3 in reabsorbing HCO.	7 alpha-hydroxy-4-cholesten-3-one	121-124	solute carrier family 4 member 7	Rattus norvegicus	27-32
11788449-16	2002	The increased abundance of NBCn1 may play a role in the reabsorption of NH in the mTAL and increased NBC3 in reabsorbing HCO.	7 alpha-hydroxy-4-cholesten-3-one	121-124	solute carrier family 4 member 7	Rattus norvegicus	101-105
11772400-1	2002	Kanadaptin (kidney anion exchanger adaptor protein) has recently been identified as a protein with binding activity to the cytoplasmic domain of the kidney Na(+)-independent Cl(-)/HCO(-)(3) anion exchanger 1 (kAE1).	7 alpha-hydroxy-4-cholesten-3-one	180-183	solute carrier family 4 member 1 adaptor protein	Rattus norvegicus	0-10
11772400-1	2002	Kanadaptin (kidney anion exchanger adaptor protein) has recently been identified as a protein with binding activity to the cytoplasmic domain of the kidney Na(+)-independent Cl(-)/HCO(-)(3) anion exchanger 1 (kAE1).	7 alpha-hydroxy-4-cholesten-3-one	180-183	solute carrier family 4 member 1 adaptor protein	Rattus norvegicus	12-50
11698238-2	2001	We showed previously that nerve growth factor (NGF) inhibits HCO absorption in the rat medullary thick ascending limb (MTAL) via an extracellular signal-regulated kinase (ERK)-dependent pathway.	7 alpha-hydroxy-4-cholesten-3-one	61-64	Eph receptor B1	Rattus norvegicus	171-174
11698238-0	2001	Neurotrophin-3 inhibits HCO absorption via a cAMP-dependent pathway in renal thick ascending limb.	7 alpha-hydroxy-4-cholesten-3-one	24-27	neurotrophin 3	Rattus norvegicus	0-14
11698263-1	2001	The Na(+)/H(+) exchangers NHE2 and NHE3 are involved in epithelial Na(+) and HCO absorption.	7 alpha-hydroxy-4-cholesten-3-one	77-80	solute carrier family 9 member A3	Homo sapiens	35-39
11698238-5	2001	In contrast, neurotrophin-3 (NT-3, 0.7 nM) inhibited HCO absorption by 40% (half-maximal inhibition at approximately 0.4 nM).	7 alpha-hydroxy-4-cholesten-3-one	53-56	neurotrophin 3	Rattus norvegicus	13-27
11698238-5	2001	In contrast, neurotrophin-3 (NT-3, 0.7 nM) inhibited HCO absorption by 40% (half-maximal inhibition at approximately 0.4 nM).	7 alpha-hydroxy-4-cholesten-3-one	53-56	neurotrophin 3	Rattus norvegicus	29-33
11698238-2	2001	We showed previously that nerve growth factor (NGF) inhibits HCO absorption in the rat medullary thick ascending limb (MTAL) via an extracellular signal-regulated kinase (ERK)-dependent pathway.	7 alpha-hydroxy-4-cholesten-3-one	61-64	nerve growth factor	Rattus norvegicus	26-45
11705743-5	2001	These in vivo phenotypic correlates of the absorptive defect suggest that the NaCl, HCO, and fluid absorption that is dependent on apical Na(+)/H(+) exchange is due overwhelmingly to the activity of NHE3, with little contribution from NHE2.	7 alpha-hydroxy-4-cholesten-3-one	84-87	solute carrier family 9 (sodium/hydrogen exchanger), member 3	Mus musculus	199-203
11698238-2	2001	We showed previously that nerve growth factor (NGF) inhibits HCO absorption in the rat medullary thick ascending limb (MTAL) via an extracellular signal-regulated kinase (ERK)-dependent pathway.	7 alpha-hydroxy-4-cholesten-3-one	61-64	nerve growth factor	Rattus norvegicus	47-50
11698238-11	2001	These results demonstrate that NT-3 inhibits HCO absorption via a cAMP- and PKA-dependent pathway.	7 alpha-hydroxy-4-cholesten-3-one	45-48	neurotrophin 3	Rattus norvegicus	31-35
11698238-11	2001	These results demonstrate that NT-3 inhibits HCO absorption via a cAMP- and PKA-dependent pathway.	7 alpha-hydroxy-4-cholesten-3-one	45-48	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	76-79
11443061-7	2001	Ion substitution and drug treatment protocols suggested that HCO secretion compensated for reduced Cl(-) secretion in NKCC1-/- airway epithelia.	7 alpha-hydroxy-4-cholesten-3-one	61-64	solute carrier family 12, member 2	Mus musculus	118-123
11502558-7	2001	To further investigate the origin of this increased intracellular acidification observed in CFTR-transfected cells, the activity of the DIDS-inhibitable Cl(-)/HCO exchanger was studied.	7 alpha-hydroxy-4-cholesten-3-one	159-162	cystic fibrosis transmembrane conductance regulator	Cricetulus griseus	92-96
11668039-4	2001	Cl(-)/HCO exchange activity, assayed with the pH-sensitive dye 2",7"-bis(2-carboxyethyl)-5(6)-carboxyfluorescein in cells grown on coverslips, increased about twofold in cells transfected with functional CFTR.	7 alpha-hydroxy-4-cholesten-3-one	6-9	CF transmembrane conductance regulator	Homo sapiens	204-208
11668039-10	2001	We propose that the pancreatic HCO secretion defect in CF patients is partly due to the downregulation of apical Cl(-)/HCO exchange activity mediated by DRA (and possibly PAT1).	7 alpha-hydroxy-4-cholesten-3-one	31-34	solute carrier family 26 member 3	Homo sapiens	153-156
11668039-10	2001	We propose that the pancreatic HCO secretion defect in CF patients is partly due to the downregulation of apical Cl(-)/HCO exchange activity mediated by DRA (and possibly PAT1).	7 alpha-hydroxy-4-cholesten-3-one	31-34	solute carrier family 36 member 1	Homo sapiens	171-175
11443048-4	2001	This higher excitability is partly based on an upregulation of the Na(+) current density (608.2 +/- 123.2 pA/pF in NHE1 mutant vs. 334.7 +/- 63.7 pA/pF in wild type in HCO/CO(2)).	7 alpha-hydroxy-4-cholesten-3-one	168-171	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	115-119
11457720-4	2001	Although Na(+)-H(+) exchanger isoform NHE3 accounts for the largest component of H(+) secretion in the proximal tubule, 40-50% of the rates of HCO absorption or cellular H(+) extrusion persist in NHE3 null mice.	7 alpha-hydroxy-4-cholesten-3-one	143-146	solute carrier family 9 (sodium/hydrogen exchanger), member 3	Mus musculus	38-42
11875259-3	2001	Cystic fibrosis transmembrane conductance regulator (CFTR) is highly expressed in the pancreatic ductal epithelium and plays a key role in ductal HCO(3)(-) secretion.	7 alpha-hydroxy-4-cholesten-3-one	146-150	CF transmembrane conductance regulator	Homo sapiens	0-51
11408268-3	2001	We postulated that one or more isoforms of the Na(+)/H(+) exchanger (NHE) family is located on the apical surface of human duodenal mucosal epithelial cells and thereby contributes to duodenal mucosal HCO transport.	7 alpha-hydroxy-4-cholesten-3-one	201-204	solute carrier family 9 member C1	Homo sapiens	47-67
11408268-3	2001	We postulated that one or more isoforms of the Na(+)/H(+) exchanger (NHE) family is located on the apical surface of human duodenal mucosal epithelial cells and thereby contributes to duodenal mucosal HCO transport.	7 alpha-hydroxy-4-cholesten-3-one	201-204	solute carrier family 9 member C1	Homo sapiens	69-72
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	213-216	solute carrier family 9 member A2	Homo sapiens	20-24
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	213-216	solute carrier family 9 member A3	Homo sapiens	29-33
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	213-216	solute carrier family 9 member A2	Homo sapiens	151-155
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	213-216	solute carrier family 9 member A3	Homo sapiens	160-164
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	213-216	solute carrier family 9 member A2	Homo sapiens	151-155
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	213-216	solute carrier family 9 member A3	Homo sapiens	160-164
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	213-216	solute carrier family 9 member C1	Homo sapiens	20-23
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	290-293	solute carrier family 9 member A2	Homo sapiens	20-24
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	290-293	solute carrier family 9 member A2	Homo sapiens	151-155
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	290-293	solute carrier family 9 member A3	Homo sapiens	160-164
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	290-293	solute carrier family 9 member A2	Homo sapiens	151-155
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	290-293	solute carrier family 9 member A3	Homo sapiens	160-164
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	290-293	solute carrier family 9 member C1	Homo sapiens	20-23
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	290-293	solute carrier family 9 member A2	Homo sapiens	20-24
11875262-4	2001	Using electrophysiological techniques on basolaterally permeabilized preparations of microperfused native sweat ducts, we investigated whether: a) CFTR can act as a HCO(3)(-) conductive channel, b) different conditions for stimulating CFTR can alter its selectivity to HCO(3)(-) and, c) pancreatic insufficiency correlate with HCO(3)(-) conductance in different CFTR mutations.	7 alpha-hydroxy-4-cholesten-3-one	165-168	CF transmembrane conductance regulator	Homo sapiens	147-151
11875262-6	2001	HCO(3)(-) conductance in the apical plasma membranes of sweat duct appears to be mediated by CFTR and not by any other Cl(-) channel because HCO(3)(-) conductance is abolished when CFTR is: a) deactivated by removing cAMP and ATP, b) blocked by 1 mM DIDS (4,4"-diisothiocyanostilbene-2,2"-disulfonic acid) in the cytoplasmic bath and, c) absent in the plasma membranes of DeltaF508 CF ducts.	7 alpha-hydroxy-4-cholesten-3-one	0-3	CF transmembrane conductance regulator	Homo sapiens	93-97
11875262-6	2001	HCO(3)(-) conductance in the apical plasma membranes of sweat duct appears to be mediated by CFTR and not by any other Cl(-) channel because HCO(3)(-) conductance is abolished when CFTR is: a) deactivated by removing cAMP and ATP, b) blocked by 1 mM DIDS (4,4"-diisothiocyanostilbene-2,2"-disulfonic acid) in the cytoplasmic bath and, c) absent in the plasma membranes of DeltaF508 CF ducts.	7 alpha-hydroxy-4-cholesten-3-one	0-3	CF transmembrane conductance regulator	Homo sapiens	181-185
11875263-12	2001	The hyperpolarization of V(ap) and V(bl) caused by 1-EBIO provides a driving force for Cl(-) exit across the apical membrane, inhibits the influx of HCO(3)(-) on the Na(+):HCO(3)(-) cotransporter across the basolateral membrane, activates the basolateral membrane Na(+):K:2Cl(-) cotransporter and thereby provides the switch from HCO(3)(-) secretion to Cl(-) secretion.	7 alpha-hydroxy-4-cholesten-3-one	149-152	solute carrier family 4 member 4	Homo sapiens	166-195
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	290-293	solute carrier family 9 member A2	Homo sapiens	151-155
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	290-293	solute carrier family 9 member A3	Homo sapiens	160-164
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	290-293	solute carrier family 9 member A2	Homo sapiens	151-155
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	290-293	solute carrier family 9 member A3	Homo sapiens	160-164
11408268-10	2001	We conclude that 1) NHE2 and NHE3 are localized principally to the brush border of human duodenal villus epithelial cells; 2) sequential inhibition of NHE2 and NHE3 isoforms resulted in step-wise increases in net HCO(3)(-) output; 3) NHE2 and NHE3 participate in human duodenal villus cell HCO(3)(-) transport; and 4) the contribution of NHE-related transport events should be considered when studying duodenal HCO(3)(-) transport processes.	7 alpha-hydroxy-4-cholesten-3-one	290-293	solute carrier family 9 member C1	Homo sapiens	20-23
11875267-5	2001	Ussing-chamber experiments with an NBC-specific inhibitor revealed that NBC, coupled to basolateral Cl(-)/HCO(3)(-) exchange, was an important alternative Cl(-) supply pathway to Na(+)K(+)2Cl(-) cotransport (NKCC) during cAMP-stimulated colonic Cl(-) secretion.	7 alpha-hydroxy-4-cholesten-3-one	106-109	solute carrier family 4 (anion exchanger), member 4	Mus musculus	35-38
11875267-5	2001	Ussing-chamber experiments with an NBC-specific inhibitor revealed that NBC, coupled to basolateral Cl(-)/HCO(3)(-) exchange, was an important alternative Cl(-) supply pathway to Na(+)K(+)2Cl(-) cotransport (NKCC) during cAMP-stimulated colonic Cl(-) secretion.	7 alpha-hydroxy-4-cholesten-3-one	106-109	solute carrier family 4 (anion exchanger), member 4	Mus musculus	72-75
11875259-3	2001	Cystic fibrosis transmembrane conductance regulator (CFTR) is highly expressed in the pancreatic ductal epithelium and plays a key role in ductal HCO(3)(-) secretion.	7 alpha-hydroxy-4-cholesten-3-one	146-150	CF transmembrane conductance regulator	Homo sapiens	53-57
11875259-5	2001	Experimental data suggests that HCO(3)(-) secretion occurs via apical Cl(-)/HCO(3)(-) exchangers working in parallel with Cl(-) channels (CFTR and calcium activated chloride channels, CaCC).	7 alpha-hydroxy-4-cholesten-3-one	32-35	CF transmembrane conductance regulator	Homo sapiens	138-142
11875259-5	2001	Experimental data suggests that HCO(3)(-) secretion occurs via apical Cl(-)/HCO(3)(-) exchangers working in parallel with Cl(-) channels (CFTR and calcium activated chloride channels, CaCC).	7 alpha-hydroxy-4-cholesten-3-one	32-35	chloride channel accessory 1	Homo sapiens	184-188
11875260-3	2001	In pancreatic ducts HCO(3)(-) secretion is mediated by cystic fibrosis transmembrane conductance regulator (CFTR) activated luminal Cl(-)/HCO(3)(-) exchange activity and HCO(3)(-) absorption is achieved by Na(+)-dependent mechanisms including Na(+)/H(+) exchanger 3 (NHE3).	7 alpha-hydroxy-4-cholesten-3-one	20-23	CF transmembrane conductance regulator	Homo sapiens	55-106
11875260-3	2001	In pancreatic ducts HCO(3)(-) secretion is mediated by cystic fibrosis transmembrane conductance regulator (CFTR) activated luminal Cl(-)/HCO(3)(-) exchange activity and HCO(3)(-) absorption is achieved by Na(+)-dependent mechanisms including Na(+)/H(+) exchanger 3 (NHE3).	7 alpha-hydroxy-4-cholesten-3-one	20-23	CF transmembrane conductance regulator	Homo sapiens	108-112
11875260-3	2001	In pancreatic ducts HCO(3)(-) secretion is mediated by cystic fibrosis transmembrane conductance regulator (CFTR) activated luminal Cl(-)/HCO(3)(-) exchange activity and HCO(3)(-) absorption is achieved by Na(+)-dependent mechanisms including Na(+)/H(+) exchanger 3 (NHE3).	7 alpha-hydroxy-4-cholesten-3-one	20-23	solute carrier family 9 member A3	Homo sapiens	243-265
11875260-3	2001	In pancreatic ducts HCO(3)(-) secretion is mediated by cystic fibrosis transmembrane conductance regulator (CFTR) activated luminal Cl(-)/HCO(3)(-) exchange activity and HCO(3)(-) absorption is achieved by Na(+)-dependent mechanisms including Na(+)/H(+) exchanger 3 (NHE3).	7 alpha-hydroxy-4-cholesten-3-one	20-23	solute carrier family 9 member A3	Homo sapiens	267-271
11179033-5	2001	AT-1 cell Cl(-)/HCO(3)(-) activity was stimulated two- to threefold by extracellular ATP and ANG II.	7 alpha-hydroxy-4-cholesten-3-one	16-19	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	93-99
11292633-8	2001	Thus CA IV expression may be regulated to accommodate the maturational increase in HCO absorption in the proximal tubule.	7 alpha-hydroxy-4-cholesten-3-one	83-86	carbonic anhydrase 4	Oryctolagus cuniculus	5-10
11302728-5	2001	Human AE4 shares 84% identity with the recently reported rabbit AE4, a sodium independent, Cl(-)/HCO(-)(3) exchanger located on the apical membrane of beta-intercalated kidney cells.	7 alpha-hydroxy-4-cholesten-3-one	97-100	solute carrier family 4 member 9	Homo sapiens	6-9
11302728-5	2001	Human AE4 shares 84% identity with the recently reported rabbit AE4, a sodium independent, Cl(-)/HCO(-)(3) exchanger located on the apical membrane of beta-intercalated kidney cells.	7 alpha-hydroxy-4-cholesten-3-one	97-100	anion exchange protein 4	Oryctolagus cuniculus	64-67
10993873-7	2000	Functional analyses of the NCBE protein expressed in Xenopus laevis oocytes and HEK293 cells demonstrate that it transports extracellular Na(+) and HCO(3)(-) into cells in exchange for intracellular Cl(-) and H(+), thus raising the intracellular pH.	7 alpha-hydroxy-4-cholesten-3-one	148-151	solute carrier family 4, sodium bicarbonate transporter, member 10 L homeolog	Xenopus laevis	27-31
10993873-8	2000	Thus, we conclude that NCBE is a Na(+)-driven Cl(-)/HCO(3)(-) exchanger that regulates intracellular pH in native cells.	7 alpha-hydroxy-4-cholesten-3-one	52-55	solute carrier family 4 member 10	Homo sapiens	23-27
10966931-9	2000	Our data show that a large component of HCO(3)(-) and fluid absorption in the proximal tubule is controlled by nNOS.	7 alpha-hydroxy-4-cholesten-3-one	40-43	nitric oxide synthase 1, neuronal	Mus musculus	111-115
11053051-13	2000	The localization of NBC(N)1 in medullary TAL cells and medullary collecting duct intercalated cells suggests that NBC(N)1 may be important for electroneutral basolateral HCO(3)(-) transport in these cells.	7 alpha-hydroxy-4-cholesten-3-one	170-173	solute carrier family 4 member 7	Rattus norvegicus	20-27
11053051-13	2000	The localization of NBC(N)1 in medullary TAL cells and medullary collecting duct intercalated cells suggests that NBC(N)1 may be important for electroneutral basolateral HCO(3)(-) transport in these cells.	7 alpha-hydroxy-4-cholesten-3-one	170-173	solute carrier family 4 member 7	Rattus norvegicus	114-121
11029292-4	2000	The phosphatidylinositol 3-kinase (PI 3-K) inhibitors wortmannin (100 nM) and LY-294002 (20 microM) blocked completely the stimulation of HCO(3)(-) absorption by hyposmolality.	7 alpha-hydroxy-4-cholesten-3-one	138-141	phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit gamma	Rattus norvegicus	4-33
10898717-5	2000	Cl(-)/HCO(3)(-) exchange activity increased by approximately 300% in cells transfected with functional CFTR, with activities increasing from 0.034 pH/min in CFT-1 cells to 0.11 in CFT-WT cells (P < 0.001, n = 8).	7 alpha-hydroxy-4-cholesten-3-one	6-9	CF transmembrane conductance regulator	Homo sapiens	103-107
10746996-9	2000	These results show that ET-1 increases the activity of the Na(+)-independent Cl(-)-HCO(3)(-) exchanger in cardiac tissue through the ET(A) receptors.	7 alpha-hydroxy-4-cholesten-3-one	83-86	endothelin 1	Homo sapiens	24-28
10611158-8	2000	DBcAMP-stimulated HCO(3)(-) secretion was closely linked to active Cl(-) secretion because HCO(3)(-) secretion was substantially reduced by removal of bath Cl(-), by addition of bath bumetanide, an inhibitor of Na-K-2Cl cotransport and Cl(-) secretion, and by addition of lumen NPPB, a Cl(-) channel inhibitor.	7 alpha-hydroxy-4-cholesten-3-one	18-21	natriuretic peptide B	Rattus norvegicus	278-282
10627304-4	2000	The change in intracellular pH (pH(i)) resulting from the change in pH(0) seems to be a prerequisite for the motility decrease since other means to decrease pH(i), namely Na(+)-free solution (in the absence of HCO(-)(3)) and nigericin-containing solution, mimicked the extracellular acidification.	7 alpha-hydroxy-4-cholesten-3-one	210-214	glucose-6-phosphate isomerase 1	Mus musculus	32-37
10729744-2	2000	The alpha form secretes acid by an apical H(+) ATPase and a basolateral Cl:HCO(3) exchanger which is an alternatively spliced form of the red cell band 3 (kAE1), while the beta form secretes HCO(3) by having these transporters on the reverse membranes.	7 alpha-hydroxy-4-cholesten-3-one	75-78	O-sialoglycoprotein endopeptidase	Homo sapiens	155-159
10644659-7	2000	We sought to ascertain if the magnitude of the acute stimulated response to ANG II by the Na(+)/H(+) and Na(+)-dependent Cl(-)/HCO(-)(3) exchanger is changed.	7 alpha-hydroxy-4-cholesten-3-one	127-130	angiogenin	Homo sapiens	76-79
10444585-7	1999	Net rates of HCO(-)(3) (J(HCO3)) and fluid absorption (J(v)) were reduced by 54 and 63%, respectively, in NHE3 null mice compared with controls.	7 alpha-hydroxy-4-cholesten-3-one	13-16	solute carrier family 9 (sodium/hydrogen exchanger), member 3	Mus musculus	106-110
10529183-3	1999	The efficiency of either Zn-Cam or Co-Cam for CO(2) hydration (k(cat)/K(m)) was severalfold greater than HCO(3-) dehydration at physiological pH values, a result consistent with the proposed physiological function for Cam during growth on acetate.	7 alpha-hydroxy-4-cholesten-3-one	105-108	calmodulin 3	Homo sapiens	38-41
10529183-3	1999	The efficiency of either Zn-Cam or Co-Cam for CO(2) hydration (k(cat)/K(m)) was severalfold greater than HCO(3-) dehydration at physiological pH values, a result consistent with the proposed physiological function for Cam during growth on acetate.	7 alpha-hydroxy-4-cholesten-3-one	105-108	calmodulin 3	Homo sapiens	38-41
10444464-10	1999	Our observations suggest that secretion of HCO(-)(3) by human pancreatic duct cells involves the basolateral uptake of Na(+) and HCO(-)(3) via NBC, an electrogenic Na(+)-HCO(-)(3) cotransporter.	7 alpha-hydroxy-4-cholesten-3-one	43-46	solute carrier family 4 member 4	Homo sapiens	164-193
10444464-10	1999	Our observations suggest that secretion of HCO(-)(3) by human pancreatic duct cells involves the basolateral uptake of Na(+) and HCO(-)(3) via NBC, an electrogenic Na(+)-HCO(-)(3) cotransporter.	7 alpha-hydroxy-4-cholesten-3-one	129-132	solute carrier family 4 member 4	Homo sapiens	164-193
10362780-0	1999	HCO-3 reabsorption in renal collecting duct of NHE-3-deficient mouse: a compensatory response.	7 alpha-hydroxy-4-cholesten-3-one	0-3	solute carrier family 9 (sodium/hydrogen exchanger), member 3	Mus musculus	47-52
10424714-5	1999	The HCO stimulatory effect of sulprostone in the stomach was significantly inhibited by ONO-AE-829, the selective EP1 antagonist.	7 alpha-hydroxy-4-cholesten-3-one	4-7	prostaglandin E receptor 1 (subtype EP1)	Mus musculus	114-117
9843781-8	1998	Administration of hCG to female rats in vivo caused a significant increase in HCO-3 and K+ secretion from the duodenum and pancreas.	7 alpha-hydroxy-4-cholesten-3-one	78-81	hypertrichosis 2 (generalised, congenital)	Homo sapiens	18-21
9886916-3	1999	We further demonstrate that 1) HCO-3 uptake across the basolateral membranes of pancreatic duct cells is mediated via NBC and 2) cAMP potentiates NBC activity through activation of CFTR-mediated Cl- secretion.	7 alpha-hydroxy-4-cholesten-3-one	31-34	CF transmembrane conductance regulator	Homo sapiens	181-185
9815033-5	1998	Depolarization of cholangiocytes increased basal pHi and the activity of Cl-/HCO-3 exchange, suggesting that an electrogenic Na+-HCO-3 symport might function as a counterregulatory pHi mechanism.	7 alpha-hydroxy-4-cholesten-3-one	77-80	glucose-6-phosphate isomerase	Rattus norvegicus	181-184
8707250-1	1996	Serum concentrations of 7alpha-hydroxy-4-cholesten-3-one (alpha-HC) have recently been shown to reflect the activity of cholesterol 7 alpha-hydroxylase in humans.	7 alpha-hydroxy-4-cholesten-3-one	24-56	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	120-151
9729505-3	1998	At constant external pH, BLMV 36Cl-/HCO-3 and 36Cl-/Cl- exchanges exhibited a sigmoidal pattern of activation as internal pH (pHi) increased from 6.1 to 8.0, whereas LMV 36Cl-/Cl- exchange was unchanged between pHi 6.7 and 7.8.	7 alpha-hydroxy-4-cholesten-3-one	36-39	glucose-6-phosphate isomerase	Rattus norvegicus	126-129
9204898-3	1997	TW Hya itself displays circumstellar CO, HCN, CN, and HCO+ emission.	7 alpha-hydroxy-4-cholesten-3-one	54-58	lysine demethylase 5D	Homo sapiens	3-6
8891880-1	1996	Intracellular pH (pHi) regulation in the heart relies on the activity of three membrane mechanisms: the Na+/H+ exchange and an Na+, HCO3(-)-dependent transport, both activated after an acid load, and the Cl-/HCO(3-) exchange, activated by an intracellular alkalinization.	7 alpha-hydroxy-4-cholesten-3-one	132-135	glucose-6-phosphate isomerase	Rattus norvegicus	18-21
2060639-0	1991	The plasma level of 7 alpha-hydroxy-4-cholesten-3-one reflects the activity of hepatic cholesterol 7 alpha-hydroxylase in man.	7 alpha-hydroxy-4-cholesten-3-one	20-53	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	87-118
8081463-6	1994	The plasma levels of 7 alpha-hydroxy-4-cholesten-3-one were correlated with the cholesterol 7 alpha-hydroxylase activity to a higher degree than those of any other form of 7 alpha-hydroxycholesterol (r = 0.84, n = 16, p < 0.0001).	7 alpha-hydroxy-4-cholesten-3-one	21-54	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	80-111
1849960-13	1991	The MM fit shows that the symmetric half-saturation constant, Ks1/2, is 20.2 (HCO-3) and 23.9 (Cl-) mM, and J(eff,s)max is 0.51 (HCO3-) and 0.32 (Cl-) nmol/(cm2.s).	7 alpha-hydroxy-4-cholesten-3-one	78-81	zinc finger protein 382	Homo sapiens	62-67
2610336-3	1989	158, 228-232) for measuring cholesterol 7 alpha-hydroxylase activity was modified by using a C-18 reverse-phase column to separate 7 alpha-hydroxy-4-cholesten-3-one and 4-cholesten-3-one and by adding 7 beta-hydroxycholesterol to each reaction mixture as an internal recovery standard.	7 alpha-hydroxy-4-cholesten-3-one	131-164	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	28-59
2166273-9	1990	In acidified cultured DCTb cells, a partial pHi recovery was induced in sodium-free media by 15 mM HCO(-3) in the presence of an outward chloride gradient.	7 alpha-hydroxy-4-cholesten-3-one	99-103	glucose-6-phosphate isomerase	Oryctolagus cuniculus	44-47
2221061-2	1990	Tissue pH is calculated by using the Henderson-Hasselbalch equation and measurements of arterial [HCO-3] and CO2 tension (PCO3) of saline contained in a Silastic balloon within the lumen of the gut.	7 alpha-hydroxy-4-cholesten-3-one	98-101	vasoactive intestinal peptide	Sus scrofa	7-9
24213040-7	1989	The average pHi was 7.29 (+-0.11) for cells in the presence of 2 mM HCO 3 (-) .	7 alpha-hydroxy-4-cholesten-3-one	68-71	glucose-6-phosphate isomerase	Homo sapiens	12-15
24213040-8	1989	In the absence of HCO 3 (-) the pHi was decreased by 0.8 pH unit.	7 alpha-hydroxy-4-cholesten-3-one	18-21	glucose-6-phosphate isomerase	Homo sapiens	32-35
2556038-7	1989	4,4"-Diisothiocyanostilbene-2,2"-disulfonic acid (DIDS, 50 microM), an inhibitor of HCO-3 transport systems, blocked this Na+-dependent pHi recovery in all three superficial subtypes and the JS3 but had no effect in either the JS1 or JS2.	7 alpha-hydroxy-4-cholesten-3-one	84-87	glucose-6-phosphate isomerase	Oryctolagus cuniculus	136-139
16666689-2	1989	DCDP is an effective inhibitor of PEP carboxylase from Zea mays or Panicum miliaceum; 50% inhibition was obtained at 70 or 350 micromolar, respectively, in the presence of 1 millimolar PEP and 1 millimolar HCO(3) (-).	7 alpha-hydroxy-4-cholesten-3-one	206-209	phosphoenolpyruvate carboxylase 2	Zea mays	34-37
6403922-5	1983	It is concluded that in these experiments clearing of HCO-3 from the CSF is critically dependent on plasma [HCO-3].	7 alpha-hydroxy-4-cholesten-3-one	54-57	colony stimulating factor 2	Canis lupus familiaris	69-72
3198770-2	1988	A new inborn error in bile acid synthesis, manifest in identical infant twins as severe intrahepatic cholestasis, is described involving the delta 4-3-oxosteroid 5 beta-reductase catalyzed conversion of the key intermediates, 7 alpha-hydroxy-4-cholesten-3-one and 7 alpha,12 alpha-dihydroxy-4-cholesten-3-one for chenodeoxycholic and cholic acid synthesis, to the respective 3 alpha-hydroxy-5 beta (H) products.	7 alpha-hydroxy-4-cholesten-3-one	226-259	aldo-keto reductase family 1 member D1	Homo sapiens	141-178
6736016-1	1984	delta 4-3-Ketosteroid 5 beta-reductase was purified about 230-fold from 100,000 X g supernatant of rat liver homogenate using 7 alpha-hydroxy-4-cholesten-3-one as substrate throughout.	7 alpha-hydroxy-4-cholesten-3-one	126-159	aldo-keto reductase family 1, member D1	Rattus norvegicus	0-38
6423637-5	1984	The purified cytochrome P-450 catalyzed 26-hydroxylation of cholesterol, 5-cholestene-3 beta,7 alpha-diol, 7 alpha-hydroxy-4-cholesten-3-one, 5 beta-cholestane-3 alpha,7 alpha-diol, and 5 beta-cholestane-3 alpha,7 alpha,12 alpha-triol up to 1000 times more efficiently than the mitochondria.	7 alpha-hydroxy-4-cholesten-3-one	107-140	cytochrome P-450	Oryctolagus cuniculus	13-29
6721879-4	1984	In unbuffered solutions, a new Cl-pH-equilibrium is reached very fast and proceeds by the Cl-/HCO-3-exchange.	7 alpha-hydroxy-4-cholesten-3-one	94-97	calcium binding protein, spermatid associated 1	Homo sapiens	31-36
2883187-2	1987	The pHi of NG108-15 cells suspended in nominally HCO-3-free, Na+-containing buffer could be reduced by the external application of acetate.	7 alpha-hydroxy-4-cholesten-3-one	49-52	glucose-6-phosphate isomerase 1	Mus musculus	4-7
24232647-0	1986	An efficient method for the determination of K m values for HCO 3 (-) of phosphoenolpyruvate carboxylase.	7 alpha-hydroxy-4-cholesten-3-one	60-63	phosphoenolpyruvate carboxykinase 1	Homo sapiens	73-104
24232647-4	1986	The method is discussed and the K m values for HCO 3 (-) of PEPCase from several C4-species are presented.	7 alpha-hydroxy-4-cholesten-3-one	47-50	phosphoenolpyruvate carboxykinase 1	Homo sapiens	60-67
4003549-5	1985	Among exogenous hormones, the most effective stimulant of HCO-3 secretion was PP, which caused a significant increase in HCO-3 output from the gastric and duodenal mucosa at doses (125-500 pmol X kg-1 X h-1) that raised plasma PP to postprandial levels.	7 alpha-hydroxy-4-cholesten-3-one	58-61	pancreatic polypeptide	Canis lupus familiaris	78-80
3978424-6	1985	The presence of a distinct, HCO-3-dependent pHi regulatory mechanism is postulated.	7 alpha-hydroxy-4-cholesten-3-one	28-31	glucose-6-phosphate isomerase	Homo sapiens	44-47
3989871-3	1985	In 20 mM HEPES buffered solution, steady state pHi is close to that in control CO2/HCO-3 (25 mM HCO-3, 5% CO2) solution.	7 alpha-hydroxy-4-cholesten-3-one	83-87	glucose-6-phosphate isomerase	Oryctolagus cuniculus	47-50
6419623-7	1983	The pHi tended to be more alkaline in SO2-4 -Ringer, suggesting the presence of a HCO-3/Cl- exchange mechanism.	7 alpha-hydroxy-4-cholesten-3-one	82-85	glucose-6-phosphate isomerase	Homo sapiens	4-7
6614175-3	1983	Increases in peritubular HCO -/3 concentration without changing pH resulted in drastic decreases in aiCl.	7 alpha-hydroxy-4-cholesten-3-one	25-28	C-type lectin domain family 2 member B	Homo sapiens	100-104
6403922-8	1983	The experiments therefore suggest a dual contribution for the clearing of HCO-3 from the CSF after its experimental increase: diffusion along the CSF-plasma gradient for HCO-3 and a carbonic anhydrase dependent clearing of HCO-3.	7 alpha-hydroxy-4-cholesten-3-one	74-77	colony stimulating factor 2	Canis lupus familiaris	89-92
6403922-8	1983	The experiments therefore suggest a dual contribution for the clearing of HCO-3 from the CSF after its experimental increase: diffusion along the CSF-plasma gradient for HCO-3 and a carbonic anhydrase dependent clearing of HCO-3.	7 alpha-hydroxy-4-cholesten-3-one	74-77	colony stimulating factor 2	Canis lupus familiaris	146-149
6403922-8	1983	The experiments therefore suggest a dual contribution for the clearing of HCO-3 from the CSF after its experimental increase: diffusion along the CSF-plasma gradient for HCO-3 and a carbonic anhydrase dependent clearing of HCO-3.	7 alpha-hydroxy-4-cholesten-3-one	170-173	colony stimulating factor 2	Canis lupus familiaris	89-92
6403922-5	1983	It is concluded that in these experiments clearing of HCO-3 from the CSF is critically dependent on plasma [HCO-3].	7 alpha-hydroxy-4-cholesten-3-one	108-111	colony stimulating factor 2	Canis lupus familiaris	69-72
6819139-0	1982	A 13C nuclear magnetic resonance study of CO2/HCO-3 exchange catalyzed by human carbonic anhydrase I.	7 alpha-hydroxy-4-cholesten-3-one	46-49	carbonic anhydrase 1	Homo sapiens	80-100
6819139-1	1982	Rates of CO2/HCO-3 exchange, catalyzed by human carbonic anhydrase I (or B) at chemical equilibrium, were estimated from the nuclear magnetic resonance linewidths of 13C-labeled substrates.	7 alpha-hydroxy-4-cholesten-3-one	13-16	carbonic anhydrase 1	Homo sapiens	48-68
6808459-3	1982	In dogs with normal plasma [HCO(-3)], CSF [HCO(-3)]fell by ca.	7 alpha-hydroxy-4-cholesten-3-one	28-31	colony stimulating factor 2	Canis lupus familiaris	38-41
6808459-3	1982	In dogs with normal plasma [HCO(-3)], CSF [HCO(-3)]fell by ca.	7 alpha-hydroxy-4-cholesten-3-one	43-46	colony stimulating factor 2	Canis lupus familiaris	38-41
6808459-0	1982	Correction of CSF HCO(-3) after its experimental increase in normocapnia.	7 alpha-hydroxy-4-cholesten-3-one	18-21	colony stimulating factor 2	Canis lupus familiaris	14-17
6808459-6	1982	It is concluded that correction of CSF [HCO(-3)] is partially dependent on a sufficiently low plasma [HCO(-3)].	7 alpha-hydroxy-4-cholesten-3-one	40-43	colony stimulating factor 2	Canis lupus familiaris	35-38
6808459-2	1982	In anesthetized normocapnic dogs CSF [HCO(-3)] was increased to 33 mmol/l by perfusing the brain ventricles for 45 min with a mock CSF containing a high [HCO(-3)].	7 alpha-hydroxy-4-cholesten-3-one	38-41	colony stimulating factor 2	Canis lupus familiaris	33-36
6808459-6	1982	It is concluded that correction of CSF [HCO(-3)] is partially dependent on a sufficiently low plasma [HCO(-3)].	7 alpha-hydroxy-4-cholesten-3-one	102-105	colony stimulating factor 2	Canis lupus familiaris	35-38
6808459-7	1982	The small and persistent fall of CSF [HCO(-3)] which at high plasma [HCO(-3)] occurs against a concentration gradient with blood suggests moreover the contribution of more specific mechanism(s) for lowering CSF [HCO(-3)] after its experimental increase.	7 alpha-hydroxy-4-cholesten-3-one	38-41	colony stimulating factor 2	Canis lupus familiaris	33-36
6808459-7	1982	The small and persistent fall of CSF [HCO(-3)] which at high plasma [HCO(-3)] occurs against a concentration gradient with blood suggests moreover the contribution of more specific mechanism(s) for lowering CSF [HCO(-3)] after its experimental increase.	7 alpha-hydroxy-4-cholesten-3-one	38-41	colony stimulating factor 2	Canis lupus familiaris	207-210
6808459-7	1982	The small and persistent fall of CSF [HCO(-3)] which at high plasma [HCO(-3)] occurs against a concentration gradient with blood suggests moreover the contribution of more specific mechanism(s) for lowering CSF [HCO(-3)] after its experimental increase.	7 alpha-hydroxy-4-cholesten-3-one	69-72	colony stimulating factor 2	Canis lupus familiaris	33-36
441571-8	1979	(III) In order to show interdependence of the rate of fall in CSF [HCO-3] with rate of fall in cisternal PCO2 six dogs were mechanically hyperventilated and PaCO2 reduced to 21 torr rapidly and maintained there for six hours.	7 alpha-hydroxy-4-cholesten-3-one	67-70	colony stimulating factor 2	Canis lupus familiaris	62-65
441571-13	1979	It is speculated that the coupling of CSF [HCO-3] reduction in metabolic acidosis to CSF PCO2 fall is primarily for the benefit of CNS H+ homeostasis.	7 alpha-hydroxy-4-cholesten-3-one	43-46	colony stimulating factor 2	Canis lupus familiaris	38-41
441571-13	1979	It is speculated that the coupling of CSF [HCO-3] reduction in metabolic acidosis to CSF PCO2 fall is primarily for the benefit of CNS H+ homeostasis.	7 alpha-hydroxy-4-cholesten-3-one	43-46	colony stimulating factor 2	Canis lupus familiaris	85-88
9514-7	1976	The pH rise can be reversed by the addition of HCO(-3) (4 muM) or 2,4-dinitrophenol (90 muM).	7 alpha-hydroxy-4-cholesten-3-one	47-50	latexin	Homo sapiens	58-61
17740-20	1977	It was concluded that H+ ions are not passively distributed across the muscle cell membrane, and that the pHi is closely controlled by the active transport of H+, OH- or HCO-3 ions.	7 alpha-hydroxy-4-cholesten-3-one	170-173	glucose-6-phosphate isomerase 1	Mus musculus	106-109
23428-21	1977	These results suggest that Cl(-)-HCO(3) (-) exchange is also involved in the pH(i) regulating system and that it is a separate mechanism.	7 alpha-hydroxy-4-cholesten-3-one	33-36	glucose-6-phosphate isomerase 1	Mus musculus	77-82
23428-22	1977	Under the conditions used, Cl(-)-HCO(3) (-) exchange formed about 20% of the pH(i) regulating system.9.	7 alpha-hydroxy-4-cholesten-3-one	33-36	glucose-6-phosphate isomerase 1	Mus musculus	77-82
23429-12	1977	It is concluded that the pH(i) regulating system involves tightly linked Cl(-)-HCO(3) (-) and Na(+)-H(+) exchange, with Na entry down its concentration gradient probably providing the energy to drive the movement inwards of HCO(3) (-) and the movement outward of Cl(-) and H(+) ions.	7 alpha-hydroxy-4-cholesten-3-one	79-82	glucose-6-phosphate isomerase	Homo sapiens	25-27
23429-12	1977	It is concluded that the pH(i) regulating system involves tightly linked Cl(-)-HCO(3) (-) and Na(+)-H(+) exchange, with Na entry down its concentration gradient probably providing the energy to drive the movement inwards of HCO(3) (-) and the movement outward of Cl(-) and H(+) ions.	7 alpha-hydroxy-4-cholesten-3-one	224-227	glucose-6-phosphate isomerase	Homo sapiens	25-27
9514-7	1976	The pH rise can be reversed by the addition of HCO(-3) (4 muM) or 2,4-dinitrophenol (90 muM).	7 alpha-hydroxy-4-cholesten-3-one	47-50	latexin	Homo sapiens	88-91
130854-3	1976	Should gastrin induce the formation of histamine in endocrinous cells and the histamine activate carboanhydrase in parietal cells, our data confirm the supposition that HCO-3-ions stimulate ATP-ase sustaining the exchange between HCO-3-cells and C1- of blood to form HCl in the endothelial cells of blood capillaries adjacent to the parietal cells.	7 alpha-hydroxy-4-cholesten-3-one	169-172	gastrin	Rattus norvegicus	7-14
956369-1	1976	Renal micropuncture and clearance experiments were carried out in rats to study the effect of parathyroid hormone (PTH) on renal tubular HCO-/3 reabsorption.	7 alpha-hydroxy-4-cholesten-3-one	137-140	parathyroid hormone	Rattus norvegicus	94-113
30471425-7	2019	7alpha-Hydroxycholest-4-en-3-one is a ligand for the pregnane X receptor (PXR), activation of which is known to up-regulate the expression of CYP3A11, which we confirm has sterol 26-hydroxylase activity.	7 alpha-hydroxy-4-cholesten-3-one	0-32	nuclear receptor subfamily 1, group I, member 2	Mus musculus	53-72
4385432-4	1968	7alpha-Hydroxycholest-4-en-3-one was metabolized into 7alpha-12alpha-dihydroxycholest-4-en-3-one in the presence of microsomal fraction fortified with NADPH and into 5beta-cholestane-3alpha,7alpha-diol in the presence of 100,000 g supernatant fluid.	7 alpha-hydroxy-4-cholesten-3-one	0-32	2,4-dienoyl-CoA reductase 1	Homo sapiens	151-156
30122083-8	2020	Plasma levels of 7alpha-hydroxy-4-cholesten-3-one (C4), a marker of CYP7A1 activity, were quantified using HPLC-MS/MS.	7 alpha-hydroxy-4-cholesten-3-one	17-49	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	68-74
30471425-7	2019	7alpha-Hydroxycholest-4-en-3-one is a ligand for the pregnane X receptor (PXR), activation of which is known to up-regulate the expression of CYP3A11, which we confirm has sterol 26-hydroxylase activity.	7 alpha-hydroxy-4-cholesten-3-one	0-32	nuclear receptor subfamily 1, group I, member 2	Mus musculus	74-77
30471425-7	2019	7alpha-Hydroxycholest-4-en-3-one is a ligand for the pregnane X receptor (PXR), activation of which is known to up-regulate the expression of CYP3A11, which we confirm has sterol 26-hydroxylase activity.	7 alpha-hydroxy-4-cholesten-3-one	0-32	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	142-149
30471425-9	2019	We hereby suggest that a lack of a motor neuron phenotype in some CTX patients and Cyp27a1-/- mice may involve increased levels of 7alpha-hydroxycholest-4-en-3-one and activation PXR, as well as increased levels of sterol 26-hydroxylase and the production of neuroprotective sterols capable of activating LXR.	7 alpha-hydroxy-4-cholesten-3-one	131-163	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	83-90
30682184-2	2019	Hepatic BA production, measured by serum levels of the precursor 7alpha-hydroxy-4-cholesten-3-one (C4), is regulated by the farnesoid-X-receptor (FXR)-dependent ileal hormone fibroblast growth factor 19 (FGF19).	7 alpha-hydroxy-4-cholesten-3-one	65-97	nuclear receptor subfamily 1 group H member 4	Homo sapiens	124-144
30682184-2	2019	Hepatic BA production, measured by serum levels of the precursor 7alpha-hydroxy-4-cholesten-3-one (C4), is regulated by the farnesoid-X-receptor (FXR)-dependent ileal hormone fibroblast growth factor 19 (FGF19).	7 alpha-hydroxy-4-cholesten-3-one	65-97	nuclear receptor subfamily 1 group H member 4	Homo sapiens	146-149
30682184-2	2019	Hepatic BA production, measured by serum levels of the precursor 7alpha-hydroxy-4-cholesten-3-one (C4), is regulated by the farnesoid-X-receptor (FXR)-dependent ileal hormone fibroblast growth factor 19 (FGF19).	7 alpha-hydroxy-4-cholesten-3-one	65-97	fibroblast growth factor 19	Homo sapiens	204-209
26180239-6	2015	Adding HMGB1 to the bath decreased HCO(3)(-) absorption by 24% in isolated, perfused rat and mouse MTALs.	7 alpha-hydroxy-4-cholesten-3-one	35-38	high mobility group box 1	Rattus norvegicus	7-12
30399365-2	2018	The oxysterol 12alpha-hydroxylase enzyme is cytochrome P450 8B1 (P450 8B1), which regioselectively and stereoselectively incorporates the 12alpha-hydroxy group in 7alpha-hydroxycholest-4-en-3-one, the biosynthetic precursor of cholic acid.	7 alpha-hydroxy-4-cholesten-3-one	163-195	cytochrome P450 family 8 subfamily B member 1	Homo sapiens	44-63
29692737-9	2018	Both GALR2 and GALR3 antagonists reversed the inhibitory effects of spexin on concentrations of serum TBA and 7 alpha-hydroxy-4-cholesten-3-one (C4), and hepatic CYP7A1 expression.	7 alpha-hydroxy-4-cholesten-3-one	110-143	galanin receptor 2	Mus musculus	5-10
29692737-9	2018	Both GALR2 and GALR3 antagonists reversed the inhibitory effects of spexin on concentrations of serum TBA and 7 alpha-hydroxy-4-cholesten-3-one (C4), and hepatic CYP7A1 expression.	7 alpha-hydroxy-4-cholesten-3-one	110-143	galanin receptor 3	Mus musculus	15-20
29692737-9	2018	Both GALR2 and GALR3 antagonists reversed the inhibitory effects of spexin on concentrations of serum TBA and 7 alpha-hydroxy-4-cholesten-3-one (C4), and hepatic CYP7A1 expression.	7 alpha-hydroxy-4-cholesten-3-one	110-143	spexin hormone	Mus musculus	68-74
29983448-6	2018	Moreover, the radical HCS is found to be more abundant than its oxygen analogue, HCO.	7 alpha-hydroxy-4-cholesten-3-one	81-84	holocarboxylase synthetase	Homo sapiens	22-25
28039331-4	2017	LS-Xbp1-/- mice had lower serum 7alpha-hydroxy-4-cholesten-3-one (C4) levels compared with Xbp1fl/fl mice, indicating reduced cholesterol 7alpha-hydroxylase (CYP7A1) synthetic activity.	7 alpha-hydroxy-4-cholesten-3-one	32-64	X-box binding protein 1	Mus musculus	3-7
27552660-1	2016	We report on potential energies for the transition state, reactant, and product complexes along the reaction pathways for hydrogen transfer reactions to hydroperoxyl radical from formaldehyde H2CO + HO2   HCO + H2O2 and another hydroperoxyl radical 2HO2   H2O2 + O2 in the presence of one carbon dioxide molecule.	7 alpha-hydroxy-4-cholesten-3-one	205-208	heme oxygenase 2	Homo sapiens	199-202
29615519-7	2018	Long-term administration of the long-acting FGF21 analogs in obese cynomolgus monkeys suppressed plasma total bile acid and 7alpha-hydroxy-4-cholesten-3-one levels, a biomarker for bile acid synthesis.	7 alpha-hydroxy-4-cholesten-3-one	124-156	fibroblast growth factor 21	Macaca fascicularis	44-49
28916735-8	2017	This proliferative barrier imposed by fatty acid metabolism in hCOs could be rescued by simultaneous activation of both beta-catenin and YAP1 using genetic approaches or a small molecule activating both pathways.	7 alpha-hydroxy-4-cholesten-3-one	63-67	catenin beta 1	Homo sapiens	120-132
28916735-8	2017	This proliferative barrier imposed by fatty acid metabolism in hCOs could be rescued by simultaneous activation of both beta-catenin and YAP1 using genetic approaches or a small molecule activating both pathways.	7 alpha-hydroxy-4-cholesten-3-one	63-67	Yes1 associated transcriptional regulator	Homo sapiens	137-141
28915417-0	2017	LC-MS/MS quantification of 7alpha-hydroxy-4-cholesten-3-one (C4) in rat and monkey plasma.	7 alpha-hydroxy-4-cholesten-3-one	27-59	complement C4A	Rattus norvegicus	61-63
28915417-1	2017	7alpha-hydroxy-4-cholesten-3-one (C4) is an oxidative enzymatic product of cholesterol metabolism via cholesterol 7alpha-hydroxylase, an enzyme also known as cholesterol 7-alpha-monooxygenase or cytochrome P450 7A1 (CYP7A1).	7 alpha-hydroxy-4-cholesten-3-one	0-32	complement C4A	Rattus norvegicus	34-36
28915417-1	2017	7alpha-hydroxy-4-cholesten-3-one (C4) is an oxidative enzymatic product of cholesterol metabolism via cholesterol 7alpha-hydroxylase, an enzyme also known as cholesterol 7-alpha-monooxygenase or cytochrome P450 7A1 (CYP7A1).	7 alpha-hydroxy-4-cholesten-3-one	0-32	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	102-132
28915417-1	2017	7alpha-hydroxy-4-cholesten-3-one (C4) is an oxidative enzymatic product of cholesterol metabolism via cholesterol 7alpha-hydroxylase, an enzyme also known as cholesterol 7-alpha-monooxygenase or cytochrome P450 7A1 (CYP7A1).	7 alpha-hydroxy-4-cholesten-3-one	0-32	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	158-191
28915417-1	2017	7alpha-hydroxy-4-cholesten-3-one (C4) is an oxidative enzymatic product of cholesterol metabolism via cholesterol 7alpha-hydroxylase, an enzyme also known as cholesterol 7-alpha-monooxygenase or cytochrome P450 7A1 (CYP7A1).	7 alpha-hydroxy-4-cholesten-3-one	0-32	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	195-214
28915417-1	2017	7alpha-hydroxy-4-cholesten-3-one (C4) is an oxidative enzymatic product of cholesterol metabolism via cholesterol 7alpha-hydroxylase, an enzyme also known as cholesterol 7-alpha-monooxygenase or cytochrome P450 7A1 (CYP7A1).	7 alpha-hydroxy-4-cholesten-3-one	0-32	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	216-222
28485583-4	2017	Diffuse reflectance infrared Fourier transform spectroscopy results revealed the high C2H5OH production and selectivity of Pd2Cu NPs/P25 can be ascribed to boosting *CO (adsorption CO) hydrogenation to *HCO, the rate-determining step for the CO2 hydrogenation to C2H5OH.	7 alpha-hydroxy-4-cholesten-3-one	203-206	tubulin polymerization promoting protein	Homo sapiens	133-136
28352920-11	2017	The Ecm enhancement for sigma(HOCO+) at Ecm   0.5-5.0 eV can be attributed to the direct collision mechanism, whereas the formation of HOCO+ at low Ecm < 0.4 eV may involve a complex mechanism, which is mediated by the formation of a loosely sticking complex between HCO+ and OH.	7 alpha-hydroxy-4-cholesten-3-one	270-274	multimerin 1	Homo sapiens	4-7
28352920-11	2017	The Ecm enhancement for sigma(HOCO+) at Ecm   0.5-5.0 eV can be attributed to the direct collision mechanism, whereas the formation of HOCO+ at low Ecm < 0.4 eV may involve a complex mechanism, which is mediated by the formation of a loosely sticking complex between HCO+ and OH.	7 alpha-hydroxy-4-cholesten-3-one	270-274	multimerin 1	Homo sapiens	40-43
28352920-11	2017	The Ecm enhancement for sigma(HOCO+) at Ecm   0.5-5.0 eV can be attributed to the direct collision mechanism, whereas the formation of HOCO+ at low Ecm < 0.4 eV may involve a complex mechanism, which is mediated by the formation of a loosely sticking complex between HCO+ and OH.	7 alpha-hydroxy-4-cholesten-3-one	270-274	multimerin 1	Homo sapiens	40-43
27598558-1	2016	The serum concentration of 7alpha-hydroxy-4-cholesten-3-one (C4), a marker of cholesterol 7alpha-hydroxylase activity, has recently become an attractive diagnostic tool for researchers interested in cholesterol and bile acid metabolism.	7 alpha-hydroxy-4-cholesten-3-one	27-59	complement C4A (Rodgers blood group)	Homo sapiens	61-63
27598558-1	2016	The serum concentration of 7alpha-hydroxy-4-cholesten-3-one (C4), a marker of cholesterol 7alpha-hydroxylase activity, has recently become an attractive diagnostic tool for researchers interested in cholesterol and bile acid metabolism.	7 alpha-hydroxy-4-cholesten-3-one	27-59	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	78-108
27118869-10	2016	SLC26A3 as a tumour suppressor is restricted to colon; it is a Cl(-)/HCO(-) 3 exchanger, facilitating the efflux of HCO(-) 3 The likely mechanism for the tumour-suppressive function of SLC26A3 is related to intracellular pH regulation.	7 alpha-hydroxy-4-cholesten-3-one	69-72	solute carrier family 26 member 3	Homo sapiens	0-7
27118869-10	2016	SLC26A3 as a tumour suppressor is restricted to colon; it is a Cl(-)/HCO(-) 3 exchanger, facilitating the efflux of HCO(-) 3 The likely mechanism for the tumour-suppressive function of SLC26A3 is related to intracellular pH regulation.	7 alpha-hydroxy-4-cholesten-3-one	69-72	solute carrier family 26 member 3	Homo sapiens	185-192
27106353-4	2016	The plasma concentration of 7alpha-hydroxy-4-cholesten-3-one (C4), a marker of CYP7A1 activity, was determined in all the experiments at 90-min intervals.	7 alpha-hydroxy-4-cholesten-3-one	28-60	complement C4A (Rodgers blood group)	Homo sapiens	62-64
26180239-12	2015	We conclude that HMGB1 inhibits MTAL HCO(3)(-) absorption through a RAGE-dependent pathway distinct from TLR4-mediated inhibition by LPS.	7 alpha-hydroxy-4-cholesten-3-one	37-40	high mobility group box 1	Mus musculus	17-22
26233137-2	2015	This potential energy surface is used in low energy quantum scattering calculations to provide a set of (de)-excitation cross sections and rate coefficients among the first 20 rotational levels of HCS(+) by He in the range of temperature from 5 K to 100 K. The paper discusses the impact of the new ab initio potential energy surface on the cross sections at low energy and provides a comparison with the HCO(+)-He system.	7 alpha-hydroxy-4-cholesten-3-one	405-408	holocarboxylase synthetase	Homo sapiens	197-200
26332081-10	2015	Our simulations suggest that the intense fluctuations in intra and extracellular concentrations of Na(+), K(+) and Cl(-) that accompany NEA are able to affect the combined action of the Na(+)/H(+) exchanger (NHE), [HCO(-)(3)]/Cl(-) exchanger (HCE), H(+) pump and the catalytic activity of intra and extracellular carbonic anhydrase.	7 alpha-hydroxy-4-cholesten-3-one	215-218	solute carrier family 9 member C1	Homo sapiens	208-211
26332081-10	2015	Our simulations suggest that the intense fluctuations in intra and extracellular concentrations of Na(+), K(+) and Cl(-) that accompany NEA are able to affect the combined action of the Na(+)/H(+) exchanger (NHE), [HCO(-)(3)]/Cl(-) exchanger (HCE), H(+) pump and the catalytic activity of intra and extracellular carbonic anhydrase.	7 alpha-hydroxy-4-cholesten-3-one	215-218	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	243-246
26157392-1	2015	Congenital chloride diarrhea is an autosomal recessive disease caused by mutations in the intestinal lumenal membrane Cl(-)/HCO(-) 3 exchanger, SLC26A3.	7 alpha-hydroxy-4-cholesten-3-one	124-127	solute carrier family 26 member 3	Homo sapiens	144-151
25611968-5	2015	The temperature range of available direct rate constant data of the high-temperature key reaction HCO + O2   CO + HO2 has been extended up to 1705 K and confirms a temperature dependence consistent with a dominating direct abstraction channel.	7 alpha-hydroxy-4-cholesten-3-one	98-101	heme oxygenase 2	Homo sapiens	114-117
25257781-1	2014	Anion exchanger 1 (AE1) is a 95 kDa glycoprotein that facilitates Cl(-)=HCO(-)(3) exchange across the erythrocyte plasma membrane.	7 alpha-hydroxy-4-cholesten-3-one	72-75	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	0-17
25257781-1	2014	Anion exchanger 1 (AE1) is a 95 kDa glycoprotein that facilitates Cl(-)=HCO(-)(3) exchange across the erythrocyte plasma membrane.	7 alpha-hydroxy-4-cholesten-3-one	72-75	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	19-22
24478712-2	2013	It has been demonstrated the existence of at least two functional isoforms, one that promotes the co-influx of 1 molecule of Na(+) per 1 molecule of HCO(-) 3 (electroneutral isoform; NBCn1) and the other one that generates the co-influx of 1 molecule of Na(+) per 2 molecules of HCO(-) 3 (electrogenic isoform; NBCe1).	7 alpha-hydroxy-4-cholesten-3-one	149-155	solute carrier family 4 member 7	Homo sapiens	183-188
25080475-5	2014	Administration of M70 in healthy human volunteers potently reduces serum levels of 7alpha-hydroxy-4-cholesten-3-one, a surrogate marker for the hepatic activity of cholesterol 7alpha-hydroxylase (CYP7A1), the enzyme responsible for catalyzing the first and rate-limiting step in the classical bile acid synthetic pathway.	7 alpha-hydroxy-4-cholesten-3-one	83-115	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	196-202
24478712-2	2013	It has been demonstrated the existence of at least two functional isoforms, one that promotes the co-influx of 1 molecule of Na(+) per 1 molecule of HCO(-) 3 (electroneutral isoform; NBCn1) and the other one that generates the co-influx of 1 molecule of Na(+) per 2 molecules of HCO(-) 3 (electrogenic isoform; NBCe1).	7 alpha-hydroxy-4-cholesten-3-one	279-285	solute carrier family 4 member 7	Homo sapiens	183-188
24478713-6	2013	Analysis of HCO(-) 3 transport systems and pHi regulation in cholangiocytes from normal and Ae2 (-/-) a,b mice confirmed that AE2 is the transporter responsible for the Cl(-)/HCO(-) 3exchange in these cells.	7 alpha-hydroxy-4-cholesten-3-one	12-15	solute carrier family 4 (anion exchanger), member 2	Mus musculus	126-129
21976599-0	2012	Participation of the Cl-/HCO(3)- exchangers SLC26A3 and SLC26A6, the Cl- channel CFTR, and the regulatory factor SLC9A3R1 in mouse sperm capacitation.	7 alpha-hydroxy-4-cholesten-3-one	25-28	solute carrier family 26, member 3	Mus musculus	44-51
23121098-1	2013	Building on previous studies involving coupled cluster quartic force fields for the description of spectroscopic constants and vibrational frequencies of astronomically relevant molecules, this work applies the same techniques to the elucidation of such properties for the bent 1 (3)A" state of HCN and the isoelectronic 1 (3)A" HCO(+).	7 alpha-hydroxy-4-cholesten-3-one	329-332	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	295-298
23926603-4	2013	report on the function of an exciting new paracrine mediator, the mitochondrial the citric acid(TCA) cycle intermediate alpha-ketoglutarate (alphaKG), which via its OXGR1 receptor plays an unexpected, nontraditional role in the adaptive regulation of renal HCO(3-) secretion and salt reabsorption.	7 alpha-hydroxy-4-cholesten-3-one	257-260	oxoglutarate receptor 1	Homo sapiens	165-170
23324180-1	2013	In the basolateral membrane of proximal-tubule cells, NBCe1-A (SLC4A4, variant A), operating with an apparent Na(+):HCO(3)(-) stoichiometry of 1:3, contributes to the reclamation of HCO(3)(-) from the glomerular filtrate, thereby preventing whole body acidosis.	7 alpha-hydroxy-4-cholesten-3-one	116-119	solute carrier family 4 member 4	Homo sapiens	54-61
23324180-1	2013	In the basolateral membrane of proximal-tubule cells, NBCe1-A (SLC4A4, variant A), operating with an apparent Na(+):HCO(3)(-) stoichiometry of 1:3, contributes to the reclamation of HCO(3)(-) from the glomerular filtrate, thereby preventing whole body acidosis.	7 alpha-hydroxy-4-cholesten-3-one	116-119	solute carrier family 4 member 4	Homo sapiens	63-69
23111110-5	2013	Accumulation of 7alpha-hydroxy-4-cholesten-3-one in patients with lack of sterol 27-hydroxylase (Cerebrotendinous xanthomatosis was shown to be an important pathogenetic factor.	7 alpha-hydroxy-4-cholesten-3-one	16-48	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	74-95
22890707-8	2012	These data therefore suggest that prestin can act as a weak Cl(-)/HCO(3)(-) antiporter and it is proposed that, in addition to participating in wide band cochlear sound amplification, prestin may also be involved in the slow time scale (>10 s) phenomena where changes in cell stiffness and internal pressure have been implicated.	7 alpha-hydroxy-4-cholesten-3-one	66-69	solute carrier family 26 member 5	Homo sapiens	34-41
22908201-4	2012	CFTR mediates the exit of both HCO(3)(-) and Cl(-) across the apical membrane.	7 alpha-hydroxy-4-cholesten-3-one	31-35	CF transmembrane conductance regulator	Homo sapiens	0-4
22455795-1	2012	Anion metathesis of imidazol(in)ium chlorides with KHCO(3) afforded an easy one step access to air stable imidazol(in)ium hydrogen carbonates, denoted as [NHC(H)][HCO(3)].	7 alpha-hydroxy-4-cholesten-3-one	52-55	high mobility group nucleosomal binding domain 4	Homo sapiens	155-158
23750782-4	2013	The commonly used AGN tracer HCN/HCO+ is strongly time-dependent, with ratios that vary over orders of magnitude for times longer than 10(4) years.	7 alpha-hydroxy-4-cholesten-3-one	33-37	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	29-32
23945020-5	2013	Reduction of HCo(III) also results in cleavage of the H-Co bond from HCo(II) or HCo(I), leading to formation of the Co(I) complex [Co(I)(L2)(CH3CN)](+).	7 alpha-hydroxy-4-cholesten-3-one	13-16	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	81-86
23945020-5	2013	Reduction of HCo(III) also results in cleavage of the H-Co bond from HCo(II) or HCo(I), leading to formation of the Co(I) complex [Co(I)(L2)(CH3CN)](+).	7 alpha-hydroxy-4-cholesten-3-one	13-16	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	116-121
23945020-5	2013	Reduction of HCo(III) also results in cleavage of the H-Co bond from HCo(II) or HCo(I), leading to formation of the Co(I) complex [Co(I)(L2)(CH3CN)](+).	7 alpha-hydroxy-4-cholesten-3-one	69-72	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	116-121
23945020-5	2013	Reduction of HCo(III) also results in cleavage of the H-Co bond from HCo(II) or HCo(I), leading to formation of the Co(I) complex [Co(I)(L2)(CH3CN)](+).	7 alpha-hydroxy-4-cholesten-3-one	69-72	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	116-121
23574760-6	2013	The concentration of 7alpha-hydroxy-4-cholesten-3-one (C4), a marker for hepatic bile acid biosynthesis, was significantly elevated, whereas the levels of fibroblast growth factor 19 (FGF19), a marker for intestinal bile acid flux, were reduced in patients with CD compared with patients with UC and controls.	7 alpha-hydroxy-4-cholesten-3-one	21-53	complement C4A (Rodgers blood group)	Homo sapiens	55-57
23019197-8	2012	The further knockout of p21, which is a downstream effector of telomere shortening-induced senescence, rescued villus atrophy of duodenal mucosa, and basal and forskolin-stimulated duodenal HCO(3)(-) secretion and I(sc) in mTERC(-/-) p21(-/-) double-knockout mice were not different from wild-type controls.	7 alpha-hydroxy-4-cholesten-3-one	190-193	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	24-27
22802585-11	2012	Basolateral Cl(-)/HCO(3)(-) exchange measured by basolateral pH-stat in cells with permeabilized apical membranes was abolished in AE2-KD monolayers, and the intracellular alkalinization resulting from basolateral Cl(-) removal was reduced by ~80% in AE2-KD cells.	7 alpha-hydroxy-4-cholesten-3-one	18-22	solute carrier family 4 member 2	Homo sapiens	131-134
22895259-0	2012	Deletion of Slc26a6 alters the stoichiometry of apical Cl-/HCO-3 exchange in mouse pancreatic duct.	7 alpha-hydroxy-4-cholesten-3-one	59-62	solute carrier family 26, member 6	Mus musculus	12-19
22185591-13	2012	Serum VEGF inversely correlated with TLC, pH, PO(2) and HCO(3), and positively correlated with PCo(2) and FiO(2).	7 alpha-hydroxy-4-cholesten-3-one	56-59	vascular endothelial growth factor A	Homo sapiens	6-10
22357733-2	2012	Previous studies have shown that the choroid plexus epithelium (CPE) from mice lacking the Na(+)-dependent Cl(-)/HCO(3)(-) exchanger (NCBE) encoded by Slc4a10 leads to retargeting of the Na(+)/H(+) exchanger 1 (NHE1) from the luminal to the basolateral plasma membrane.	7 alpha-hydroxy-4-cholesten-3-one	113-116	solute carrier family 4, sodium bicarbonate cotransporter-like, member 10	Mus musculus	151-158
22159080-10	2012	Kinetic analysis of HCO(3)(-) currents reveals that fNBCe1 has a much higher transport capacity (higher maximum current) and lower affinity (higher K(m)) than human kidney NBCe1 (hkNBCe1) does in the physiological range (membrane potential = -80 mV; [HCO(3)(-)] = 10 mM).	7 alpha-hydroxy-4-cholesten-3-one	20-23	solute carrier family 4 member 4 S homeolog	Xenopus laevis	53-58
22159080-10	2012	Kinetic analysis of HCO(3)(-) currents reveals that fNBCe1 has a much higher transport capacity (higher maximum current) and lower affinity (higher K(m)) than human kidney NBCe1 (hkNBCe1) does in the physiological range (membrane potential = -80 mV; [HCO(3)(-)] = 10 mM).	7 alpha-hydroxy-4-cholesten-3-one	251-254	solute carrier family 4 member 4 S homeolog	Xenopus laevis	53-58
22331414-1	2012	The renal electrogenic Na(+)/HCO(3)(-) cotransporter (NBCe1-A) contributes to the basolateral step of transepithelial HCO(3)(-) reabsorption in proximal tubule epithelia, contributing to the buffering of blood pH.	7 alpha-hydroxy-4-cholesten-3-one	29-32	solute carrier family 4 member 4 L homeolog	Xenopus laevis	54-59
21976599-0	2012	Participation of the Cl-/HCO(3)- exchangers SLC26A3 and SLC26A6, the Cl- channel CFTR, and the regulatory factor SLC9A3R1 in mouse sperm capacitation.	7 alpha-hydroxy-4-cholesten-3-one	25-28	solute carrier family 26, member 6	Mus musculus	56-63
21595652-1	2011	BACKGROUND AND PURPOSE: Na(+) /HCO(3) (-) co-transport (NBC) regulates intracellular pH (pH(i) ) in the heart.	7 alpha-hydroxy-4-cholesten-3-one	31-34	glucose-6-phosphate isomerase	Homo sapiens	89-94
21871436-1	2011	Impaired trafficking of human kidney anion exchanger 1 (kAE1) to the basolateral membrane of alpha-intercalated cells of the kidney collecting duct leads to the defect of the Cl(-)/HCO(3)(-) exchange and the failure of proton (H(+)) secretion at the apical membrane of these cells, causing distal renal tubular acidosis (dRTA).	7 alpha-hydroxy-4-cholesten-3-one	181-184	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	37-54
21914796-6	2011	Pendrin-mediated anion exchange activity was confirmed by shRNA pendrin knockdown (KD), which markedly reduced cAMP-activated Cl(-)/HCO(3)(-) exchange.	7 alpha-hydroxy-4-cholesten-3-one	132-135	solute carrier family 26 member 4	Homo sapiens	0-7
21914796-6	2011	Pendrin-mediated anion exchange activity was confirmed by shRNA pendrin knockdown (KD), which markedly reduced cAMP-activated Cl(-)/HCO(3)(-) exchange.	7 alpha-hydroxy-4-cholesten-3-one	132-135	solute carrier family 26 member 4	Homo sapiens	64-71
21997505-2	2011	identify Slc26a11, a novel member of the Slc26 anion exchanger family, as an electrogenic (Cl(-))(n)/HCO(3)(-) exchanger.	7 alpha-hydroxy-4-cholesten-3-one	101-104	solute carrier family 26 member 11	Homo sapiens	9-17
21593449-2	2011	Optimal stimulation of pancreatic HCO(3)(-) secretion likely requires coupled activities of the cystic fibrosis transmembrane regulator (CFTR) anion channel and apical SLC26 Cl(-)/HCO(3)(-) exchangers.	7 alpha-hydroxy-4-cholesten-3-one	34-37	CF transmembrane conductance regulator	Homo sapiens	137-141
21593481-6	2011	Vas deferens epithelial cells were isolated and electrophysiological results support that CFTR(-/-) monolayers can exhibit Na(+) reabsorption but reveal no anion secretion following exposure to cAMP-generating compounds, suggesting that CFTR-dependent Cl(-) and/or HCO(3)(-) transport is completely impaired.	7 alpha-hydroxy-4-cholesten-3-one	265-268	CF transmembrane conductance regulator	Sus scrofa	90-94
21679700-7	2011	7alpha-Hydroxy-4-cholesten-3-one, an early bile acid synthesis marker, showed an inverse response with a significant decrease at 60 min which proves the efficient and rapid downregulation of CYP7A1 via FXR activation through bile acid signaling.	7 alpha-hydroxy-4-cholesten-3-one	0-32	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	191-197
21679700-7	2011	7alpha-Hydroxy-4-cholesten-3-one, an early bile acid synthesis marker, showed an inverse response with a significant decrease at 60 min which proves the efficient and rapid downregulation of CYP7A1 via FXR activation through bile acid signaling.	7 alpha-hydroxy-4-cholesten-3-one	0-32	nuclear receptor subfamily 1 group H member 4	Homo sapiens	202-205
21543742-11	2011	Taken together, these data suggest that association of functional CAII with AE1 increases Cl(-)/HCO(3)(-) exchange activity, consistent with the HCO(3)(-) transport metabolon model.	7 alpha-hydroxy-4-cholesten-3-one	96-99	carbonic anhydrase 2	Homo sapiens	66-70
21543742-11	2011	Taken together, these data suggest that association of functional CAII with AE1 increases Cl(-)/HCO(3)(-) exchange activity, consistent with the HCO(3)(-) transport metabolon model.	7 alpha-hydroxy-4-cholesten-3-one	96-99	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	76-79
21543742-11	2011	Taken together, these data suggest that association of functional CAII with AE1 increases Cl(-)/HCO(3)(-) exchange activity, consistent with the HCO(3)(-) transport metabolon model.	7 alpha-hydroxy-4-cholesten-3-one	145-148	carbonic anhydrase 2	Homo sapiens	66-70
21571816-1	2011	The electroneutral Na(+)-HCO(3)(-) cotransporter NBCn1 (SLC4A7) contributes to intracellular pH maintenance and transepithelial HCO(3)(-) movement.	7 alpha-hydroxy-4-cholesten-3-one	25-28	solute carrier family 4, sodium bicarbonate cotransporter, member 7 L homeolog	Xenopus laevis	49-54
21543742-11	2011	Taken together, these data suggest that association of functional CAII with AE1 increases Cl(-)/HCO(3)(-) exchange activity, consistent with the HCO(3)(-) transport metabolon model.	7 alpha-hydroxy-4-cholesten-3-one	145-148	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	76-79
21571816-1	2011	The electroneutral Na(+)-HCO(3)(-) cotransporter NBCn1 (SLC4A7) contributes to intracellular pH maintenance and transepithelial HCO(3)(-) movement.	7 alpha-hydroxy-4-cholesten-3-one	25-28	solute carrier family 4, sodium bicarbonate cotransporter, member 7 L homeolog	Xenopus laevis	56-62
21474426-9	2011	Genistein, an activator of CFTR, which does not increase intracellular cAMP, also stimulated HCO(3)(-) secretion, whereas glibenclamide, a Cl(-) channel blocker, and bumetanide, a Na(+)-K(+)-2Cl(-) blocker, decreased it.	7 alpha-hydroxy-4-cholesten-3-one	93-96	CF transmembrane conductance regulator	Homo sapiens	27-31
21427702-2	2011	We screened for Caenorhabditis elegans mutants defective for inhibitory neurotransmission and identified mutations in ABTS-1, a Na(+)-driven Cl(-)-HCO(3)(-) exchanger that extrudes chloride from cells, like KCC-2, but also alkalinizes them.	7 alpha-hydroxy-4-cholesten-3-one	147-150	Anion exchange protein	Caenorhabditis elegans	118-124
21413028-13	2011	The exchanger AE2 also occurred on the basolateral surface of osteoblasts, consistent with Cl(-) /HCO 3- exchange for elimination of metabolic carbonate.	7 alpha-hydroxy-4-cholesten-3-one	98-101	solute carrier family 4 member 2	Homo sapiens	14-17
21394828-2	2011	Life-long secretory diarrhea is caused by mutations in the solute carrier family 26 member 3 (SLC26A3) gene disrupting the epithelial Cl(-) /HCO 3- transport in the ileum and colon.	7 alpha-hydroxy-4-cholesten-3-one	141-144	solute carrier family 26 member 3	Homo sapiens	59-92
21394828-2	2011	Life-long secretory diarrhea is caused by mutations in the solute carrier family 26 member 3 (SLC26A3) gene disrupting the epithelial Cl(-) /HCO 3- transport in the ileum and colon.	7 alpha-hydroxy-4-cholesten-3-one	141-144	solute carrier family 26 member 3	Homo sapiens	94-101
21427702-2	2011	We screened for Caenorhabditis elegans mutants defective for inhibitory neurotransmission and identified mutations in ABTS-1, a Na(+)-driven Cl(-)-HCO(3)(-) exchanger that extrudes chloride from cells, like KCC-2, but also alkalinizes them.	7 alpha-hydroxy-4-cholesten-3-one	147-150	K+/Cl- Cotransporter	Caenorhabditis elegans	207-212
22116353-13	2011	In conclusion, systemic pH, the hormone aldosterone, and the peptide UGN influence renal tubular pendrin gene expression and, perhaps, pendrin-mediated Cl(-)/HCO(3)(-) exchange at the transcriptional level.	7 alpha-hydroxy-4-cholesten-3-one	158-161	guanylate cyclase activator 2B	Homo sapiens	69-72
21345585-4	2011	Since the uptake of As(V) should be interfered by several anions of natural occurrence in waters, the effect of Cl(-), SO(4)(2-), NO(3)(-), HPO(4)(2-), HCO(3)(-) on retention was evaluated and discussed.	7 alpha-hydroxy-4-cholesten-3-one	152-155	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	20-25
21054167-4	2011	This transport is mediated by apical Na(+)/H(+) (NHE2/3) and Cl(-)/HCO(3)(-) (Slc26a3/a6 and others) exchangers that provide the major route of NaCl absorption.	7 alpha-hydroxy-4-cholesten-3-one	67-70	solute carrier family 26 member 3	Homo sapiens	78-85
21317537-2	2011	Secretion of ductal fluid and HCO(3)(-) in secretory glands is fueled by Na(+)/HCO(3)(-) cotransport mediated by basolateral solute carrier family 4 member 4 (NBCe1-B) and by Cl(-)/HCO(3)(-) exchange mediated by luminal solute carrier family 26, member 6 (Slc26a6) and CFTR.	7 alpha-hydroxy-4-cholesten-3-one	30-33	solute carrier family 4 (anion exchanger), member 4	Mus musculus	125-157
21317537-2	2011	Secretion of ductal fluid and HCO(3)(-) in secretory glands is fueled by Na(+)/HCO(3)(-) cotransport mediated by basolateral solute carrier family 4 member 4 (NBCe1-B) and by Cl(-)/HCO(3)(-) exchange mediated by luminal solute carrier family 26, member 6 (Slc26a6) and CFTR.	7 alpha-hydroxy-4-cholesten-3-one	30-33	solute carrier family 26, member 6	Mus musculus	220-254
21317537-2	2011	Secretion of ductal fluid and HCO(3)(-) in secretory glands is fueled by Na(+)/HCO(3)(-) cotransport mediated by basolateral solute carrier family 4 member 4 (NBCe1-B) and by Cl(-)/HCO(3)(-) exchange mediated by luminal solute carrier family 26, member 6 (Slc26a6) and CFTR.	7 alpha-hydroxy-4-cholesten-3-one	30-33	solute carrier family 26, member 6	Mus musculus	256-263
21317537-2	2011	Secretion of ductal fluid and HCO(3)(-) in secretory glands is fueled by Na(+)/HCO(3)(-) cotransport mediated by basolateral solute carrier family 4 member 4 (NBCe1-B) and by Cl(-)/HCO(3)(-) exchange mediated by luminal solute carrier family 26, member 6 (Slc26a6) and CFTR.	7 alpha-hydroxy-4-cholesten-3-one	30-33	cystic fibrosis transmembrane conductance regulator	Mus musculus	269-273
21317537-2	2011	Secretion of ductal fluid and HCO(3)(-) in secretory glands is fueled by Na(+)/HCO(3)(-) cotransport mediated by basolateral solute carrier family 4 member 4 (NBCe1-B) and by Cl(-)/HCO(3)(-) exchange mediated by luminal solute carrier family 26, member 6 (Slc26a6) and CFTR.	7 alpha-hydroxy-4-cholesten-3-one	79-82	solute carrier family 4 (anion exchanger), member 4	Mus musculus	125-157
21317537-2	2011	Secretion of ductal fluid and HCO(3)(-) in secretory glands is fueled by Na(+)/HCO(3)(-) cotransport mediated by basolateral solute carrier family 4 member 4 (NBCe1-B) and by Cl(-)/HCO(3)(-) exchange mediated by luminal solute carrier family 26, member 6 (Slc26a6) and CFTR.	7 alpha-hydroxy-4-cholesten-3-one	79-82	solute carrier family 26, member 6	Mus musculus	220-254
21317537-2	2011	Secretion of ductal fluid and HCO(3)(-) in secretory glands is fueled by Na(+)/HCO(3)(-) cotransport mediated by basolateral solute carrier family 4 member 4 (NBCe1-B) and by Cl(-)/HCO(3)(-) exchange mediated by luminal solute carrier family 26, member 6 (Slc26a6) and CFTR.	7 alpha-hydroxy-4-cholesten-3-one	79-82	solute carrier family 26, member 6	Mus musculus	256-263
21317537-2	2011	Secretion of ductal fluid and HCO(3)(-) in secretory glands is fueled by Na(+)/HCO(3)(-) cotransport mediated by basolateral solute carrier family 4 member 4 (NBCe1-B) and by Cl(-)/HCO(3)(-) exchange mediated by luminal solute carrier family 26, member 6 (Slc26a6) and CFTR.	7 alpha-hydroxy-4-cholesten-3-one	79-82	cystic fibrosis transmembrane conductance regulator	Mus musculus	269-273
22116364-5	2011	First, pendrin-mediated Cl(-) transport is coupled with Na(+) reabsorption by the Na(+)-dependent Cl(-)/HCO(3)(-) exchanger NDCBE to mediate NaCl reabsorption in B-ICs.	7 alpha-hydroxy-4-cholesten-3-one	104-107	solute carrier family 26, member 4	Mus musculus	7-14
22116364-5	2011	First, pendrin-mediated Cl(-) transport is coupled with Na(+) reabsorption by the Na(+)-dependent Cl(-)/HCO(3)(-) exchanger NDCBE to mediate NaCl reabsorption in B-ICs.	7 alpha-hydroxy-4-cholesten-3-one	104-107	solute carrier family 4 (anion exchanger), member 8	Mus musculus	124-129
22116353-13	2011	In conclusion, systemic pH, the hormone aldosterone, and the peptide UGN influence renal tubular pendrin gene expression and, perhaps, pendrin-mediated Cl(-)/HCO(3)(-) exchange at the transcriptional level.	7 alpha-hydroxy-4-cholesten-3-one	158-161	solute carrier family 26 member 4	Homo sapiens	135-142
22116358-1	2011	Pendrin (SLC26A4, PDS) is an electroneutral anion exchanger transporting I(-), Cl(-), HCO(3)(-), OH(-), SCN(-) and formate.	7 alpha-hydroxy-4-cholesten-3-one	86-89	solute carrier family 26 member 4	Homo sapiens	0-7
22116358-1	2011	Pendrin (SLC26A4, PDS) is an electroneutral anion exchanger transporting I(-), Cl(-), HCO(3)(-), OH(-), SCN(-) and formate.	7 alpha-hydroxy-4-cholesten-3-one	86-89	solute carrier family 26 member 4	Homo sapiens	9-16
22116358-1	2011	Pendrin (SLC26A4, PDS) is an electroneutral anion exchanger transporting I(-), Cl(-), HCO(3)(-), OH(-), SCN(-) and formate.	7 alpha-hydroxy-4-cholesten-3-one	86-89	solute carrier family 26 member 4	Homo sapiens	18-21
21151921-3	2010	Here we reported the involvement of CFTR, a cAMP-activated anion channel conducting both Cl(-) and HCO(3)(-), in mediating prostate HCO(3)(-) secretion and its possible role in bacterial killing.	7 alpha-hydroxy-4-cholesten-3-one	99-102	CF transmembrane conductance regulator	Rattus norvegicus	36-40
21625623-5	2011	Inhibition of CFTR or depletion of HCO(3) (-) could reduce FSH-stimulated, sAC-dependent cAMP production and phosphorylation of CREB, the key transcription factor in spermatogenesis.	7 alpha-hydroxy-4-cholesten-3-one	35-38	adenylate cyclase 10	Rattus norvegicus	75-78
21625623-5	2011	Inhibition of CFTR or depletion of HCO(3) (-) could reduce FSH-stimulated, sAC-dependent cAMP production and phosphorylation of CREB, the key transcription factor in spermatogenesis.	7 alpha-hydroxy-4-cholesten-3-one	35-38	cAMP responsive element binding protein 1	Homo sapiens	128-132
20962000-6	2010	This was mediated via membrane Cl(-)/HCO(3)(-) exchange (the AE1 gene product), irrespective of whether recovery was from an intracellular acid or base load, and with no evident contribution from other transporters such as Na(+)/H(+) exchange.	7 alpha-hydroxy-4-cholesten-3-one	37-40	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	61-64