PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33810109-1	2021	Cystic fibrosis (CF) is the most common autosomal recessive disease in the Caucasian population and is caused by mutations in the CF transmembrane conductance regulator (CFTR) gene that encodes for a chloride/bicarbonate channel expressed on the membrane of epithelial cells of the airways and of the intestine, as well as in cells with exocrine and endocrine functions.	Bicarbonates	209-220	CF transmembrane conductance regulator	Homo sapiens	130-168	
1385255-3	1992	Evidence suggests that the cystic fibrosis transmembrane conductance regulator is a cyclic adenosine monophosphate-regulated Cl- conductance in the luminal membrane that plays a pivotal role in ductal bicarbonate secretion by recirculating the Cl- imported into duct cells through Cl(-)-HCO3- exchange.	Bicarbonates	201-212	CF transmembrane conductance regulator	Homo sapiens	27-78	
1385255-3	1992	Evidence suggests that the cystic fibrosis transmembrane conductance regulator is a cyclic adenosine monophosphate-regulated Cl- conductance in the luminal membrane that plays a pivotal role in ductal bicarbonate secretion by recirculating the Cl- imported into duct cells through Cl(-)-HCO3- exchange.	Bicarbonates	287-291	CF transmembrane conductance regulator	Homo sapiens	27-78	
7681623-6	1993	Physiologically, these CFTR channels act in parallel with chloride-bicarbonate exchangers to facilitate bicarbonate secretion across the apical plasma membrane of the duct cell.	Bicarbonates	67-78	CF transmembrane conductance regulator	Homo sapiens	23-27	
7681623-6	1993	Physiologically, these CFTR channels act in parallel with chloride-bicarbonate exchangers to facilitate bicarbonate secretion across the apical plasma membrane of the duct cell.	Bicarbonates	104-115	CF transmembrane conductance regulator	Homo sapiens	23-27	
33810109-1	2021	Cystic fibrosis (CF) is the most common autosomal recessive disease in the Caucasian population and is caused by mutations in the CF transmembrane conductance regulator (CFTR) gene that encodes for a chloride/bicarbonate channel expressed on the membrane of epithelial cells of the airways and of the intestine, as well as in cells with exocrine and endocrine functions.	Bicarbonates	209-220	CF transmembrane conductance regulator	Homo sapiens	170-174	
34668421-8	2021	Finally, we assess the impact of bicarbonate on the activity of SLC26A9 and CFTR.	Bicarbonates	33-44	CF transmembrane conductance regulator	Homo sapiens	76-80	
34922851-1	2021	BACKGROUND: In cystic fibrosis (CF), loss of CF transmembrane conductance regulator (CFTR)-dependent bicarbonate secretion precipitates the accumulation of viscous mucus in the lumen of respiratory and gastrointestinal epithelial tissues.	Bicarbonates	101-112	CF transmembrane conductance regulator	Homo sapiens	45-83	
34922851-1	2021	BACKGROUND: In cystic fibrosis (CF), loss of CF transmembrane conductance regulator (CFTR)-dependent bicarbonate secretion precipitates the accumulation of viscous mucus in the lumen of respiratory and gastrointestinal epithelial tissues.	Bicarbonates	101-112	CF transmembrane conductance regulator	Homo sapiens	85-89	
34922851-2	2021	We investigated whether the combination of elexacaftor (ELX), ivacaftor (IVA) and tezacaftor (TEZ), apart from its well-documented effect on chloride transport, also restores Phe508del-CFTR-mediated bicarbonate transport.	Bicarbonates	199-210	CF transmembrane conductance regulator	Homo sapiens	185-189	
34922851-6	2021	In biliary epithelium, it failed to enhance CFTR-mediated bicarbonate transport but effectively rescued CFTR-mediated chloride transport, known to be requisite for bicarbonate secretion through the chloride-bicarbonate exchanger AE2 (SLC4A2), which was highly expressed by cholangiocytes.	Bicarbonates	164-175	CF transmembrane conductance regulator	Homo sapiens	104-108	
34922851-6	2021	In biliary epithelium, it failed to enhance CFTR-mediated bicarbonate transport but effectively rescued CFTR-mediated chloride transport, known to be requisite for bicarbonate secretion through the chloride-bicarbonate exchanger AE2 (SLC4A2), which was highly expressed by cholangiocytes.	Bicarbonates	207-218	CF transmembrane conductance regulator	Homo sapiens	104-108	
34189282-4	2021	Since the apical HCO3 - efflux through CFTR often required the intracellular H+/HCO3 - production and/or the Na+-dependent basolateral HCO3 - uptake, the intracellular pH (pHi) balance might be disturbed, especially as a consequence of increased endogenous H+ and HCO3 - production.	Bicarbonates	17-21	CF transmembrane conductance regulator	Homo sapiens	39-43	
34407318-1	2021	Cystic fibrosis transmembrane conductance regulator (CFTR) modulators are small molecules that directly impact the CFTR protein, improving the function of the CFTR chloride and bicarbonate channel.	Bicarbonates	177-188	CF transmembrane conductance regulator	Homo sapiens	0-51	
34407318-1	2021	Cystic fibrosis transmembrane conductance regulator (CFTR) modulators are small molecules that directly impact the CFTR protein, improving the function of the CFTR chloride and bicarbonate channel.	Bicarbonates	177-188	CF transmembrane conductance regulator	Homo sapiens	53-57	
34407318-1	2021	Cystic fibrosis transmembrane conductance regulator (CFTR) modulators are small molecules that directly impact the CFTR protein, improving the function of the CFTR chloride and bicarbonate channel.	Bicarbonates	177-188	CF transmembrane conductance regulator	Homo sapiens	115-119	
34692569-3	2021	The loss of CFTR function alters chloride, bicarbonate, and water transport through the plasma membrane, promoting the production of a thick and sticky mucus in which bacteria including Pseudomonas aeruginosa and Burkholderia cenocepacia can produce chronic infections that eventually decrease the lung function and increase the risk of mortality.	Bicarbonates	43-54	CF transmembrane conductance regulator	Homo sapiens	12-16	
34326672-1	2021	Cystic fibrosis (CF) is a life-shortening monogenic disease caused by mutations in the gene encoding the CF transmembrane conductance regulator (CFTR) protein, an anion channel that transports chloride and bicarbonate across epithelia.	Bicarbonates	206-217	CF transmembrane conductance regulator	Homo sapiens	105-143	
34326672-1	2021	Cystic fibrosis (CF) is a life-shortening monogenic disease caused by mutations in the gene encoding the CF transmembrane conductance regulator (CFTR) protein, an anion channel that transports chloride and bicarbonate across epithelia.	Bicarbonates	206-217	CF transmembrane conductance regulator	Homo sapiens	145-149	
34090606-2	2021	Mutations in CFTR, the gene encoding the epithelial ion channel that normally transports chloride and bicarbonate, lead to impaired mucus hydration and clearance.	Bicarbonates	102-113	CF transmembrane conductance regulator	Homo sapiens	13-17	
34831067-7	2021	Yet, the CFTR protein also regulates numerous other pathways, such as the transport of HCO3-, glutathione and thiocyanate, immune cells, and the metabolism of lipids.	Bicarbonates	87-92	CF transmembrane conductance regulator	Homo sapiens	9-13	
34680949-1	2021	CFTR encodes for a chloride and bicarbonate channel expressed at the apical membrane of polarized epithelial cells.	Bicarbonates	32-43	CF transmembrane conductance regulator	Homo sapiens	0-4	
34166230-1	2021	Without CFTR-mediated HCO3- secretion, airway epithelia of newborns with cystic fibrosis (CF) produce an abnormally acidic airway surface liquid (ASL), and the decreased pH impairs respiratory host defenses.	Bicarbonates	22-26	CF transmembrane conductance regulator	Homo sapiens	8-12	
34027905-3	2021	RECENT FINDINGS: In the beta-intercalated cells of the collecting duct , CFTR functions in very similar terms as established in the exocrine pancreatic duct and both CFTR and SLC26A4 (pendrin) orchestrate regulated HCO3- secretion.	Bicarbonates	215-219	CF transmembrane conductance regulator	Homo sapiens	166-170	
34202364-1	2021	Cystic fibrosis (CF) is an autosomal recessive disease caused by mutations in the cystic fibrosis transmembrane regulator (CFTR) gene: the gene product responsible for transporting chloride and bicarbonate ions through the apical membrane of most epithelial cells.	Bicarbonates	194-205	CF transmembrane conductance regulator	Homo sapiens	82-121	
34202364-1	2021	Cystic fibrosis (CF) is an autosomal recessive disease caused by mutations in the cystic fibrosis transmembrane regulator (CFTR) gene: the gene product responsible for transporting chloride and bicarbonate ions through the apical membrane of most epithelial cells.	Bicarbonates	194-205	CF transmembrane conductance regulator	Homo sapiens	123-127	
34189282-4	2021	Since the apical HCO3 - efflux through CFTR often required the intracellular H+/HCO3 - production and/or the Na+-dependent basolateral HCO3 - uptake, the intracellular pH (pHi) balance might be disturbed, especially as a consequence of increased endogenous H+ and HCO3 - production.	Bicarbonates	80-86	CF transmembrane conductance regulator	Homo sapiens	39-43	
34189282-4	2021	Since the apical HCO3 - efflux through CFTR often required the intracellular H+/HCO3 - production and/or the Na+-dependent basolateral HCO3 - uptake, the intracellular pH (pHi) balance might be disturbed, especially as a consequence of increased endogenous H+ and HCO3 - production.	Bicarbonates	135-141	CF transmembrane conductance regulator	Homo sapiens	39-43	
34189282-4	2021	Since the apical HCO3 - efflux through CFTR often required the intracellular H+/HCO3 - production and/or the Na+-dependent basolateral HCO3 - uptake, the intracellular pH (pHi) balance might be disturbed, especially as a consequence of increased endogenous H+ and HCO3 - production.	Bicarbonates	264-270	CF transmembrane conductance regulator	Homo sapiens	39-43	
34068986-9	2021	We suggest that cinnamaldehyde stimulates the secretion of HCO3- via apical CFTR and basolateral Na+-HCO3- cotransport, preventing acidosis and damage to the epithelium and the colonic microbiome.	Bicarbonates	59-63	CF transmembrane conductance regulator	Homo sapiens	76-80	
34707004-2	2021	Cystic fibrosis transmembrane conduction regulator (CFTR) is an apical membrane chloride channel, which is very important for the regulation of epithelial fluid, chloride ion, and bicarbonate transport.	Bicarbonates	180-191	CF transmembrane conductance regulator	Homo sapiens	52-56	
35453033-1	2022	Defects of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) protein affect the homeostasis of chloride, bicarbonate, sodium, and water in the airway surface liquid, influencing the mucus composition and viscosity, which induces a severe condition of infection and inflammation along the whole life of CF patients.	Bicarbonates	123-134	CF transmembrane conductance regulator	Homo sapiens	15-71	
35623009-1	2022	INTRODUCTION: Cystic fibrosis transmembrane conductance regulator (CFTR)-mediated chloride and bicarbonate secretion is integral to the pancreas" ability to produce the alkaline pancreatic juice required for proper activation of enzymes for digestion.	Bicarbonates	95-106	CF transmembrane conductance regulator	Homo sapiens	14-65	
35623009-1	2022	INTRODUCTION: Cystic fibrosis transmembrane conductance regulator (CFTR)-mediated chloride and bicarbonate secretion is integral to the pancreas" ability to produce the alkaline pancreatic juice required for proper activation of enzymes for digestion.	Bicarbonates	95-106	CF transmembrane conductance regulator	Homo sapiens	67-71	
35453033-1	2022	Defects of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) protein affect the homeostasis of chloride, bicarbonate, sodium, and water in the airway surface liquid, influencing the mucus composition and viscosity, which induces a severe condition of infection and inflammation along the whole life of CF patients.	Bicarbonates	123-134	CF transmembrane conductance regulator	Homo sapiens	73-77	
34990652-1	2022	An attractive approach to treat people with Cystic Fibrosis (CF), a life-shortening disease caused by mutant CFTR, is to compensate for the absence of this chloride/bicarbonate channel by activating alternative (non-CFTR) chloride channels.	Bicarbonates	165-176	CF transmembrane conductance regulator	Homo sapiens	109-113	
35392868-4	2022	We hypothesize that bicarbonate-containing aerosols could be beneficial for patients with CFTR dysfunctions.	Bicarbonates	20-31	CF transmembrane conductance regulator	Homo sapiens	90-94	
35455747-6	2022	The effect of the CFTR modulator combination ELX/TEZ/IVA on CFTR-mediated Cl- and HCO3- secretion was assessed in organoid-derived intestinal epithelial monolayers.	Bicarbonates	82-86	CF transmembrane conductance regulator	Homo sapiens	60-64	
35455747-9	2022	RESULTS: ELX/TEZ/IVA markedly enhanced CFTR-mediated bicarbonate and chloride transport across intestinal epithelium of both patients.	Bicarbonates	53-64	CF transmembrane conductance regulator	Homo sapiens	39-43	
35455747-11	2022	CONCLUSIONS: Current measurements in organoid-derived intestinal monolayers can readily be used to monitor CFTR-dependent epithelial Cl- and HCO3- transport.	Bicarbonates	141-146	CF transmembrane conductance regulator	Homo sapiens	107-111	
35156780-1	2022	Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) is a chloride and bicarbonate channel in secretory epithelia with a critical role in maintaining fluid homeostasis.	Bicarbonates	77-88	CF transmembrane conductance regulator	Homo sapiens	0-51	
35269829-1	2022	The multi-organ disease cystic fibrosis (CF) is caused by mutations in the gene encoding the CF transmembrane conductance regulator (CFTR) protein, a cAMP regulated chloride (Cl-) and bicarbonate (HCO3-) ion channel expressed at the apical plasma membrane (PM) of epithelial cells.	Bicarbonates	184-195	CF transmembrane conductance regulator	Homo sapiens	93-131	
35269829-1	2022	The multi-organ disease cystic fibrosis (CF) is caused by mutations in the gene encoding the CF transmembrane conductance regulator (CFTR) protein, a cAMP regulated chloride (Cl-) and bicarbonate (HCO3-) ion channel expressed at the apical plasma membrane (PM) of epithelial cells.	Bicarbonates	197-202	CF transmembrane conductance regulator	Homo sapiens	93-131	
35269829-1	2022	The multi-organ disease cystic fibrosis (CF) is caused by mutations in the gene encoding the CF transmembrane conductance regulator (CFTR) protein, a cAMP regulated chloride (Cl-) and bicarbonate (HCO3-) ion channel expressed at the apical plasma membrane (PM) of epithelial cells.	Bicarbonates	197-202	CF transmembrane conductance regulator	Homo sapiens	133-137	
35227018-3	2022	While pendrin drives chloride reabsorption and bicarbonate, thiocyanate or iodide secretion within the apical compartment, CFTR represents a pathway for the apical efflux of chloride, bicarbonate, and possibly iodide.	Bicarbonates	184-195	CF transmembrane conductance regulator	Homo sapiens	123-127	
35227018-4	2022	In the airways, pendrin and CFTR seems to be involved in alkalinization of the apical fluid via bicarbonate secretion, especially during inflammation, while CFTR also controls the volume of the apical fluid via a cAMP-dependent chloride secretion, which is stimulated by pendrin.	Bicarbonates	96-107	CF transmembrane conductance regulator	Homo sapiens	28-32	
35156780-1	2022	Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) is a chloride and bicarbonate channel in secretory epithelia with a critical role in maintaining fluid homeostasis.	Bicarbonates	77-88	CF transmembrane conductance regulator	Homo sapiens	53-57	
33861752-4	2021	The cystic fibrosis transmembrane conductance regulator (CFTR), an anion channel widely distributed at the apical membrane of epithelial cells, plays a crucial role in mediating the secretion of Cl- and HCO3-.	Bicarbonates	203-208	CF transmembrane conductance regulator	Homo sapiens	57-61	
33963548-0	2021	The molecular mechanism of CFTR- and secretin-dependent renal bicarbonate excretion.	Bicarbonates	62-73	CF transmembrane conductance regulator	Homo sapiens	27-31	
33963548-1	2021	This review summarizes the newly discovered molecular mechanism of secretin-stimulated urine HCO3 - excretion and the role of CFTR in renal HCO3 - excretion.	Bicarbonates	140-144	CF transmembrane conductance regulator	Homo sapiens	126-130	
33949881-1	2021	Cystic fibrosis is a deadly multi-organ disorder caused by loss of function mutations in the gene that encodes for the cystic fibrosis transmembrane conductance regulator (CFTR) chloride/bicarbonate ion channel.	Bicarbonates	187-198	CF transmembrane conductance regulator	Homo sapiens	119-170	
33949881-1	2021	Cystic fibrosis is a deadly multi-organ disorder caused by loss of function mutations in the gene that encodes for the cystic fibrosis transmembrane conductance regulator (CFTR) chloride/bicarbonate ion channel.	Bicarbonates	187-198	CF transmembrane conductance regulator	Homo sapiens	172-176	
33655768-0	2021	Impact of hypoxia and AMPK on CFTR-mediated bicarbonate secretion in human cholangiocyte organoids.	Bicarbonates	44-55	CF transmembrane conductance regulator	Homo sapiens	30-34	
33655768-1	2021	BACKGROUND AND AIMS: Cholangiocytes express cystic fibrosis transmembrane conductance regulator (CFTR) which is involved in bicarbonate secretion for the protection against bile toxicity.	Bicarbonates	124-135	CF transmembrane conductance regulator	Homo sapiens	44-95	
33655768-1	2021	BACKGROUND AND AIMS: Cholangiocytes express cystic fibrosis transmembrane conductance regulator (CFTR) which is involved in bicarbonate secretion for the protection against bile toxicity.	Bicarbonates	124-135	CF transmembrane conductance regulator	Homo sapiens	97-101	
34031755-12	2021	These findings suggest that the activation of cAMP-dependent HCO3- secretion through CFTR would be partly involved in the IND-mediated pH normalization in gland secretion and may be suitable for the maintenance of airway defense against exacerbating factors including LPS.	Bicarbonates	61-65	CF transmembrane conductance regulator	Homo sapiens	85-89	
33655768-9	2021	Forskolin-stimulation in absence of intracellular chloride showed ion-transport, indicating that bicarbonate could be secreted by CFTR.	Bicarbonates	97-108	CF transmembrane conductance regulator	Homo sapiens	130-134	
33923029-1	2021	Cystic fibrosis (CF) is caused by genetic mutations of the CF transmembrane conductance regulator (CFTR), leading to disrupted transport of Cl- and bicarbonate and CF lung disease featuring bacterial colonization and chronic infection in conducting airways.	Bicarbonates	148-159	CF transmembrane conductance regulator	Homo sapiens	99-103	
34004101-6	2021	CFTR is involved in the entry of HCO3- into Sertoli cells to trigger cAMP-dependent transcription and its defects lead to suppression of FSH-dependent gene expression of spermatogenesis, loss of sequence in the Wnt cascade, destruction of the PGE2-dependent transepithelial interaction and, as a consequence, the blood-testicular barrier.CF is characterized, along with classical signs, by endocrine dysfunction of the pancreas, osteoporosis with suppression of osteoblastogenesis, and a defect in spermatogenesis.	Bicarbonates	33-37	CF transmembrane conductance regulator	Homo sapiens	0-4	
33376814-1	2021	: Regulation of HCO3 -Transport and extracellular pH by CFTR.	Bicarbonates	16-20	CF transmembrane conductance regulator	Homo sapiens	56-60	
33532041-2	2021	Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene disrupts the capacity of the protein to function as a channel, transporting chloride ions and bicarbonate across epithelial cell membranes.	Bicarbonates	175-186	CF transmembrane conductance regulator	Homo sapiens	17-68	
33532041-2	2021	Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene disrupts the capacity of the protein to function as a channel, transporting chloride ions and bicarbonate across epithelial cell membranes.	Bicarbonates	175-186	CF transmembrane conductance regulator	Homo sapiens	70-74	
33481676-2	2021	It has been postulated that a reduced HCO3- transport in CF through CFTR may lead to a decreased airway surface liquid (ASL) pH.	Bicarbonates	38-42	CF transmembrane conductance regulator	Homo sapiens	68-72	
33376814-3	2021	Expression of functional CFTR may normally regulate extracellular pH via control of bicarbonate efflux.	Bicarbonates	84-95	CF transmembrane conductance regulator	Homo sapiens	25-29	
33376814-4	2021	Reports also suggest that the CFTR may be a Cl-/HCO3- exchanger.	Bicarbonates	48-52	CF transmembrane conductance regulator	Homo sapiens	30-34	
33376814-6	2021	We compared evidentiary support of four possible models of CFTR"s role in the transport of bicarbonate: 1) CFTR as a Cl-channel that permits bicarbonate conductance, 2) CFTR as an anion Cl-/HCO3- exchanger (AE), 3.)	Bicarbonates	91-102	CF transmembrane conductance regulator	Homo sapiens	59-63	
33376814-6	2021	We compared evidentiary support of four possible models of CFTR"s role in the transport of bicarbonate: 1) CFTR as a Cl-channel that permits bicarbonate conductance, 2) CFTR as an anion Cl-/HCO3- exchanger (AE), 3.)	Bicarbonates	91-102	CF transmembrane conductance regulator	Homo sapiens	107-111	
33376814-6	2021	We compared evidentiary support of four possible models of CFTR"s role in the transport of bicarbonate: 1) CFTR as a Cl-channel that permits bicarbonate conductance, 2) CFTR as an anion Cl-/HCO3- exchanger (AE), 3.)	Bicarbonates	91-102	CF transmembrane conductance regulator	Homo sapiens	107-111	
33376814-6	2021	We compared evidentiary support of four possible models of CFTR"s role in the transport of bicarbonate: 1) CFTR as a Cl-channel that permits bicarbonate conductance, 2) CFTR as an anion Cl-/HCO3- exchanger (AE), 3.)	Bicarbonates	141-152	CF transmembrane conductance regulator	Homo sapiens	59-63	
33376814-6	2021	We compared evidentiary support of four possible models of CFTR"s role in the transport of bicarbonate: 1) CFTR as a Cl-channel that permits bicarbonate conductance, 2) CFTR as an anion Cl-/HCO3- exchanger (AE), 3.)	Bicarbonates	141-152	CF transmembrane conductance regulator	Homo sapiens	107-111	
33376814-6	2021	We compared evidentiary support of four possible models of CFTR"s role in the transport of bicarbonate: 1) CFTR as a Cl-channel that permits bicarbonate conductance, 2) CFTR as an anion Cl-/HCO3- exchanger (AE), 3.)	Bicarbonates	141-152	CF transmembrane conductance regulator	Homo sapiens	107-111	
33376814-6	2021	We compared evidentiary support of four possible models of CFTR"s role in the transport of bicarbonate: 1) CFTR as a Cl-channel that permits bicarbonate conductance, 2) CFTR as an anion Cl-/HCO3- exchanger (AE), 3.)	Bicarbonates	190-194	CF transmembrane conductance regulator	Homo sapiens	59-63	
33376814-8	2021	CFTR as a Cl-channel that allows for transport of bicarbonate and regulates an independent AE.	Bicarbonates	50-61	CF transmembrane conductance regulator	Homo sapiens	0-4	
33376814-10	2021	This data, as well as that published by others, suggest that while CFTR may support and regulate bicarbonate flux it is unlikely it directly performs Cl-/HCO3- anion exchange.	Bicarbonates	97-108	CF transmembrane conductance regulator	Homo sapiens	67-71	
32520327-1	2020	Cystic fibrosis (CF) is an autosomal recessive disorder caused by mutations in the CF transmembrane conductance regulator (CFTR) gene, encoding an anion channel that conducts chloride and bicarbonate across epithelial membranes.	Bicarbonates	188-199	CF transmembrane conductance regulator	Homo sapiens	83-121	
32606316-2	2020	The resulting defect in the cystic fibrosis transmembrane conductance regulator protein (CFTR) results in defective chloride and bicarbonate secretion, as well as dysregulation of epithelial sodium channels (ENaC).	Bicarbonates	129-140	CF transmembrane conductance regulator	Homo sapiens	28-79	
32606316-2	2020	The resulting defect in the cystic fibrosis transmembrane conductance regulator protein (CFTR) results in defective chloride and bicarbonate secretion, as well as dysregulation of epithelial sodium channels (ENaC).	Bicarbonates	129-140	CF transmembrane conductance regulator	Homo sapiens	89-93	
32703846-9	2020	In patients, treatment with the CFTR modulator drug lumacaftor-ivacaftor increased the renal ability to excrete HCO3 -.	Bicarbonates	112-118	CF transmembrane conductance regulator	Homo sapiens	32-36	
32520327-1	2020	Cystic fibrosis (CF) is an autosomal recessive disorder caused by mutations in the CF transmembrane conductance regulator (CFTR) gene, encoding an anion channel that conducts chloride and bicarbonate across epithelial membranes.	Bicarbonates	188-199	CF transmembrane conductance regulator	Homo sapiens	123-127	
32168979-5	2020	We also demonstrate the ability of the bicarbonate sensory cellular test system to measure intracellular bicarbonate concentration changes in response to activation and specific inhibition of wild-type human CFTR protein when co-expressed with the bicarbonate sensing and reporting units in living cells.	Bicarbonates	39-50	CF transmembrane conductance regulator	Homo sapiens	208-212	
32587127-2	2020	The secretion of Cl- and HCO3- is mainly regulated by cystic fibrosis transmembrane conductance regulator (CFTR) or via the calciumactivated Cl- channel anoctamin-1 (ANO1) in nasal gland serous cells.	Bicarbonates	25-30	CF transmembrane conductance regulator	Homo sapiens	54-105	
32587127-2	2020	The secretion of Cl- and HCO3- is mainly regulated by cystic fibrosis transmembrane conductance regulator (CFTR) or via the calciumactivated Cl- channel anoctamin-1 (ANO1) in nasal gland serous cells.	Bicarbonates	25-30	CF transmembrane conductance regulator	Homo sapiens	107-111	
32439937-0	2020	Correctors modify the bicarbonate permeability of F508del-CFTR.	Bicarbonates	22-33	CF transmembrane conductance regulator	Homo sapiens	58-62	
32439937-5	2020	Interestingly, the permeability of bicarbonate increases in the cells containing corrected p.F508del CFTR channels is greater than the increase of the halide permeability.	Bicarbonates	35-46	CF transmembrane conductance regulator	Homo sapiens	101-105	
32439937-6	2020	These different increases of the permeability of bicarbonate and halides are consistent with the concept that the structural conformation of the pore of the corrector-rescued p.F508del channels would be different than the normal wild type CFTR protein.	Bicarbonates	49-60	CF transmembrane conductance regulator	Homo sapiens	239-243	
32512832-2	2020	Our aim was to establish and characterize co-culture models of human CF bronchial epithelial (CFBE) cell lines expressing a wild-type (WT) or mutant (deltaF508) CF transmembrane conductance regulator (CFTR) channel with human vascular endothelial cells and investigate the effects of bicarbonate.	Bicarbonates	284-295	CF transmembrane conductance regulator	Homo sapiens	201-205	
32168979-5	2020	We also demonstrate the ability of the bicarbonate sensory cellular test system to measure intracellular bicarbonate concentration changes in response to activation and specific inhibition of wild-type human CFTR protein when co-expressed with the bicarbonate sensing and reporting units in living cells.	Bicarbonates	105-116	CF transmembrane conductance regulator	Homo sapiens	208-212	
32168979-5	2020	We also demonstrate the ability of the bicarbonate sensory cellular test system to measure intracellular bicarbonate concentration changes in response to activation and specific inhibition of wild-type human CFTR protein when co-expressed with the bicarbonate sensing and reporting units in living cells.	Bicarbonates	105-116	CF transmembrane conductance regulator	Homo sapiens	208-212	
32168979-6	2020	A valuable benefit of the bicarbonate sensory cellular test system could be the screening of novel anionophore library compounds for bicarbonate transport activity with efficiencies close to the natural anion channel CFTR, which is not functional in the respiratory epithelia of cystic fibrosis patients.	Bicarbonates	26-37	CF transmembrane conductance regulator	Homo sapiens	217-221	
32168979-6	2020	A valuable benefit of the bicarbonate sensory cellular test system could be the screening of novel anionophore library compounds for bicarbonate transport activity with efficiencies close to the natural anion channel CFTR, which is not functional in the respiratory epithelia of cystic fibrosis patients.	Bicarbonates	133-144	CF transmembrane conductance regulator	Homo sapiens	217-221	
31561038-6	2020	RESULTS: Among the WNK1, SPAK, and OSR1 kinases that constitute a [Cl-]i-sensitive kinase cascade, the expression of WNK1 alone was sufficient to increase the CFTR bicarbonate permeability (PHCO3/PCl) and conductance (GHCO3) in patch clamp recordings.	Bicarbonates	164-175	CF transmembrane conductance regulator	Homo sapiens	159-163	
31721070-1	2020	BACKGROUND: Among the many consequences of loss of CFTR protein function, a significant reduction of the secretion of bicarbonate (HCO3-) in cystic fibrosis (CF) is a major pathogenic feature.	Bicarbonates	118-129	CF transmembrane conductance regulator	Homo sapiens	51-55	
31561038-0	2020	Regulation of CFTR Bicarbonate Channel Activity by WNK1: Implications for Pancreatitis and CFTR-related disorders.	Bicarbonates	19-30	CF transmembrane conductance regulator	Homo sapiens	14-18	
31561038-0	2020	Regulation of CFTR Bicarbonate Channel Activity by WNK1: Implications for Pancreatitis and CFTR-related disorders.	Bicarbonates	19-30	CF transmembrane conductance regulator	Homo sapiens	91-95	
31561038-1	2020	BACKGRAOUD & AIMS: Aberrant epithelial bicarbonate (HCO3-) secretion caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene is associated with several diseases including cystic fibrosis and pancreatitis.	Bicarbonates	43-54	CF transmembrane conductance regulator	Homo sapiens	100-151	
31561038-1	2020	BACKGRAOUD & AIMS: Aberrant epithelial bicarbonate (HCO3-) secretion caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene is associated with several diseases including cystic fibrosis and pancreatitis.	Bicarbonates	43-54	CF transmembrane conductance regulator	Homo sapiens	153-157	
31659725-5	2019	The role of the CFTR protein as an ion channel transporting chloride and bicarbonate and its repercussions on different epithelial cell-lined organs and mucus are now better understood.	Bicarbonates	73-84	CF transmembrane conductance regulator	Homo sapiens	16-20	
32061340-1	2020	The cystic fibrosis transmembrane conductance regulator (CFTR) is an anion channel responsible for the direct transport of bicarbonate and chloride.	Bicarbonates	123-134	CF transmembrane conductance regulator	Homo sapiens	4-55	
32061340-1	2020	The cystic fibrosis transmembrane conductance regulator (CFTR) is an anion channel responsible for the direct transport of bicarbonate and chloride.	Bicarbonates	123-134	CF transmembrane conductance regulator	Homo sapiens	57-61	
30761610-1	2019	Cystic fibrosis (CF) is a severe, monogenic, autosomal recessive disease caused by mutations in the CFTR (cystic fibrosis transmembrane regulator) gene, where disturbed chloride and bicarbonate transportation in epithelial cells results in a multiorgan disease with primarily pulmonary infections and pancreatic insufficiency.	Bicarbonates	182-193	CF transmembrane conductance regulator	Homo sapiens	100-104	
31715083-3	2019	A similar pathogenesis cascade is observed in all of these organs: loss of CFTR function leads to altered ion transport, consisting of decreased chloride and bicarbonate secretion via the CFTR channel and increased sodium absorption via epithelial sodium channel upregulation.	Bicarbonates	158-169	CF transmembrane conductance regulator	Homo sapiens	75-79	
31715088-3	2019	CFTR primarily functions as a chloride channel that transports ions across the apical membrane of epithelial cells but has other functions, including bicarbonate secretion and inhibition of sodium transport.	Bicarbonates	150-161	CF transmembrane conductance regulator	Homo sapiens	0-4	
31532390-1	2019	Cystic Fibrosis (CF) is a monogenic disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, resulting in defective CFTR-mediated chloride and bicarbonate transport, with dysregulation of epithelial sodium channels (ENaC).	Bicarbonates	186-197	CF transmembrane conductance regulator	Homo sapiens	71-122	
31532390-1	2019	Cystic Fibrosis (CF) is a monogenic disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, resulting in defective CFTR-mediated chloride and bicarbonate transport, with dysregulation of epithelial sodium channels (ENaC).	Bicarbonates	186-197	CF transmembrane conductance regulator	Homo sapiens	124-128	
31532390-1	2019	Cystic Fibrosis (CF) is a monogenic disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, resulting in defective CFTR-mediated chloride and bicarbonate transport, with dysregulation of epithelial sodium channels (ENaC).	Bicarbonates	186-197	CF transmembrane conductance regulator	Homo sapiens	159-163	
30742493-10	2019	The dependence of DeltapHi on pendrin suggests there is minimal electrical coupling between Cl- and HCO3- fluxes and that CFTR activation increases anion exchange-mediated HCO3- influx.	Bicarbonates	172-176	CF transmembrane conductance regulator	Homo sapiens	122-126	
31745411-3	2019	Homozygous CFTR gene mutation results in viscous and acidic bile secretions secondary to deficient surface fluid and bicarbonate efflux.	Bicarbonates	117-128	CF transmembrane conductance regulator	Homo sapiens	11-15	
30738802-0	2019	Lumacaftor-rescued F508del-CFTR has a modified bicarbonate permeability.	Bicarbonates	47-58	CF transmembrane conductance regulator	Homo sapiens	27-31	
30738802-3	2019	We studied the permeability properties of the CFTR mutant F508del treated with the corrector lumacaftor, showing that the rescued protein has selectivity properties different than the wild type CFTR, showing an augmented bicarbonate permeability.	Bicarbonates	221-232	CF transmembrane conductance regulator	Homo sapiens	46-50	
30738802-3	2019	We studied the permeability properties of the CFTR mutant F508del treated with the corrector lumacaftor, showing that the rescued protein has selectivity properties different than the wild type CFTR, showing an augmented bicarbonate permeability.	Bicarbonates	221-232	CF transmembrane conductance regulator	Homo sapiens	194-198	
30738802-5	2019	Our findings rather support the idea that a combination of correctors would be required to address the CFTR-dependent bicarbonate permeability.	Bicarbonates	118-129	CF transmembrane conductance regulator	Homo sapiens	103-107	
30761610-1	2019	Cystic fibrosis (CF) is a severe, monogenic, autosomal recessive disease caused by mutations in the CFTR (cystic fibrosis transmembrane regulator) gene, where disturbed chloride and bicarbonate transportation in epithelial cells results in a multiorgan disease with primarily pulmonary infections and pancreatic insufficiency.	Bicarbonates	182-193	CF transmembrane conductance regulator	Homo sapiens	106-145	
31027466-3	2019	CFTR, an adenosine triphosphate binding anion channel, has multiple functions, but primarily regulates the movement of chloride anions, thiocyanate and bicarbonate across luminal cell membranes.	Bicarbonates	152-163	CF transmembrane conductance regulator	Homo sapiens	0-4	
30867598-1	2019	Loss-of-function mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) compromise epithelial HCO3- and Cl- secretion, reduce airway surface liquid pH, and impair respiratory host defences in people with cystic fibrosis1-3.	Bicarbonates	115-120	CF transmembrane conductance regulator	Homo sapiens	34-85	
30867598-1	2019	Loss-of-function mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) compromise epithelial HCO3- and Cl- secretion, reduce airway surface liquid pH, and impair respiratory host defences in people with cystic fibrosis1-3.	Bicarbonates	115-120	CF transmembrane conductance regulator	Homo sapiens	87-91	
30599064-4	2019	Alternatively, it was postulated that a reduced HCO3- transport through CFTR leads to a decreased ASL pH, favoring bacterial colonization.	Bicarbonates	48-52	CF transmembrane conductance regulator	Homo sapiens	72-76	
30289627-2	2018	Loss of CFTR function disrupts chloride, bicarbonate and regulation of sodium transport, producing a cascade of mucus obstruction, inflammation, pulmonary infection, and ultimately damage in numerous organs.	Bicarbonates	41-52	CF transmembrane conductance regulator	Homo sapiens	8-12	
30506051-4	2018	The CFTR is an anion transporter of chloride (Cl-) and bicarbonate (HCO3 -) that is located on the apical surface of respiratory epithelium and exocrine glandular epithelium.	Bicarbonates	55-66	CF transmembrane conductance regulator	Homo sapiens	4-8	
30506051-4	2018	The CFTR is an anion transporter of chloride (Cl-) and bicarbonate (HCO3 -) that is located on the apical surface of respiratory epithelium and exocrine glandular epithelium.	Bicarbonates	68-72	CF transmembrane conductance regulator	Homo sapiens	4-8	
30618777-3	2018	CFTR plays a central role in the pancreatic ductal secretory functions by carrying Cl- and HCO3 - ions across the apical membrane.	Bicarbonates	91-95	CF transmembrane conductance regulator	Homo sapiens	0-4	
30361244-2	2018	There are currently alternative hypotheses that attempt to describe the abnormally viscous and elastic mucus that is a hallmark of CF airways disease, including: 1) loss of CF transmembrane regulator (CFTR)-dependent airway surface volume (water) secretion, producing mucus hyperconcentration-dependent increased viscosity, and 2) impaired bicarbonate secretion by CFTR, producing acidification of airway surfaces and increased mucus viscosity.A series of experiments was conducted to determine the contributions of mucus concentration versus pH to the rheological properties of airway mucus across length scales from the nanoscopic to macroscopic.For length scales greater than the nanoscopic, i.e. those relevant to mucociliary clearance, the effect of mucus concentration dominated over the effect of airway acidification.Mucus hydration and chemical reduction of disulfide bonds that connect mucin monomers are more promising therapeutic approaches than alkalisation.	Bicarbonates	340-351	CF transmembrane conductance regulator	Homo sapiens	201-205	
30063865-2	2018	CFTR is an ion channel regulating transport of chloride, bicarbonate, and water, and influencing sodium resorption.	Bicarbonates	57-68	CF transmembrane conductance regulator	Homo sapiens	0-4	
30416443-2	2018	Defective chloride and bicarbonate secretion, arising from CFTR mutations, cause a multi-organ disease.	Bicarbonates	23-34	CF transmembrane conductance regulator	Homo sapiens	59-63	
30131695-1	2018	Cystic fibrosis (CF) is a genetic lethal disease, originated from the defective function of the CFTR protein, a chloride and bicarbonate permeable transmembrane channel.	Bicarbonates	125-136	CF transmembrane conductance regulator	Homo sapiens	96-100	
29750923-2	2018	CFTR functions as a cyclic adenosine monophosphate-dependent anion channel that transports chloride and bicarbonate across epithelial surfaces, and disruption of these ion transport processes plays a central role in the pathogenesis of CF.	Bicarbonates	104-115	CF transmembrane conductance regulator	Homo sapiens	0-4	
30063324-2	2018	Much of this research is driven by the biological relevance of anion transport and the search to find new treatments for diseases such as cystic fibrosis, which is caused by genetic problems leading to faulty cystic fibrosis transmembrane conductance regulator (CFTR) channels, which in turn lead to reduced chloride and bicarbonate transport through epithelial cell membranes.	Bicarbonates	321-332	CF transmembrane conductance regulator	Homo sapiens	209-260	
30063324-2	2018	Much of this research is driven by the biological relevance of anion transport and the search to find new treatments for diseases such as cystic fibrosis, which is caused by genetic problems leading to faulty cystic fibrosis transmembrane conductance regulator (CFTR) channels, which in turn lead to reduced chloride and bicarbonate transport through epithelial cell membranes.	Bicarbonates	321-332	CF transmembrane conductance regulator	Homo sapiens	262-266	
30089726-2	2018	Loss of CFTR-mediated HCO3- secretion reduces the pH of airway surface liquid (ASL) in vitro and in neonatal humans and pigs in vivo.	Bicarbonates	22-26	CF transmembrane conductance regulator	Homo sapiens	8-12	
29933921-7	2018	Immediately a different hypothesis arose, postulating a reduced ASL pH as the cause for the increased susceptibility to infections, due to a diminished bicarbonate secretion through CFTR.	Bicarbonates	152-163	CF transmembrane conductance regulator	Homo sapiens	182-186	
29517421-1	2018	Pancreatic ductular epithelial cells comprise the majority of duct cells in pancreas, control cystic fibrosis transmembrane conductance regulator (CFTR)-dependent bicarbonate ([Formula: see text]) secretion, but are difficult to grow as a polarized monolayer.	Bicarbonates	163-174	CF transmembrane conductance regulator	Homo sapiens	94-145	
29517421-1	2018	Pancreatic ductular epithelial cells comprise the majority of duct cells in pancreas, control cystic fibrosis transmembrane conductance regulator (CFTR)-dependent bicarbonate ([Formula: see text]) secretion, but are difficult to grow as a polarized monolayer.	Bicarbonates	163-174	CF transmembrane conductance regulator	Homo sapiens	147-151	
29517421-11	2018	NEW & NOTEWORTHY Pancreas ductular epithelial cells control cystic fibrosis transmembrane conductance regulator (CFTR)-dependent bicarbonate secretion.	Bicarbonates	133-144	CF transmembrane conductance regulator	Homo sapiens	64-115	
29517421-11	2018	NEW & NOTEWORTHY Pancreas ductular epithelial cells control cystic fibrosis transmembrane conductance regulator (CFTR)-dependent bicarbonate secretion.	Bicarbonates	133-144	CF transmembrane conductance regulator	Homo sapiens	117-121	
29517421-12	2018	Their function is critical because when CFTR is deficient in cystic fibrosis bicarbonate secretion is lost and the pancreas is damaged.	Bicarbonates	77-88	CF transmembrane conductance regulator	Homo sapiens	40-44	
29845767-0	2018	Editorial Focus: CFTR-dependent bicarbonate secretion by Calu-3 cells.	Bicarbonates	32-43	CF transmembrane conductance regulator	Homo sapiens	17-21	
29743243-0	2018	CFTR/ENaC-dependent regulation of membrane potential during human sperm capacitation is initiated by bicarbonate uptake through NBC.	Bicarbonates	101-112	CF transmembrane conductance regulator	Homo sapiens	0-4	
29743243-7	2018	We observed that inhibition of both CFTR and NBC decreased HCO3- influx, resulting in lower PKA activity, and that events downstream of the cAMP activation of PKA are essential for the regulation of Em.	Bicarbonates	59-63	CF transmembrane conductance regulator	Homo sapiens	36-40	
29536650-0	2018	Most bicarbonate secretion by Calu-3 cells is mediated by CFTR and independent of pendrin.	Bicarbonates	5-16	CF transmembrane conductance regulator	Homo sapiens	58-62	
29536650-8	2018	While the conclusions cannot be extrapolated to other airway epithelia, the present results demonstrate that most HCO3- secretion by Calu-3 cells is mediated by CFTR.	Bicarbonates	114-118	CF transmembrane conductance regulator	Homo sapiens	161-165	
28875346-1	2018	Cystic fibrosis transmembrane conductance regulator (CFTR) is the essential chloride and bicarbonate channel in the apical membrane of epithelial cells.	Bicarbonates	89-100	CF transmembrane conductance regulator	Homo sapiens	0-51	
28875346-1	2018	Cystic fibrosis transmembrane conductance regulator (CFTR) is the essential chloride and bicarbonate channel in the apical membrane of epithelial cells.	Bicarbonates	89-100	CF transmembrane conductance regulator	Homo sapiens	53-57	
29079751-1	2017	Chloride absorption and bicarbonate excretion through exchange by the solute carrier family 26 member 3 (SLC26A3) and cystic fibrosis transmembrane conductance regulator (CFTR) are crucial for many tissues including sperm and epithelia of the male reproductive tract.	Bicarbonates	24-35	CF transmembrane conductance regulator	Homo sapiens	118-169	
30384810-3	2018	Interestingly, the cystic fibrosis transmembrane conductance regulator encoded by CFTR gene, an ATP-binding cassette transporter-class ion channel that conducts chloride and bicarbonate anions across membrane of epithelial cells, has recently been suggested to play a role in the development and progression of many types of cancer.	Bicarbonates	174-185	CF transmembrane conductance regulator	Homo sapiens	19-70	
30384810-3	2018	Interestingly, the cystic fibrosis transmembrane conductance regulator encoded by CFTR gene, an ATP-binding cassette transporter-class ion channel that conducts chloride and bicarbonate anions across membrane of epithelial cells, has recently been suggested to play a role in the development and progression of many types of cancer.	Bicarbonates	174-185	CF transmembrane conductance regulator	Homo sapiens	82-86	
28345252-3	2017	Recently, soluble adenylyl cyclase (sAC), which is activated by HCO3- or Ca2+ , emerges to provide an alternative way to activate cAMP/PKA pathway with the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-activated Cl- /HCO3- -conducting anion channel, as a key player.	Bicarbonates	64-68	CF transmembrane conductance regulator	Homo sapiens	156-207	
28345252-3	2017	Recently, soluble adenylyl cyclase (sAC), which is activated by HCO3- or Ca2+ , emerges to provide an alternative way to activate cAMP/PKA pathway with the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-activated Cl- /HCO3- -conducting anion channel, as a key player.	Bicarbonates	64-68	CF transmembrane conductance regulator	Homo sapiens	209-213	
28345252-3	2017	Recently, soluble adenylyl cyclase (sAC), which is activated by HCO3- or Ca2+ , emerges to provide an alternative way to activate cAMP/PKA pathway with the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-activated Cl- /HCO3- -conducting anion channel, as a key player.	Bicarbonates	238-242	CF transmembrane conductance regulator	Homo sapiens	156-207	
28345252-3	2017	Recently, soluble adenylyl cyclase (sAC), which is activated by HCO3- or Ca2+ , emerges to provide an alternative way to activate cAMP/PKA pathway with the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-activated Cl- /HCO3- -conducting anion channel, as a key player.	Bicarbonates	238-242	CF transmembrane conductance regulator	Homo sapiens	209-213	
28345252-4	2017	This review summarizes new progress in the investigation of the CFTR/HCO3- -dependent sAC signalling and its essential role in various reproductive processes, particularly in ovarian functions.	Bicarbonates	69-73	CF transmembrane conductance regulator	Homo sapiens	64-68	
28345252-5	2017	We present the evidence for a CFTR/HCO3- -dependent nuclear sAC signalling cascade that amplifies the FSH-stimulated cAMP/PKA pathway, traditionally thought to involve tmAC, in granulosa for the regulation of oestrogen production and granulosa cell proliferation.	Bicarbonates	35-39	CF transmembrane conductance regulator	Homo sapiens	30-34	
28345252-6	2017	The implication of the CFTR/HCO3- /sAC pathway in amplifying other receptor-activated cAMP/PKA signalling in a wide variety of cell types and pathophysiological processes, including aging, is also discussed.	Bicarbonates	28-32	CF transmembrane conductance regulator	Homo sapiens	23-27	
28732801-3	2017	METHODS: The present short review reports early findings as well as recent insights into the role of CFTR for bicarbonate transport and its defects in CF.	Bicarbonates	110-121	CF transmembrane conductance regulator	Homo sapiens	101-105	
29079751-1	2017	Chloride absorption and bicarbonate excretion through exchange by the solute carrier family 26 member 3 (SLC26A3) and cystic fibrosis transmembrane conductance regulator (CFTR) are crucial for many tissues including sperm and epithelia of the male reproductive tract.	Bicarbonates	24-35	CF transmembrane conductance regulator	Homo sapiens	171-175	
28554723-5	2017	The disease is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene which encodes the CFTR protein, a protein kinase A-activated ATP-gated anion channel that regulates the transport of electrolytes such as chloride and bicarbonate.	Bicarbonates	257-268	CF transmembrane conductance regulator	Homo sapiens	42-93	
28869532-1	2017	The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP- and cGMP-regulated chloride (Cl-) and bicarbonate (HCO3-) channel localized primarily at the apical plasma membrane of epithelial cells lining the airway, gut and exocrine glands, where it is responsible for transepithelial salt and water transport.	Bicarbonates	112-123	CF transmembrane conductance regulator	Homo sapiens	4-55	
28869532-1	2017	The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP- and cGMP-regulated chloride (Cl-) and bicarbonate (HCO3-) channel localized primarily at the apical plasma membrane of epithelial cells lining the airway, gut and exocrine glands, where it is responsible for transepithelial salt and water transport.	Bicarbonates	112-123	CF transmembrane conductance regulator	Homo sapiens	57-61	
28869532-1	2017	The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP- and cGMP-regulated chloride (Cl-) and bicarbonate (HCO3-) channel localized primarily at the apical plasma membrane of epithelial cells lining the airway, gut and exocrine glands, where it is responsible for transepithelial salt and water transport.	Bicarbonates	125-129	CF transmembrane conductance regulator	Homo sapiens	4-55	
28869532-1	2017	The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP- and cGMP-regulated chloride (Cl-) and bicarbonate (HCO3-) channel localized primarily at the apical plasma membrane of epithelial cells lining the airway, gut and exocrine glands, where it is responsible for transepithelial salt and water transport.	Bicarbonates	125-129	CF transmembrane conductance regulator	Homo sapiens	57-61	
27714810-6	2017	We observed that inhibition of CFTR affects HCO3- -entrance dependent events resulting in lower PKA activity.	Bicarbonates	44-48	CF transmembrane conductance regulator	Homo sapiens	31-35	
28554723-5	2017	The disease is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene which encodes the CFTR protein, a protein kinase A-activated ATP-gated anion channel that regulates the transport of electrolytes such as chloride and bicarbonate.	Bicarbonates	257-268	CF transmembrane conductance regulator	Homo sapiens	95-99	
28554723-5	2017	The disease is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene which encodes the CFTR protein, a protein kinase A-activated ATP-gated anion channel that regulates the transport of electrolytes such as chloride and bicarbonate.	Bicarbonates	257-268	CF transmembrane conductance regulator	Homo sapiens	124-128	
27876591-2	2017	CFTR is an anion channel that conducts bicarbonate and chloride across cell membranes.	Bicarbonates	39-50	CF transmembrane conductance regulator	Homo sapiens	0-4	
27699454-3	2017	If allowed to leave the ER, CFTR is modified at the Golgi and reaches the post-Golgi compartments to be delivered to the plasma membrane where it functions as a cAMP- and phosphorylation-regulated chloride/bicarbonate channel.	Bicarbonates	206-217	CF transmembrane conductance regulator	Homo sapiens	28-32	
28445932-1	2017	Cystic fibrosis transmembrane conductance regulator (CFTR) is classified as an anion channel transporter of Cl- and HCO3-.	Bicarbonates	116-120	CF transmembrane conductance regulator	Homo sapiens	0-51	
28445932-1	2017	Cystic fibrosis transmembrane conductance regulator (CFTR) is classified as an anion channel transporter of Cl- and HCO3-.	Bicarbonates	116-120	CF transmembrane conductance regulator	Homo sapiens	53-57	
28094839-1	2017	BACKGROUND AND PURPOSE: Cystic fibrosis (CF) is a debilitating disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which codes for a Cl-/HCO3 - channel.	Bicarbonates	185-189	CF transmembrane conductance regulator	Homo sapiens	98-149	
28094839-1	2017	BACKGROUND AND PURPOSE: Cystic fibrosis (CF) is a debilitating disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which codes for a Cl-/HCO3 - channel.	Bicarbonates	185-189	CF transmembrane conductance regulator	Homo sapiens	151-155	
28300821-10	2017	These data provide in vivo evidence that CFTR is an important regulator of bicarbonate secretion, which may be a translational link between CFTR function and clinical improvement.	Bicarbonates	75-86	CF transmembrane conductance regulator	Homo sapiens	41-45	
28300821-10	2017	These data provide in vivo evidence that CFTR is an important regulator of bicarbonate secretion, which may be a translational link between CFTR function and clinical improvement.	Bicarbonates	75-86	CF transmembrane conductance regulator	Homo sapiens	140-144	
27226582-1	2016	The cystic fibrosis transmembrane conductance regulator (CFTR, ABCC7), mutations of which cause cystic fibrosis, belongs to the ATP-binding cassette (ABC) transporter family and works as a channel for small anions, such as chloride and bicarbonate.	Bicarbonates	236-247	CF transmembrane conductance regulator	Homo sapiens	4-55	
27615377-6	2016	The cystic fibrosis transmembrane conductance regulator (CFTR) and the solute-linked carrier 26 gene family A6 (SLC26A6) are two key bicarbonate transport proteins that mediate duodenal mucosal bicarbonate secretion.	Bicarbonates	133-144	CF transmembrane conductance regulator	Homo sapiens	4-55	
27615377-6	2016	The cystic fibrosis transmembrane conductance regulator (CFTR) and the solute-linked carrier 26 gene family A6 (SLC26A6) are two key bicarbonate transport proteins that mediate duodenal mucosal bicarbonate secretion.	Bicarbonates	133-144	CF transmembrane conductance regulator	Homo sapiens	57-61	
27615377-6	2016	The cystic fibrosis transmembrane conductance regulator (CFTR) and the solute-linked carrier 26 gene family A6 (SLC26A6) are two key bicarbonate transport proteins that mediate duodenal mucosal bicarbonate secretion.	Bicarbonates	194-205	CF transmembrane conductance regulator	Homo sapiens	4-55	
27615377-6	2016	The cystic fibrosis transmembrane conductance regulator (CFTR) and the solute-linked carrier 26 gene family A6 (SLC26A6) are two key bicarbonate transport proteins that mediate duodenal mucosal bicarbonate secretion.	Bicarbonates	194-205	CF transmembrane conductance regulator	Homo sapiens	57-61	
27615377-9	2016	The cystic fibrosis transmembrane conductance regulator (CFTR) and the solute-linked carrier 26 gene family A6 (SLC26A6) are two key bicarbonate transport proteins that mediate duodenal mucosal bicarbonate secretion, which is an important protective factor against acid-induced duodenal injury.	Bicarbonates	133-144	CF transmembrane conductance regulator	Homo sapiens	4-55	
27615377-9	2016	The cystic fibrosis transmembrane conductance regulator (CFTR) and the solute-linked carrier 26 gene family A6 (SLC26A6) are two key bicarbonate transport proteins that mediate duodenal mucosal bicarbonate secretion, which is an important protective factor against acid-induced duodenal injury.	Bicarbonates	133-144	CF transmembrane conductance regulator	Homo sapiens	57-61	
27615377-9	2016	The cystic fibrosis transmembrane conductance regulator (CFTR) and the solute-linked carrier 26 gene family A6 (SLC26A6) are two key bicarbonate transport proteins that mediate duodenal mucosal bicarbonate secretion, which is an important protective factor against acid-induced duodenal injury.	Bicarbonates	194-205	CF transmembrane conductance regulator	Homo sapiens	4-55	
27615377-9	2016	The cystic fibrosis transmembrane conductance regulator (CFTR) and the solute-linked carrier 26 gene family A6 (SLC26A6) are two key bicarbonate transport proteins that mediate duodenal mucosal bicarbonate secretion, which is an important protective factor against acid-induced duodenal injury.	Bicarbonates	194-205	CF transmembrane conductance regulator	Homo sapiens	57-61	
27365309-8	2016	We showed that translocation is driven by an electrochemical gradient generated by apical accumulation of Cl(-) and HCO3(-) through CFTR.	Bicarbonates	116-120	CF transmembrane conductance regulator	Homo sapiens	132-136	
27341355-5	2016	Alcohol consumption impairs cystic fibrosis transmembrane conductance regulator (CFTR) activity leading to decreased bicarbonate secretion and patients with susceptible CFTR mutations can develop clinical pancreatitis.	Bicarbonates	117-128	CF transmembrane conductance regulator	Homo sapiens	28-79	
27341355-5	2016	Alcohol consumption impairs cystic fibrosis transmembrane conductance regulator (CFTR) activity leading to decreased bicarbonate secretion and patients with susceptible CFTR mutations can develop clinical pancreatitis.	Bicarbonates	117-128	CF transmembrane conductance regulator	Homo sapiens	81-85	
26245938-8	2016	Oncocytes expressed cystic fibrosis transmembrane conductance regulator and sodium/potassium ATPase, ion channels that play a role in bicarbonate secretion.	Bicarbonates	134-145	CF transmembrane conductance regulator	Homo sapiens	20-71	
27226582-1	2016	The cystic fibrosis transmembrane conductance regulator (CFTR, ABCC7), mutations of which cause cystic fibrosis, belongs to the ATP-binding cassette (ABC) transporter family and works as a channel for small anions, such as chloride and bicarbonate.	Bicarbonates	236-247	CF transmembrane conductance regulator	Homo sapiens	57-61	
27226582-1	2016	The cystic fibrosis transmembrane conductance regulator (CFTR, ABCC7), mutations of which cause cystic fibrosis, belongs to the ATP-binding cassette (ABC) transporter family and works as a channel for small anions, such as chloride and bicarbonate.	Bicarbonates	236-247	CF transmembrane conductance regulator	Homo sapiens	63-68	
26134505-4	2015	We have recently shown that bicarbonate ions passing through CFTR are necessary for proper unfolding of the MUC2 mucin, thus highlighting the importance of bicarbonate ion transport via the CFTR and the ability of these ions to raise the pH and chelate calcium bound to the mucin as the important steps in forming normal mucus.	Bicarbonates	28-39	CF transmembrane conductance regulator	Homo sapiens	61-65	
27114540-5	2016	However, recent discoveries focused attention on CFTR-mediated HCO3 (-) secretion and airway surface liquid (ASL) pH as critical for host defense and CF pathogenesis.	Bicarbonates	63-67	CF transmembrane conductance regulator	Homo sapiens	49-53	
27114540-8	2016	Likewise, heterozygous epithelia (CFTR(+/-) or CFTR(+/ F508)) expressed CFTR and secreted HCO3 (-) at ~50% of wild-type values.	Bicarbonates	90-94	CF transmembrane conductance regulator	Homo sapiens	34-38	
27114540-8	2016	Likewise, heterozygous epithelia (CFTR(+/-) or CFTR(+/ F508)) expressed CFTR and secreted HCO3 (-) at ~50% of wild-type values.	Bicarbonates	90-94	CF transmembrane conductance regulator	Homo sapiens	47-51	
27114540-8	2016	Likewise, heterozygous epithelia (CFTR(+/-) or CFTR(+/ F508)) expressed CFTR and secreted HCO3 (-) at ~50% of wild-type values.	Bicarbonates	90-94	CF transmembrane conductance regulator	Homo sapiens	47-51	
27114540-10	2016	Overexpressing CFTR increased HCO3 (-) secretion to rates greater than wild type, but ASL pH did not exceed wild-type values.	Bicarbonates	30-34	CF transmembrane conductance regulator	Homo sapiens	15-19	
27114540-11	2016	Thus, in contrast to Cl(-) secretion, the amount of CFTR is rate-limiting for HCO3 (-) secretion and for correcting host defense abnormalities.	Bicarbonates	78-82	CF transmembrane conductance regulator	Homo sapiens	52-56	
26856995-1	2016	Cystic fibrosis transmembrane conductance regulator (CFTR) is an ion channel that conducts chloride and bicarbonate ions across epithelial cell membranes.	Bicarbonates	104-115	CF transmembrane conductance regulator	Homo sapiens	0-51	
26856995-1	2016	Cystic fibrosis transmembrane conductance regulator (CFTR) is an ion channel that conducts chloride and bicarbonate ions across epithelial cell membranes.	Bicarbonates	104-115	CF transmembrane conductance regulator	Homo sapiens	53-57	
26663196-0	2016	Pore dilatation increases the bicarbonate permeability of CFTR, ANO1 and glycine receptor anion channels.	Bicarbonates	30-41	CF transmembrane conductance regulator	Homo sapiens	58-62	
26663196-4	2016	Pore dilatation increases the bicarbonate permeability (P HC O3/ Cl ) of CFTR, ANO1 and GlyR.	Bicarbonates	30-41	CF transmembrane conductance regulator	Homo sapiens	73-77	
26719229-5	2016	Abnormal CFTR mediated bicarbonate transport creates an unfavourable, acidic environment, which impairs antimicrobial function and alters mucus properties and clearance.	Bicarbonates	23-34	CF transmembrane conductance regulator	Homo sapiens	9-13	
26671068-8	2015	Together, our data show that Slc26a1, Slc26a6 and Slc26a7 are novel participants in the extracellular transport of bicarbonate during enamel maturation, and that their functional roles may be achieved by forming interaction units with Cftr.	Bicarbonates	115-126	CF transmembrane conductance regulator	Homo sapiens	235-239	
26416827-8	2015	Ivacaftor is a potentiator of CFTR channels defective in their chloride/bicarbonate gating/conductance, but present at the epithelial cell surface.	Bicarbonates	72-83	CF transmembrane conductance regulator	Homo sapiens	30-34	
26134505-4	2015	We have recently shown that bicarbonate ions passing through CFTR are necessary for proper unfolding of the MUC2 mucin, thus highlighting the importance of bicarbonate ion transport via the CFTR and the ability of these ions to raise the pH and chelate calcium bound to the mucin as the important steps in forming normal mucus.	Bicarbonates	28-39	CF transmembrane conductance regulator	Homo sapiens	190-194	
26134505-4	2015	We have recently shown that bicarbonate ions passing through CFTR are necessary for proper unfolding of the MUC2 mucin, thus highlighting the importance of bicarbonate ion transport via the CFTR and the ability of these ions to raise the pH and chelate calcium bound to the mucin as the important steps in forming normal mucus.	Bicarbonates	156-167	CF transmembrane conductance regulator	Homo sapiens	61-65	
26134505-4	2015	We have recently shown that bicarbonate ions passing through CFTR are necessary for proper unfolding of the MUC2 mucin, thus highlighting the importance of bicarbonate ion transport via the CFTR and the ability of these ions to raise the pH and chelate calcium bound to the mucin as the important steps in forming normal mucus.	Bicarbonates	156-167	CF transmembrane conductance regulator	Homo sapiens	190-194	
26730394-1	2015	Cystic fibrosis (CF) results from mutations in the CF transmembrane conductance regulator (CFTR) gene, which codes for a chloride/bicarbonate channel in the apical epithelial membranes.	Bicarbonates	130-141	CF transmembrane conductance regulator	Homo sapiens	51-89	
26335950-2	2015	There is emerging evidence that CFTR is a bicarbonate channel, a driver of chloride-bicarbonate exchange and through its action on local pH, a regulator of other ion channels and of proteins that function optimally in a neutral environment.	Bicarbonates	42-53	CF transmembrane conductance regulator	Homo sapiens	32-36	
26335950-2	2015	There is emerging evidence that CFTR is a bicarbonate channel, a driver of chloride-bicarbonate exchange and through its action on local pH, a regulator of other ion channels and of proteins that function optimally in a neutral environment.	Bicarbonates	84-95	CF transmembrane conductance regulator	Homo sapiens	32-36	
26335950-9	2015	Basic and applied research that focuses on the role of CFTR-mediated bicarbonate secretion helps explain many of the diverse clinical manifestations that are CF.	Bicarbonates	69-80	CF transmembrane conductance regulator	Homo sapiens	55-59	
26730394-1	2015	Cystic fibrosis (CF) results from mutations in the CF transmembrane conductance regulator (CFTR) gene, which codes for a chloride/bicarbonate channel in the apical epithelial membranes.	Bicarbonates	130-141	CF transmembrane conductance regulator	Homo sapiens	91-95	
26089335-12	2015	Combination of M470V and L1156F significantly reduced CFTR expression to ~60%, impaired CFTR-mediated HCO3 (-)/Cl(-) transport activity to 50-60%, and impaired CFTR-coupled Cl(-)/HCO3 (-) exchange activity to 20-30%.	Bicarbonates	102-106	CF transmembrane conductance regulator	Homo sapiens	88-92	
26089335-12	2015	Combination of M470V and L1156F significantly reduced CFTR expression to ~60%, impaired CFTR-mediated HCO3 (-)/Cl(-) transport activity to 50-60%, and impaired CFTR-coupled Cl(-)/HCO3 (-) exchange activity to 20-30%.	Bicarbonates	102-106	CF transmembrane conductance regulator	Homo sapiens	88-92	
26001957-2	2015	STATE OF KNOWLEDGE: Abnormal CFTR function, with reduced bicarbonate and other ion transport levels through the apical surface of epithelial cells, affects the intestinal tract including the pancreas and the liver.	Bicarbonates	57-68	CF transmembrane conductance regulator	Homo sapiens	29-33	
25732475-1	2015	The underlying cause of cystic fibrosis (CF) is the loss of epithelial chloride and bicarbonate transport due to mutations in the CF transmembrane conductance regulator (CFTR) gene encoding the CFTR protein.	Bicarbonates	84-95	CF transmembrane conductance regulator	Homo sapiens	130-168	
25732475-1	2015	The underlying cause of cystic fibrosis (CF) is the loss of epithelial chloride and bicarbonate transport due to mutations in the CF transmembrane conductance regulator (CFTR) gene encoding the CFTR protein.	Bicarbonates	84-95	CF transmembrane conductance regulator	Homo sapiens	170-174	
25732475-1	2015	The underlying cause of cystic fibrosis (CF) is the loss of epithelial chloride and bicarbonate transport due to mutations in the CF transmembrane conductance regulator (CFTR) gene encoding the CFTR protein.	Bicarbonates	84-95	CF transmembrane conductance regulator	Homo sapiens	194-198	
26073863-2	2015	The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-activated Cl(-) and HCO3(-) membrane transporter.	Bicarbonates	93-97	CF transmembrane conductance regulator	Homo sapiens	4-55	
26073863-2	2015	The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-activated Cl(-) and HCO3(-) membrane transporter.	Bicarbonates	93-97	CF transmembrane conductance regulator	Homo sapiens	57-61	
24954874-7	2014	While improvements in the ability to rapidly and accurately interpret complex genetic tests are clearly needed, some results, such as pathogenic CFTR variants, including a new class of bicarbonate-defective mutations, and PRSS1 variants have immediate implications that direct management.	Bicarbonates	185-196	CF transmembrane conductance regulator	Homo sapiens	145-149	
25331955-7	2014	HCO3 (-) fluxes across epithelial cells were activated by a CFTR activator, but blocked by a CFTR inhibitor.	Bicarbonates	0-4	CF transmembrane conductance regulator	Homo sapiens	60-64	
25331955-7	2014	HCO3 (-) fluxes across epithelial cells were activated by a CFTR activator, but blocked by a CFTR inhibitor.	Bicarbonates	0-4	CF transmembrane conductance regulator	Homo sapiens	93-97	
26185361-2	2015	The ability of an epithelial cell to initiate CFTR-mediated chloride and bicarbonate transport has been recognized early as a means to regulate the thickness of the epithelial lining fluid and recently as a means to regulate the pH, thereby determining critically whether or not host defense proteins such as mucins are able to fold appropriately.	Bicarbonates	73-84	CF transmembrane conductance regulator	Homo sapiens	46-50	
24240699-5	2014	Ductal fluid and HCO3 (-) secretion are mediated by the basolateral membrane Na(+)-HCO3 (-) cotransporter NBCe1-B and the luminal membrane Cl(-)/HCO3 (-) exchanger slc26a6 and the Cl(-) channel CFTR.	Bicarbonates	17-21	CF transmembrane conductance regulator	Homo sapiens	194-198	
23215877-0	2013	Protein phosphatase 1 coordinates CFTR-dependent airway epithelial HCO3- secretion by reciprocal regulation of apical and basolateral membrane Cl(-)-HCO3- exchangers.	Bicarbonates	67-71	CF transmembrane conductance regulator	Homo sapiens	34-38	
25033378-0	2014	Mechanisms of CFTR functional variants that impair regulated bicarbonate permeation and increase risk for pancreatitis but not for cystic fibrosis.	Bicarbonates	61-72	CF transmembrane conductance regulator	Homo sapiens	14-18	
25033378-2	2014	Intracellular WNK1-SPAK activation causes CFTR to change permeability and conductance characteristics from a chloride-preferring to bicarbonate-preferring channel through unknown mechanisms.	Bicarbonates	132-143	CF transmembrane conductance regulator	Homo sapiens	42-46	
25033378-4	2014	We hypothesize that those CFTR mutations that disrupt the WNK1-SPAK activation mechanisms cause a selective, bicarbonate defect in channel function (CFTRBD) affecting organs that utilize CFTR for bicarbonate secretion (e.g. the pancreas, nasal sinus, vas deferens) but do not cause typical CF.	Bicarbonates	109-120	CF transmembrane conductance regulator	Homo sapiens	26-30	
25033378-4	2014	We hypothesize that those CFTR mutations that disrupt the WNK1-SPAK activation mechanisms cause a selective, bicarbonate defect in channel function (CFTRBD) affecting organs that utilize CFTR for bicarbonate secretion (e.g. the pancreas, nasal sinus, vas deferens) but do not cause typical CF.	Bicarbonates	109-120	CF transmembrane conductance regulator	Homo sapiens	149-153	
25033378-4	2014	We hypothesize that those CFTR mutations that disrupt the WNK1-SPAK activation mechanisms cause a selective, bicarbonate defect in channel function (CFTRBD) affecting organs that utilize CFTR for bicarbonate secretion (e.g. the pancreas, nasal sinus, vas deferens) but do not cause typical CF.	Bicarbonates	196-207	CF transmembrane conductance regulator	Homo sapiens	26-30	
25033378-4	2014	We hypothesize that those CFTR mutations that disrupt the WNK1-SPAK activation mechanisms cause a selective, bicarbonate defect in channel function (CFTRBD) affecting organs that utilize CFTR for bicarbonate secretion (e.g. the pancreas, nasal sinus, vas deferens) but do not cause typical CF.	Bicarbonates	196-207	CF transmembrane conductance regulator	Homo sapiens	149-153	
25033378-10	2014	WNK1-SPAK pathway-activated increases in CFTR bicarbonate permeability are altered by CFTRBD variants through multiple mechanisms.	Bicarbonates	46-57	CF transmembrane conductance regulator	Homo sapiens	41-45	
23916755-2	2013	While the cystic fibrosis transmembrane conductance regulator (CFTR), a Cl(-) and HCO3(-) conducting anion channel expressed in a wide variety of epithelial cells, has been implicated in the regulation of epithelial polarity, the exact role of CFTR in the pathogenesis of cancer and its possible involvement in EMT process have not been elucidated.	Bicarbonates	82-86	CF transmembrane conductance regulator	Homo sapiens	10-61	
23916755-2	2013	While the cystic fibrosis transmembrane conductance regulator (CFTR), a Cl(-) and HCO3(-) conducting anion channel expressed in a wide variety of epithelial cells, has been implicated in the regulation of epithelial polarity, the exact role of CFTR in the pathogenesis of cancer and its possible involvement in EMT process have not been elucidated.	Bicarbonates	82-86	CF transmembrane conductance regulator	Homo sapiens	63-67	
23916755-2	2013	While the cystic fibrosis transmembrane conductance regulator (CFTR), a Cl(-) and HCO3(-) conducting anion channel expressed in a wide variety of epithelial cells, has been implicated in the regulation of epithelial polarity, the exact role of CFTR in the pathogenesis of cancer and its possible involvement in EMT process have not been elucidated.	Bicarbonates	82-86	CF transmembrane conductance regulator	Homo sapiens	244-248	
23757197-1	2013	Cystic fibrosis (CF), a severe genetic disease, is caused by mutations that alter the structure and function of CFTR, a plasma membrane channel permeable to chloride and bicarbonate.	Bicarbonates	170-181	CF transmembrane conductance regulator	Homo sapiens	112-116	
23878362-6	2013	ENaC is negatively regulated by CFTR and, in patients with CF, the absence of CFTR results in a double hit of reduced Cl-/HCO3- and H2O secretion as well as ENaC hyperactivity and increased Na+ and H2O absorption.	Bicarbonates	122-126	CF transmembrane conductance regulator	Homo sapiens	32-36	
23878362-6	2013	ENaC is negatively regulated by CFTR and, in patients with CF, the absence of CFTR results in a double hit of reduced Cl-/HCO3- and H2O secretion as well as ENaC hyperactivity and increased Na+ and H2O absorption.	Bicarbonates	122-126	CF transmembrane conductance regulator	Homo sapiens	78-82	
23784542-7	2013	CCh stimulation concomitantly internalized the Na(+/)H(+) exchanger 3 (NHE3) and recruited cystic fibrosis transmembrane conductance regulator (CFTR) to the apical membranes, a process that was important for CFTR-mediated bicarbonate secretion necessary for proper gel-forming mucin unfolding.	Bicarbonates	222-233	CF transmembrane conductance regulator	Homo sapiens	91-142	
23784542-7	2013	CCh stimulation concomitantly internalized the Na(+/)H(+) exchanger 3 (NHE3) and recruited cystic fibrosis transmembrane conductance regulator (CFTR) to the apical membranes, a process that was important for CFTR-mediated bicarbonate secretion necessary for proper gel-forming mucin unfolding.	Bicarbonates	222-233	CF transmembrane conductance regulator	Homo sapiens	144-148	
24898583-5	2014	This was unaffected by the anion exchange inhibitor DIDS but inhibited by the CFTR blocker CFTRinh-172, suggesting that the HCO3- influx might occur via CFTR, rather than a solute carrier family 26 (SLC26) exchanger, as recently proposed.	Bicarbonates	124-128	CF transmembrane conductance regulator	Homo sapiens	78-82	
24898583-5	2014	This was unaffected by the anion exchange inhibitor DIDS but inhibited by the CFTR blocker CFTRinh-172, suggesting that the HCO3- influx might occur via CFTR, rather than a solute carrier family 26 (SLC26) exchanger, as recently proposed.	Bicarbonates	124-128	CF transmembrane conductance regulator	Homo sapiens	91-95	
24898583-7	2014	For pHi to rise to observed values (~7.8) through HCO3- entry via CFTR, the apical membrane potential must reverse to at least +20 mV following Cl- substitution; this was confirmed by perforated-patch recordings.	Bicarbonates	50-54	CF transmembrane conductance regulator	Homo sapiens	66-70	
24898583-9	2014	This appeared to be abolished in forskolin-stimulated cells but was unmasked by blocking apical efflux of HCO3- via CFTR.	Bicarbonates	106-110	CF transmembrane conductance regulator	Homo sapiens	116-120	
24898583-10	2014	We conclude that Calu-3 cells secrete HCO3- predominantly via CFTR, and, contrary to previous reports, the basolateral anion exchanger AE2 remains active during stimulation, providing an important pathway for basolateral Cl- uptake.	Bicarbonates	38-42	CF transmembrane conductance regulator	Homo sapiens	62-66	
24534272-2	2014	Although almost all members of this family are transporters, CFTR functions as a channel with specificity for anions, in particular chloride and bicarbonate.	Bicarbonates	145-156	CF transmembrane conductance regulator	Homo sapiens	61-65	
24224935-8	2014	These results indicate that two separate components for HCO3(-) secretion, likely via CFTR- and calcium-activated chloride channel-dependent processes, are physiologically regulated for likely roles in mucus clearance and antimicrobial innate defenses of small airways.	Bicarbonates	56-60	CF transmembrane conductance regulator	Homo sapiens	86-90	
24115633-4	2014	We also summarise recent work on Slc26a3 and Slc26a6 in uterine epithelial cells and sperm, revealing their functional role in working closely with the cystic fibrosis transmembrane conductance regulator (CFTR) for HCO3(-) transport in these cells.	Bicarbonates	215-219	CF transmembrane conductance regulator	Homo sapiens	152-203	
24115633-4	2014	We also summarise recent work on Slc26a3 and Slc26a6 in uterine epithelial cells and sperm, revealing their functional role in working closely with the cystic fibrosis transmembrane conductance regulator (CFTR) for HCO3(-) transport in these cells.	Bicarbonates	215-219	CF transmembrane conductance regulator	Homo sapiens	205-209	
24077955-9	2013	Reduction of CFTR expression in sperm from old men was correlated with lowered forward motility and decreased HCO3(-) sensitivity required for sperm capacitation.	Bicarbonates	110-114	CF transmembrane conductance regulator	Homo sapiens	13-17	
23740884-0	2013	Controversies surrounding the role of CFTR in airway bicarbonate secretion.	Bicarbonates	53-64	CF transmembrane conductance regulator	Homo sapiens	38-42	
23215877-0	2013	Protein phosphatase 1 coordinates CFTR-dependent airway epithelial HCO3- secretion by reciprocal regulation of apical and basolateral membrane Cl(-)-HCO3- exchangers.	Bicarbonates	149-153	CF transmembrane conductance regulator	Homo sapiens	34-38	
22777674-10	2012	Imposing a transepithelial HCO(3)(-) gradient across basolaterally permeabilized Calu-3 cells sustained a forskolin-stimulated current, which was sensitive to CFTR inhibitors and drastically reduced in CFTR-deficient cells.	Bicarbonates	27-33	CF transmembrane conductance regulator	Homo sapiens	159-163	
23431199-1	2013	Fluid and HCO3(-) secretion is a vital function of secretory epithelia, involving basolateral HCO3(-) entry through the Na(+)-HCO3(-) cotransporter (NBC) NBCe1-B, and luminal HCO3(-) exit mediated by cystic fibrosis transmembrane conductance regulator (CFTR) and solute carrier family 26 (SLC26) Cl(-)/HCO3(-) exchangers.	Bicarbonates	10-14	CF transmembrane conductance regulator	Homo sapiens	200-251	
23431199-1	2013	Fluid and HCO3(-) secretion is a vital function of secretory epithelia, involving basolateral HCO3(-) entry through the Na(+)-HCO3(-) cotransporter (NBC) NBCe1-B, and luminal HCO3(-) exit mediated by cystic fibrosis transmembrane conductance regulator (CFTR) and solute carrier family 26 (SLC26) Cl(-)/HCO3(-) exchangers.	Bicarbonates	10-14	CF transmembrane conductance regulator	Homo sapiens	253-257	
23431199-1	2013	Fluid and HCO3(-) secretion is a vital function of secretory epithelia, involving basolateral HCO3(-) entry through the Na(+)-HCO3(-) cotransporter (NBC) NBCe1-B, and luminal HCO3(-) exit mediated by cystic fibrosis transmembrane conductance regulator (CFTR) and solute carrier family 26 (SLC26) Cl(-)/HCO3(-) exchangers.	Bicarbonates	94-98	CF transmembrane conductance regulator	Homo sapiens	200-251	
23431199-1	2013	Fluid and HCO3(-) secretion is a vital function of secretory epithelia, involving basolateral HCO3(-) entry through the Na(+)-HCO3(-) cotransporter (NBC) NBCe1-B, and luminal HCO3(-) exit mediated by cystic fibrosis transmembrane conductance regulator (CFTR) and solute carrier family 26 (SLC26) Cl(-)/HCO3(-) exchangers.	Bicarbonates	94-98	CF transmembrane conductance regulator	Homo sapiens	253-257	
23431199-1	2013	Fluid and HCO3(-) secretion is a vital function of secretory epithelia, involving basolateral HCO3(-) entry through the Na(+)-HCO3(-) cotransporter (NBC) NBCe1-B, and luminal HCO3(-) exit mediated by cystic fibrosis transmembrane conductance regulator (CFTR) and solute carrier family 26 (SLC26) Cl(-)/HCO3(-) exchangers.	Bicarbonates	94-98	CF transmembrane conductance regulator	Homo sapiens	200-251	
23431199-1	2013	Fluid and HCO3(-) secretion is a vital function of secretory epithelia, involving basolateral HCO3(-) entry through the Na(+)-HCO3(-) cotransporter (NBC) NBCe1-B, and luminal HCO3(-) exit mediated by cystic fibrosis transmembrane conductance regulator (CFTR) and solute carrier family 26 (SLC26) Cl(-)/HCO3(-) exchangers.	Bicarbonates	94-98	CF transmembrane conductance regulator	Homo sapiens	253-257	
23431199-1	2013	Fluid and HCO3(-) secretion is a vital function of secretory epithelia, involving basolateral HCO3(-) entry through the Na(+)-HCO3(-) cotransporter (NBC) NBCe1-B, and luminal HCO3(-) exit mediated by cystic fibrosis transmembrane conductance regulator (CFTR) and solute carrier family 26 (SLC26) Cl(-)/HCO3(-) exchangers.	Bicarbonates	94-98	CF transmembrane conductance regulator	Homo sapiens	200-251	
23431199-1	2013	Fluid and HCO3(-) secretion is a vital function of secretory epithelia, involving basolateral HCO3(-) entry through the Na(+)-HCO3(-) cotransporter (NBC) NBCe1-B, and luminal HCO3(-) exit mediated by cystic fibrosis transmembrane conductance regulator (CFTR) and solute carrier family 26 (SLC26) Cl(-)/HCO3(-) exchangers.	Bicarbonates	94-98	CF transmembrane conductance regulator	Homo sapiens	253-257	
23457166-2	2013	These mutations can impact the synthesis and transfer of the CFTR protein to the apical membrane of epithelial cells, as well as influencing the gating or conductance of chloride and bicarbonate ions through the channel.	Bicarbonates	183-194	CF transmembrane conductance regulator	Homo sapiens	61-65	
23931280-3	2013	The membrane HCO3- transporters are divided in two main families: solute carrier 4 (SLC4) and solute carrier 26 (SLC26), although HCO3- concentration can also be regulated by the cystic fibrosis transmembrane regulator (CFTR).	Bicarbonates	13-17	CF transmembrane conductance regulator	Homo sapiens	179-218	
23931280-3	2013	The membrane HCO3- transporters are divided in two main families: solute carrier 4 (SLC4) and solute carrier 26 (SLC26), although HCO3- concentration can also be regulated by the cystic fibrosis transmembrane regulator (CFTR).	Bicarbonates	13-17	CF transmembrane conductance regulator	Homo sapiens	220-224	
22552906-3	2012	The lymphocyte-enhanced epithelial HCO(3)- secretion and bacterial killing activity was abolished when Calu3 cells were co-cultured with lymphocytes from CFTR knockout mice, or significantly reduced by interfering with E-cadherin, a putative binding partner of CFTR.	Bicarbonates	35-41	CF transmembrane conductance regulator	Homo sapiens	154-158	
23125206-4	2012	This process is defective in the absence of cystic fibrosis transmembrane conductance regulator (CFTR)-dependent bicarbonate transport.	Bicarbonates	113-124	CF transmembrane conductance regulator	Homo sapiens	44-95	
23125206-4	2012	This process is defective in the absence of cystic fibrosis transmembrane conductance regulator (CFTR)-dependent bicarbonate transport.	Bicarbonates	113-124	CF transmembrane conductance regulator	Homo sapiens	97-101	
22709980-7	2012	Evidence also reveals a critical role of CFTR in sperm capacitation by directly or indirectly mediating HCO(3)(-) entry that is essential for capacitation.	Bicarbonates	104-110	CF transmembrane conductance regulator	Homo sapiens	41-45	
22777674-10	2012	Imposing a transepithelial HCO(3)(-) gradient across basolaterally permeabilized Calu-3 cells sustained a forskolin-stimulated current, which was sensitive to CFTR inhibitors and drastically reduced in CFTR-deficient cells.	Bicarbonates	27-33	CF transmembrane conductance regulator	Homo sapiens	202-206	
22908201-2	2012	Studies with Calu-3 cells, an airway serous model with high expression of CFTR, also show the secretion of HCO(3)(-) when cells are stimulated with cAMP-mediated agonists.	Bicarbonates	107-113	CF transmembrane conductance regulator	Homo sapiens	74-78	
23028131-1	2012	Many cystic fibrosis transmembrane conductance regulator (CFTR)-expressing epithelia secrete bicarbonate (HCO(3)(-))-containing fluids.	Bicarbonates	93-104	CF transmembrane conductance regulator	Homo sapiens	5-56	
23028131-1	2012	Many cystic fibrosis transmembrane conductance regulator (CFTR)-expressing epithelia secrete bicarbonate (HCO(3)(-))-containing fluids.	Bicarbonates	93-104	CF transmembrane conductance regulator	Homo sapiens	58-62	
23028131-1	2012	Many cystic fibrosis transmembrane conductance regulator (CFTR)-expressing epithelia secrete bicarbonate (HCO(3)(-))-containing fluids.	Bicarbonates	106-112	CF transmembrane conductance regulator	Homo sapiens	5-56	
23028131-1	2012	Many cystic fibrosis transmembrane conductance regulator (CFTR)-expressing epithelia secrete bicarbonate (HCO(3)(-))-containing fluids.	Bicarbonates	106-112	CF transmembrane conductance regulator	Homo sapiens	58-62	
23028131-3	2012	Pancreatic juice is one of the representative fluids that contain a very high concentration of bicarbonate among bodily fluids that are secreted from CFTR-expressing epithelia.	Bicarbonates	95-106	CF transmembrane conductance regulator	Homo sapiens	150-154	
23028131-6	2012	As a central regulator of bicarbonate transport at the apical membrane, CFTR plays an essential role in both direct and indirect bicarbonate secretion.	Bicarbonates	26-37	CF transmembrane conductance regulator	Homo sapiens	72-76	
23028131-6	2012	As a central regulator of bicarbonate transport at the apical membrane, CFTR plays an essential role in both direct and indirect bicarbonate secretion.	Bicarbonates	129-140	CF transmembrane conductance regulator	Homo sapiens	72-76	
23028131-7	2012	The major role of CFTR in bicarbonate secretion would be variable depending on the tissue and cell type.	Bicarbonates	26-37	CF transmembrane conductance regulator	Homo sapiens	18-22	
23028131-8	2012	For example, in epithelial cells that produce a low concentration of bicarbonate-containing fluid (up to 80 mm), either CFTR-dependent Cl(-)/HCO(3)(-) exchange or CFTR anion channel with low bicarbonate permeability would be sufficient to generate such fluid.	Bicarbonates	69-80	CF transmembrane conductance regulator	Homo sapiens	120-124	
23028131-8	2012	For example, in epithelial cells that produce a low concentration of bicarbonate-containing fluid (up to 80 mm), either CFTR-dependent Cl(-)/HCO(3)(-) exchange or CFTR anion channel with low bicarbonate permeability would be sufficient to generate such fluid.	Bicarbonates	69-80	CF transmembrane conductance regulator	Homo sapiens	163-167	
23028131-8	2012	For example, in epithelial cells that produce a low concentration of bicarbonate-containing fluid (up to 80 mm), either CFTR-dependent Cl(-)/HCO(3)(-) exchange or CFTR anion channel with low bicarbonate permeability would be sufficient to generate such fluid.	Bicarbonates	141-147	CF transmembrane conductance regulator	Homo sapiens	120-124	
23028131-8	2012	For example, in epithelial cells that produce a low concentration of bicarbonate-containing fluid (up to 80 mm), either CFTR-dependent Cl(-)/HCO(3)(-) exchange or CFTR anion channel with low bicarbonate permeability would be sufficient to generate such fluid.	Bicarbonates	191-202	CF transmembrane conductance regulator	Homo sapiens	120-124	
23028131-8	2012	For example, in epithelial cells that produce a low concentration of bicarbonate-containing fluid (up to 80 mm), either CFTR-dependent Cl(-)/HCO(3)(-) exchange or CFTR anion channel with low bicarbonate permeability would be sufficient to generate such fluid.	Bicarbonates	191-202	CF transmembrane conductance regulator	Homo sapiens	163-167	
23028131-9	2012	However, in cells that secrete high-bicarbonate-containing fluids, a highly selective CFTR bicarbonate channel activity is required.	Bicarbonates	36-47	CF transmembrane conductance regulator	Homo sapiens	86-90	
23028131-10	2012	Therefore, understanding the molecular mechanism of transepithelial bicarbonate transport and the role of CFTR in each specific epithelium will provide therapeutic strategies to recover from epithelial defects induced by hyposecretion of bicarbonate in cystic fibrosis.	Bicarbonates	238-249	CF transmembrane conductance regulator	Homo sapiens	106-110	
21893120-0	2011	Trypsin reduces pancreatic ductal bicarbonate secretion by inhibiting CFTR Cl- channels and luminal anion exchangers.	Bicarbonates	34-45	CF transmembrane conductance regulator	Homo sapiens	70-74	
22226887-2	2012	A dysfunctional cystic fibrosis transmembrane conductance regulator impairs the efflux of cell anions such as chloride and bicarbonate, and also that of other solutes such as reduced glutathione.	Bicarbonates	123-134	CF transmembrane conductance regulator	Homo sapiens	16-67	
22121115-4	2012	The cystic fibrosis transmembrane conductance regulator (CFTR) is expressed in mature sperm and has been shown to contribute to Cl(-) and HCO(3)(-) movements during capacitation.	Bicarbonates	138-144	CF transmembrane conductance regulator	Homo sapiens	4-55	
22121115-4	2012	The cystic fibrosis transmembrane conductance regulator (CFTR) is expressed in mature sperm and has been shown to contribute to Cl(-) and HCO(3)(-) movements during capacitation.	Bicarbonates	138-144	CF transmembrane conductance regulator	Homo sapiens	57-61	
22121115-8	2012	These various results suggest that TAT1 and CFTR may form a molecular complex involved in the regulation of Cl(-) and HCO(3)(-) fluxes during sperm capacitation.	Bicarbonates	118-124	CF transmembrane conductance regulator	Homo sapiens	44-48	
22515107-5	2012	HCO3- secretion critically depends on the activity of CFTR, a cAMP-dependent anion channel localized in the apical membrane of various epithelia.	Bicarbonates	0-4	CF transmembrane conductance regulator	Homo sapiens	54-58	
22515107-7	2012	In distal ducts where the luminal HCO3- concentration is already high, most of the HCO3- secretion is mediated by HCO3- conductance of CFTR.	Bicarbonates	34-38	CF transmembrane conductance regulator	Homo sapiens	135-139	
22515107-7	2012	In distal ducts where the luminal HCO3- concentration is already high, most of the HCO3- secretion is mediated by HCO3- conductance of CFTR.	Bicarbonates	83-87	CF transmembrane conductance regulator	Homo sapiens	135-139	
22515107-7	2012	In distal ducts where the luminal HCO3- concentration is already high, most of the HCO3- secretion is mediated by HCO3- conductance of CFTR.	Bicarbonates	83-87	CF transmembrane conductance regulator	Homo sapiens	135-139	
22074182-1	2011	Cystic fibrosis transmembrane conductance regulator (CFTR) is a cell-surface anion channel that permeates chloride and bicarbonate ions.	Bicarbonates	119-130	CF transmembrane conductance regulator	Homo sapiens	0-51	
22074182-1	2011	Cystic fibrosis transmembrane conductance regulator (CFTR) is a cell-surface anion channel that permeates chloride and bicarbonate ions.	Bicarbonates	119-130	CF transmembrane conductance regulator	Homo sapiens	53-57	
21893120-7	2011	Trypsin increased intracellular Ca(2+) concentration and intracellular pH and inhibited secretion of bicarbonate by the luminal anion exchanger and the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel.	Bicarbonates	101-112	CF transmembrane conductance regulator	Homo sapiens	152-203	
21893120-7	2011	Trypsin increased intracellular Ca(2+) concentration and intracellular pH and inhibited secretion of bicarbonate by the luminal anion exchanger and the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel.	Bicarbonates	101-112	CF transmembrane conductance regulator	Homo sapiens	205-209	
21914796-0	2011	Novel role for pendrin in orchestrating bicarbonate secretion in cystic fibrosis transmembrane conductance regulator (CFTR)-expressing airway serous cells.	Bicarbonates	40-51	CF transmembrane conductance regulator	Homo sapiens	65-116	
21914796-0	2011	Novel role for pendrin in orchestrating bicarbonate secretion in cystic fibrosis transmembrane conductance regulator (CFTR)-expressing airway serous cells.	Bicarbonates	40-51	CF transmembrane conductance regulator	Homo sapiens	118-122	
21914796-1	2011	In most HCO(3)(-)-secreting epithelial tissues, SLC26 Cl(-)/HCO(3)(-) transporters work in concert with the cystic fibrosis transmembrane conductance regulator (CFTR) to regulate the magnitude and composition of the secreted fluid, a process that is vital for normal tissue function.	Bicarbonates	8-14	CF transmembrane conductance regulator	Homo sapiens	108-159	
21914796-1	2011	In most HCO(3)(-)-secreting epithelial tissues, SLC26 Cl(-)/HCO(3)(-) transporters work in concert with the cystic fibrosis transmembrane conductance regulator (CFTR) to regulate the magnitude and composition of the secreted fluid, a process that is vital for normal tissue function.	Bicarbonates	8-14	CF transmembrane conductance regulator	Homo sapiens	161-165	
21914796-1	2011	In most HCO(3)(-)-secreting epithelial tissues, SLC26 Cl(-)/HCO(3)(-) transporters work in concert with the cystic fibrosis transmembrane conductance regulator (CFTR) to regulate the magnitude and composition of the secreted fluid, a process that is vital for normal tissue function.	Bicarbonates	60-66	CF transmembrane conductance regulator	Homo sapiens	108-159	
21914796-1	2011	In most HCO(3)(-)-secreting epithelial tissues, SLC26 Cl(-)/HCO(3)(-) transporters work in concert with the cystic fibrosis transmembrane conductance regulator (CFTR) to regulate the magnitude and composition of the secreted fluid, a process that is vital for normal tissue function.	Bicarbonates	60-66	CF transmembrane conductance regulator	Homo sapiens	161-165	
21914796-2	2011	By contrast, CFTR is regarded as the only exit pathway for HCO(3)(-) in the airways.	Bicarbonates	59-65	CF transmembrane conductance regulator	Homo sapiens	13-17	
21914796-4	2011	Real-time measurement of intracellular pH from polarized cultures of human Calu-3 cells demonstrated cAMP/PKA-activated Cl(-)-dependent HCO(3)(-) transport across the luminal membrane via CFTR-dependent coupled Cl(-)/HCO(3)(-) anion exchange.	Bicarbonates	136-142	CF transmembrane conductance regulator	Homo sapiens	188-192	
21914796-4	2011	Real-time measurement of intracellular pH from polarized cultures of human Calu-3 cells demonstrated cAMP/PKA-activated Cl(-)-dependent HCO(3)(-) transport across the luminal membrane via CFTR-dependent coupled Cl(-)/HCO(3)(-) anion exchange.	Bicarbonates	217-223	CF transmembrane conductance regulator	Homo sapiens	188-192	
21328463-1	2011	Cystic fibrosis transmembrane conductance regulator (CFTR) is an apical membrane chloride channel critical to the regulation of fluid, chloride, and bicarbonate transport in epithelia and other cell types.	Bicarbonates	149-160	CF transmembrane conductance regulator	Homo sapiens	0-51	
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.	Bicarbonates	34-40	CF transmembrane conductance regulator	Homo sapiens	137-141	
21652558-1	2011	Recent advances in basic science have greatly expanded our understanding of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR), the chloride and bicarbonate channel that is encoded by the gene, which is mutated in patients with CF.	Bicarbonates	162-173	CF transmembrane conductance regulator	Homo sapiens	80-136	
21652558-1	2011	Recent advances in basic science have greatly expanded our understanding of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR), the chloride and bicarbonate channel that is encoded by the gene, which is mutated in patients with CF.	Bicarbonates	162-173	CF transmembrane conductance regulator	Homo sapiens	138-142	
21389278-0	2011	Parathyroid hormone (PTH) rapidly enhances CFTR-mediated HCO3- secretion in intestinal epithelium-like Caco-2 monolayer: a novel ion regulatory action of PTH.	Bicarbonates	57-61	CF transmembrane conductance regulator	Homo sapiens	43-47	
21389278-9	2011	In conclusion, the present study provided evidence that PTH directly and rapidly stimulated apical HCO3- secretion through CFTR in PKA- and PI3K-dependent manner, which was a novel noncalciotropic, ion regulatory action of PTH in the intestinal epithelium.	Bicarbonates	99-103	CF transmembrane conductance regulator	Homo sapiens	123-127	
21474426-10	2011	CFTR(inh)-172, a specific CFTR channel blocker, inhibited basal HCO(3)(-) secretion as well as stimulation of HCO(3)(-) secretion by IBMX.	Bicarbonates	64-70	CF transmembrane conductance regulator	Homo sapiens	0-4	
21474426-10	2011	CFTR(inh)-172, a specific CFTR channel blocker, inhibited basal HCO(3)(-) secretion as well as stimulation of HCO(3)(-) secretion by IBMX.	Bicarbonates	64-70	CF transmembrane conductance regulator	Homo sapiens	26-30	
21474426-10	2011	CFTR(inh)-172, a specific CFTR channel blocker, inhibited basal HCO(3)(-) secretion as well as stimulation of HCO(3)(-) secretion by IBMX.	Bicarbonates	110-116	CF transmembrane conductance regulator	Homo sapiens	0-4	
21328463-1	2011	Cystic fibrosis transmembrane conductance regulator (CFTR) is an apical membrane chloride channel critical to the regulation of fluid, chloride, and bicarbonate transport in epithelia and other cell types.	Bicarbonates	149-160	CF transmembrane conductance regulator	Homo sapiens	53-57	
20926782-0	2011	Regulation of CFTR chloride channel macroscopic conductance by extracellular bicarbonate.	Bicarbonates	77-88	CF transmembrane conductance regulator	Homo sapiens	14-18	
20926782-1	2011	The CFTR contributes to Cl- and HCO3- transport across epithelial cell apical membranes.	Bicarbonates	32-36	CF transmembrane conductance regulator	Homo sapiens	4-8	
20926782-2	2011	The extracellular face of CFTR is exposed to varying concentrations of Cl- and HCO3- in epithelial tissues, and there is evidence that CFTR is sensitive to changes in extracellular anion concentrations.	Bicarbonates	79-83	CF transmembrane conductance regulator	Homo sapiens	26-30	
20926782-2	2011	The extracellular face of CFTR is exposed to varying concentrations of Cl- and HCO3- in epithelial tissues, and there is evidence that CFTR is sensitive to changes in extracellular anion concentrations.	Bicarbonates	79-83	CF transmembrane conductance regulator	Homo sapiens	135-139	
20926782-3	2011	Here we present functional evidence that extracellular Cl- and HCO3- regulate anion conduction in open CFTR channels.	Bicarbonates	63-67	CF transmembrane conductance regulator	Homo sapiens	103-107	
20926782-4	2011	Using cell-attached and inside-out patch-clamp recordings from constitutively active mutant E1371Q-CFTR channels, we show that voltage-dependent inhibition of CFTR currents in intact cells is significantly stronger when the extracellular solution contains HCO3- than when it contains Cl-.	Bicarbonates	256-260	CF transmembrane conductance regulator	Homo sapiens	99-103	
20926782-4	2011	Using cell-attached and inside-out patch-clamp recordings from constitutively active mutant E1371Q-CFTR channels, we show that voltage-dependent inhibition of CFTR currents in intact cells is significantly stronger when the extracellular solution contains HCO3- than when it contains Cl-.	Bicarbonates	256-260	CF transmembrane conductance regulator	Homo sapiens	159-163	
20926782-6	2011	Strong block by endogenous cytosolic anions leading to reduced CFTR channel currents in intact cells occurs at physiologically relevant HCO3- concentrations and membrane potentials and can result in up to ~50% inhibition of current amplitude.	Bicarbonates	136-140	CF transmembrane conductance regulator	Homo sapiens	63-67	
21145458-6	2010	CFTR-(/)- epithelia showed markedly reduced Cl- and HCO3- transport.	Bicarbonates	52-56	CF transmembrane conductance regulator	Homo sapiens	0-4	
20977904-0	2011	Combined bicarbonate conductance-impairing variants in CFTR and SPINK1 variants are associated with chronic pancreatitis in patients without cystic fibrosis.	Bicarbonates	9-20	CF transmembrane conductance regulator	Homo sapiens	55-59	
20977904-2	2011	In individuals without cystic fibrosis (CF), variants of CFTR that inhibit bicarbonate conductance but maintain chloride conductance might selectively impair secretion of pancreatic juice, leading to trypsin activation and pancreatitis.	Bicarbonates	75-86	CF transmembrane conductance regulator	Homo sapiens	57-61	
20977904-10	2011	Patch-clamp recordings of cells that expressed CFTR p.R75Q showed normal chloride currents but significantly reduced bicarbonate currents (P = .0001).	Bicarbonates	117-128	CF transmembrane conductance regulator	Homo sapiens	47-51	
20977904-11	2011	CONCLUSIONS: The CFTR variant p.R75Q causes a selective defect in bicarbonate conductance and increases risk of pancreatitis.	Bicarbonates	66-77	CF transmembrane conductance regulator	Homo sapiens	17-21	
21594803-8	2011	It is therefore essential to assay bicarbonate transport when studying the effect of small molecules on CFTR function.	Bicarbonates	35-46	CF transmembrane conductance regulator	Homo sapiens	104-108	
21594803-9	2011	However, due to the chaotropic nature of the ion, the measurement of the absolute bicarbonate concentration and its permeability through CFTR is far from trivial.	Bicarbonates	82-93	CF transmembrane conductance regulator	Homo sapiens	137-141	
21151921-8	2010	The relevance of the CFTR-mediated HCO(3)(-) secretion in humans was demonstrated by the upregulated expression of CFTR and CAII in human prostatitis tissues.	Bicarbonates	35-41	CF transmembrane conductance regulator	Homo sapiens	21-25	
21151921-8	2010	The relevance of the CFTR-mediated HCO(3)(-) secretion in humans was demonstrated by the upregulated expression of CFTR and CAII in human prostatitis tissues.	Bicarbonates	35-41	CF transmembrane conductance regulator	Homo sapiens	115-119	
21594802-2	2011	CFTR functions as an ATP-gated, phosphorylation-regulated Cl- channel that mediates agonist-stimulated apical membrane epithelial Cl- and bicarbonate secretion and also regulates a variety of other transport proteins and cellular processes.	Bicarbonates	138-149	CF transmembrane conductance regulator	Homo sapiens	0-4	
21594803-0	2011	How to measure CFTR-dependent bicarbonate transport: from single channels to the intact epithelium.	Bicarbonates	30-41	CF transmembrane conductance regulator	Homo sapiens	15-19	
21145458-9	2010	These results indicate that CFTR provides the predominant transcellular pathway for Cl- and HCO3- in porcine airway epithelia, and reduced anion permeability may initiate CF airway disease.	Bicarbonates	92-96	CF transmembrane conductance regulator	Homo sapiens	28-32	
20406739-0	2010	Involvement of CFTR in oviductal HCO3- secretion and its effect on soluble adenylate cyclase-dependent early embryo development.	Bicarbonates	33-37	CF transmembrane conductance regulator	Homo sapiens	15-19	
20406739-6	2010	pH measurement showed a FSK stimulated alkalization at the apical surface, which could be inhibited by CFTR inhibitor, indicating CFTR-mediated HCO(3)(-) secretion.	Bicarbonates	144-150	CF transmembrane conductance regulator	Homo sapiens	103-107	
20406739-6	2010	pH measurement showed a FSK stimulated alkalization at the apical surface, which could be inhibited by CFTR inhibitor, indicating CFTR-mediated HCO(3)(-) secretion.	Bicarbonates	144-150	CF transmembrane conductance regulator	Homo sapiens	130-134	
20406739-10	2010	CONCLUSION: The present results suggest that CFTR-mediated oviductal HCO(3)(-) secretion may be vital for sAC-dependent early embryo development, a defect of which may contribute to the reduced fertility seen in women with CF.	Bicarbonates	69-75	CF transmembrane conductance regulator	Homo sapiens	45-49	
20639512-2	2010	Because apical HCO(3)(-) exchange depends on cystic fibrosis transmembrane conductance regulator (CFTR), malfunctioning CFTR might impair sAC-mediated CBF regulation in cells from patients with cystic fibrosis (CF).	Bicarbonates	15-21	CF transmembrane conductance regulator	Homo sapiens	45-96	
20639512-2	2010	Because apical HCO(3)(-) exchange depends on cystic fibrosis transmembrane conductance regulator (CFTR), malfunctioning CFTR might impair sAC-mediated CBF regulation in cells from patients with cystic fibrosis (CF).	Bicarbonates	15-21	CF transmembrane conductance regulator	Homo sapiens	98-102	
20639512-5	2010	Inhibition of bicarbonate influx via CFTR (CFTR(inh)172) and inhibition of sAC (KH7) and PKA activation (H89) led to larger CBF declines in normal cells, now comparable with changes seen in CF cells.	Bicarbonates	14-25	CF transmembrane conductance regulator	Homo sapiens	37-41	
20639512-5	2010	Inhibition of bicarbonate influx via CFTR (CFTR(inh)172) and inhibition of sAC (KH7) and PKA activation (H89) led to larger CBF declines in normal cells, now comparable with changes seen in CF cells.	Bicarbonates	14-25	CF transmembrane conductance regulator	Homo sapiens	43-55	
20398666-0	2010	Dynamic regulation of CFTR bicarbonate permeability by [Cl-]i and its role in pancreatic bicarbonate secretion.	Bicarbonates	27-38	CF transmembrane conductance regulator	Homo sapiens	22-26	
20398666-0	2010	Dynamic regulation of CFTR bicarbonate permeability by [Cl-]i and its role in pancreatic bicarbonate secretion.	Bicarbonates	89-100	CF transmembrane conductance regulator	Homo sapiens	22-26	
20398666-3	2010	Here, we report that a dynamic increase in the cystic fibrosis transmembrane conductance regulator (CFTR) HCO3- permeability by intracellular Cl- concentration ([Cl-]i)-sensitive mechanisms plays a pivotal role in pancreatic HCO3- secretion.	Bicarbonates	106-110	CF transmembrane conductance regulator	Homo sapiens	47-98	
20398666-3	2010	Here, we report that a dynamic increase in the cystic fibrosis transmembrane conductance regulator (CFTR) HCO3- permeability by intracellular Cl- concentration ([Cl-]i)-sensitive mechanisms plays a pivotal role in pancreatic HCO3- secretion.	Bicarbonates	106-110	CF transmembrane conductance regulator	Homo sapiens	100-104	
20398666-4	2010	METHODS: The role of [Cl-]i-sensitive kinases in CFTR-mediated HCO3- transport was examined in heterologous expression systems, PANC1 human pancreatic duct cells, and human and guinea pig pancreatic tissues using an integrated molecular and physiologic approach.	Bicarbonates	63-67	CF transmembrane conductance regulator	Homo sapiens	49-53	
20406739-2	2010	METHODS: In the present study, we investigated the expression of CFTR in porcine oviduct and its functional role in oviductal HCO(3)(-) secretion and embryo development with RT-PCR, western blot, patch-clamp, short-circuit current (I(sc)), pH measurement and embryo culture.	Bicarbonates	126-132	CF transmembrane conductance regulator	Homo sapiens	65-69	
20004757-2	2010	The gene mutated in these patients is CFTR, a Cl(-) channel involved in transepithelial salt and water transport and bicarbonate secretion.	Bicarbonates	117-128	CF transmembrane conductance regulator	Homo sapiens	38-42	
20080093-10	2010	A large fraction of the cystic fibrosis transmembrane conductance regulator (CFTR), which plays a central role in pancreatic duct HCO(3)(-) secretion, was mislocalized to the cytoplasm of duct cells before treatment.	Bicarbonates	130-136	CF transmembrane conductance regulator	Homo sapiens	24-75	
20080093-10	2010	A large fraction of the cystic fibrosis transmembrane conductance regulator (CFTR), which plays a central role in pancreatic duct HCO(3)(-) secretion, was mislocalized to the cytoplasm of duct cells before treatment.	Bicarbonates	130-136	CF transmembrane conductance regulator	Homo sapiens	77-81	
20080093-11	2010	Corticosteroids corrected the localization of CFTR to the apical membrane, accounting for the improved HCO(3)(-) secretion.	Bicarbonates	103-110	CF transmembrane conductance regulator	Homo sapiens	46-50	
20080093-14	2010	Mislocalization of CFTR may explain aberrant HCO(3)(-) secretion in other forms of pancreatitis.	Bicarbonates	45-52	CF transmembrane conductance regulator	Homo sapiens	19-23	
21242704-6	2010	In the last 10 years, several new HCO(3)(-) transporters in the Slc26 family and their interaction with the cystic fibrosis transmembrane conductance regulator-chloride channel have elucidated the HCO(3)(-) exit step at the ductal lumen.	Bicarbonates	34-39	CF transmembrane conductance regulator	Homo sapiens	108-159	
20332619-3	2010	CFTR is an ATP-hydrolyzing, cAMP/PKA-activated anion channel regulating pancreatic bicarbonate/chloride secretion across duct-facing apical membranes in epithelia.	Bicarbonates	83-94	CF transmembrane conductance regulator	Homo sapiens	0-4	
19571747-5	2009	The apical CFTR channels also appear to have sufficient HCO(3)(-) permeability to contribute directly to HCO(3)(-) secretion.	Bicarbonates	56-62	CF transmembrane conductance regulator	Homo sapiens	11-15	
19752774-0	2009	CFTR expression but not Cl- transport is involved in the stimulatory effect of bile acids on apical Cl-/HCO3- exchange activity in human pancreatic duct cells.	Bicarbonates	104-108	CF transmembrane conductance regulator	Homo sapiens	0-4	
19358684-6	2009	In the airways, a major function of DUOX is to support lactoperoxidase (LPO) to generate bactericidal OSCN(-), and there are indications that the DUOX/LPO defense system is critically dependent on the function of the CFTR Cl(-) channel, which provides both SCN(-) (for LPO function) and HCO(3)(-) (for pH adjustment) to the airway surface liquid.	Bicarbonates	287-293	CF transmembrane conductance regulator	Homo sapiens	217-221	
19571747-5	2009	The apical CFTR channels also appear to have sufficient HCO(3)(-) permeability to contribute directly to HCO(3)(-) secretion.	Bicarbonates	105-111	CF transmembrane conductance regulator	Homo sapiens	11-15	
19571747-6	2009	There is a strong possibility that the Ca(2+)-activated Cl(-) channels at the apical membrane are members of the bestrophin family which, like CFTR, are also permeable to HCO(3)(-).	Bicarbonates	171-177	CF transmembrane conductance regulator	Homo sapiens	143-147	
19538314-2	2009	DRA (downregulated in adenoma) is an intestinal chloride/bicarbonate exchanger that is functionally coupled to CFTR (cystic fibrosis transmembrane regulator) in the upper gastrointestinal tract to mediate chloride and bicarbonate secretion and to NHE3 (Na/H exchanger- isoform 3) in the lower gastrointestinal tract to mediate electroneutral NaCl absorption.	Bicarbonates	57-68	CF transmembrane conductance regulator	Homo sapiens	111-115	
19015188-4	2009	This review discusses the role of CFTR in regulating fluid volume and bicarbonate secretion in the reproductive tracts and their importance in various reproductive events.	Bicarbonates	70-81	CF transmembrane conductance regulator	Homo sapiens	34-38	
19538314-2	2009	DRA (downregulated in adenoma) is an intestinal chloride/bicarbonate exchanger that is functionally coupled to CFTR (cystic fibrosis transmembrane regulator) in the upper gastrointestinal tract to mediate chloride and bicarbonate secretion and to NHE3 (Na/H exchanger- isoform 3) in the lower gastrointestinal tract to mediate electroneutral NaCl absorption.	Bicarbonates	57-68	CF transmembrane conductance regulator	Homo sapiens	117-156	
19538314-2	2009	DRA (downregulated in adenoma) is an intestinal chloride/bicarbonate exchanger that is functionally coupled to CFTR (cystic fibrosis transmembrane regulator) in the upper gastrointestinal tract to mediate chloride and bicarbonate secretion and to NHE3 (Na/H exchanger- isoform 3) in the lower gastrointestinal tract to mediate electroneutral NaCl absorption.	Bicarbonates	218-229	CF transmembrane conductance regulator	Homo sapiens	111-115	
19538314-2	2009	DRA (downregulated in adenoma) is an intestinal chloride/bicarbonate exchanger that is functionally coupled to CFTR (cystic fibrosis transmembrane regulator) in the upper gastrointestinal tract to mediate chloride and bicarbonate secretion and to NHE3 (Na/H exchanger- isoform 3) in the lower gastrointestinal tract to mediate electroneutral NaCl absorption.	Bicarbonates	218-229	CF transmembrane conductance regulator	Homo sapiens	117-156	
19019741-0	2009	Mechanism of direct bicarbonate transport by the CFTR anion channel.	Bicarbonates	20-31	CF transmembrane conductance regulator	Homo sapiens	49-53	
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).	Bicarbonates	32-38	CF transmembrane conductance regulator	Homo sapiens	12-16	
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).	Bicarbonates	90-96	CF transmembrane conductance regulator	Homo sapiens	12-16	
19019741-3	2009	METHODS: Patch clamp recordings from membrane patches excised from cells heterologously expressing wild type and mutant forms of human CFTR were used to isolate directly CFTR-mediated HCO(3)(-) transport and characterize its functional properties.	Bicarbonates	184-190	CF transmembrane conductance regulator	Homo sapiens	135-139	
19019741-3	2009	METHODS: Patch clamp recordings from membrane patches excised from cells heterologously expressing wild type and mutant forms of human CFTR were used to isolate directly CFTR-mediated HCO(3)(-) transport and characterize its functional properties.	Bicarbonates	184-190	CF transmembrane conductance regulator	Homo sapiens	170-174	
19019741-5	2009	CFTR-mediated HCO(3)(-) currents were inhibited by open channel blockers DNDS, glibenclamide and suramin, and these inhibitions were affected by mutations within the channel pore.	Bicarbonates	14-20	CF transmembrane conductance regulator	Homo sapiens	0-4	
19019741-7	2009	CONCLUSIONS: Cl(-) and HCO(3)(-) share a common transport pathway in CFTR, and selectivity between Cl(-) and HCO(3)(-) is independent of ionic conditions.	Bicarbonates	23-29	CF transmembrane conductance regulator	Homo sapiens	69-73	
19019741-7	2009	CONCLUSIONS: Cl(-) and HCO(3)(-) share a common transport pathway in CFTR, and selectivity between Cl(-) and HCO(3)(-) is independent of ionic conditions.	Bicarbonates	109-115	CF transmembrane conductance regulator	Homo sapiens	69-73	
19019741-9	2009	We suggest that mutations in CFTR that cause cystic fibrosis by selectively disrupting HCO(3)(-) transport do not impair direct CFTR-mediated HCO(3)(-) transport, but may predominantly alter CFTR regulation of other HCO(3)(-) transport pathways.	Bicarbonates	87-93	CF transmembrane conductance regulator	Homo sapiens	29-33	
19019741-9	2009	We suggest that mutations in CFTR that cause cystic fibrosis by selectively disrupting HCO(3)(-) transport do not impair direct CFTR-mediated HCO(3)(-) transport, but may predominantly alter CFTR regulation of other HCO(3)(-) transport pathways.	Bicarbonates	142-148	CF transmembrane conductance regulator	Homo sapiens	29-33	
19019741-9	2009	We suggest that mutations in CFTR that cause cystic fibrosis by selectively disrupting HCO(3)(-) transport do not impair direct CFTR-mediated HCO(3)(-) transport, but may predominantly alter CFTR regulation of other HCO(3)(-) transport pathways.	Bicarbonates	142-148	CF transmembrane conductance regulator	Homo sapiens	29-33	
17654517-7	2008	In CFTR-corrected cells, apical Cl-/HCO3- exchange activity was further enhanced by cAMP, a key feature exhibited by normal pancreatic duct cells.	Bicarbonates	36-40	CF transmembrane conductance regulator	Homo sapiens	3-7	
18385283-7	2008	Furthermore, the dual activation of CFTR and KCa channels by apical adenosine resulted in a mixed secretion of chloride and bicarbonate, which may alter the anion composition in the secretion induced by secretagogues that elicit extracellular ATP/adenosine release.	Bicarbonates	124-135	CF transmembrane conductance regulator	Homo sapiens	36-40	
17654517-8	2008	The cAMP stimulated Cl-/HCO3- exchange was inhibited by dihydro-4,4"-diisothiocyanostilbene-2,2"-disulfonic acid (H2-DIDS), but not by a specific CFTR inhibitor, CFTR(inh)-172.	Bicarbonates	24-28	CF transmembrane conductance regulator	Homo sapiens	146-150	
17654517-8	2008	The cAMP stimulated Cl-/HCO3- exchange was inhibited by dihydro-4,4"-diisothiocyanostilbene-2,2"-disulfonic acid (H2-DIDS), but not by a specific CFTR inhibitor, CFTR(inh)-172.	Bicarbonates	24-28	CF transmembrane conductance regulator	Homo sapiens	162-166	
17654517-9	2008	Our data show that SeV vector is a potential CFTR gene transfer agent for human pancreatic duct cells and that expression of CFTR in CF cells is associated with a restoration of Cl- and HCO3- transport at the apical membrane.	Bicarbonates	186-190	CF transmembrane conductance regulator	Homo sapiens	125-129	
19074559-7	2009	IL-17A-induced bicarbonate secretion was cystic fibrosis transmembrane conductance regulator (CFTR)-dependent, mucosal chloride-dependent, partially Na(+)-dependent, and sensitive to serosal, but not mucosal, stilbene inhibition.	Bicarbonates	15-26	CF transmembrane conductance regulator	Homo sapiens	41-92	
19074559-7	2009	IL-17A-induced bicarbonate secretion was cystic fibrosis transmembrane conductance regulator (CFTR)-dependent, mucosal chloride-dependent, partially Na(+)-dependent, and sensitive to serosal, but not mucosal, stilbene inhibition.	Bicarbonates	15-26	CF transmembrane conductance regulator	Homo sapiens	94-98	
20224219-0	2009	The role of CFTR in bicarbonate secretion by pancreatic duct and airway epithelia.	Bicarbonates	20-31	CF transmembrane conductance regulator	Homo sapiens	12-16	
20224219-3	2009	CFTR is predominantly a Cl(-) channel, and it is widely believed that HCO(3)(-) secretion in the pancreatic duct is mediated mainly by a Cl(-)/HCO(3)(-) exchanger at the apical membrane.	Bicarbonates	143-149	CF transmembrane conductance regulator	Homo sapiens	0-4	
20224219-4	2009	Studies on airway epithelia, however, have suggested that CFTR, despite its low permeability to HCO(3)(-), may nonetheless be directly responsible for HCO(3)(-) secretion across the apical membrane.	Bicarbonates	96-102	CF transmembrane conductance regulator	Homo sapiens	58-62	
20224219-4	2009	Studies on airway epithelia, however, have suggested that CFTR, despite its low permeability to HCO(3)(-), may nonetheless be directly responsible for HCO(3)(-) secretion across the apical membrane.	Bicarbonates	151-157	CF transmembrane conductance regulator	Homo sapiens	58-62	
16414184-0	2006	Critical role of CFTR in uterine bicarbonate secretion and the fertilizing capacity of sperm.	Bicarbonates	33-44	CF transmembrane conductance regulator	Homo sapiens	17-21	
18209474-0	2008	Control of basal CFTR gene expression by bicarbonate-sensitive adenylyl cyclase in human pulmonary cells.	Bicarbonates	41-52	CF transmembrane conductance regulator	Homo sapiens	17-21	
18209474-1	2008	The CFTR protein, encoded by the gene whose mutations induce Cystic Fibrosis, is an anion channel devoted mainly to chloride and bicarbonate transmembrane transport, but which also regulates transport of several other ions.	Bicarbonates	129-140	CF transmembrane conductance regulator	Homo sapiens	4-8	
18209474-3	2008	Looking for a control of CFTR expression by ionic conditions, we investigated the effect of altered extracellular bicarbonate ion concentration on CFTR expression in human pulmonary Calu-3 cells.	Bicarbonates	114-125	CF transmembrane conductance regulator	Homo sapiens	147-151	
18209474-4	2008	We found that basal cftr gene transcription is enhanced when extracellular HCO(3)(-) concentration increases from 0 to 25 mmol/l.	Bicarbonates	75-81	CF transmembrane conductance regulator	Homo sapiens	20-24	
18209474-6	2008	Basal membrane content in CFTR protein exhibits the same variations as cftr mRNA in cells incubated in the presence of extracellular [HCO(3)(-)] between 0 and 25 mmol/l, and is also decreased by inhibiting sAC in the presence of HCO(3)(-).	Bicarbonates	134-140	CF transmembrane conductance regulator	Homo sapiens	26-30	
18209474-6	2008	Basal membrane content in CFTR protein exhibits the same variations as cftr mRNA in cells incubated in the presence of extracellular [HCO(3)(-)] between 0 and 25 mmol/l, and is also decreased by inhibiting sAC in the presence of HCO(3)(-).	Bicarbonates	134-140	CF transmembrane conductance regulator	Homo sapiens	71-75	
18209474-6	2008	Basal membrane content in CFTR protein exhibits the same variations as cftr mRNA in cells incubated in the presence of extracellular [HCO(3)(-)] between 0 and 25 mmol/l, and is also decreased by inhibiting sAC in the presence of HCO(3)(-).	Bicarbonates	229-235	CF transmembrane conductance regulator	Homo sapiens	26-30	
18209474-7	2008	These results show that bicarbonate-controlled sAC stimulation must be taken into account in cell physiology and that basal CFTR expression depends on an ionic parameter.	Bicarbonates	24-35	CF transmembrane conductance regulator	Homo sapiens	124-128	
17519339-1	2007	Cystic fibrosis transmembrane conductance regulator (CFTR) is an anion channel, mutations of which cause cystic fibrosis, a disease characterized by defective Cl(-) and HCO(3)(-) transport.	Bicarbonates	169-175	CF transmembrane conductance regulator	Homo sapiens	0-51	
17519339-1	2007	Cystic fibrosis transmembrane conductance regulator (CFTR) is an anion channel, mutations of which cause cystic fibrosis, a disease characterized by defective Cl(-) and HCO(3)(-) transport.	Bicarbonates	169-175	CF transmembrane conductance regulator	Homo sapiens	53-57	
17519339-4	2007	CFTR inhibitor or antibody significantly reduces the sperm capacitation, and the associated HCO(3)(-)-dependent events, including increases in intracellular pH, cAMP production and membrane hyperpolarization.	Bicarbonates	92-101	CF transmembrane conductance regulator	Homo sapiens	0-4	
17519339-6	2007	These results suggest that CFTR in sperm may be involved in the transport of HCO(3)(-) important for sperm capacitation and that CFTR mutations with impaired CFTR function may lead to reduced sperm fertilizing capacity and male infertility other than CBAVD.	Bicarbonates	77-83	CF transmembrane conductance regulator	Homo sapiens	27-31	
17700966-0	2007	Cystic fibrosis transmembrane conductance regulator and SLC26 transporters in HCO3- secretion by pancreatic duct cells.	Bicarbonates	78-82	CF transmembrane conductance regulator	Homo sapiens	0-51	
17700966-2	2007	Candidate mechanisms for HCO3(-) transport across the apical membrane include Cl(-)-HCO3(-)exchange by an SLC26 anion transporter and diffusion via the HCO3(-) conductance of cystic fibrosis transmembrane conductance regulator (CFTR).	Bicarbonates	25-29	CF transmembrane conductance regulator	Homo sapiens	175-226	
17700966-2	2007	Candidate mechanisms for HCO3(-) transport across the apical membrane include Cl(-)-HCO3(-)exchange by an SLC26 anion transporter and diffusion via the HCO3(-) conductance of cystic fibrosis transmembrane conductance regulator (CFTR).	Bicarbonates	25-29	CF transmembrane conductance regulator	Homo sapiens	228-232	
17700966-10	2007	On the other hand, the HCO3(-) conductance of CFTR could theoretically support secretion of HCO3(-) to a much higher concentrations.	Bicarbonates	23-27	CF transmembrane conductance regulator	Homo sapiens	46-50	
17700966-10	2007	On the other hand, the HCO3(-) conductance of CFTR could theoretically support secretion of HCO3(-) to a much higher concentrations.	Bicarbonates	92-96	CF transmembrane conductance regulator	Homo sapiens	46-50	
16414184-1	2006	Cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-activated Cl- channel expressed in a wide variety of epithelial cells, mutations of which are responsible for hallmark defective Cl- and HCO3- secretion seen in cystic fibrosis (CF).	Bicarbonates	206-210	CF transmembrane conductance regulator	Homo sapiens	0-51	
16414184-1	2006	Cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-activated Cl- channel expressed in a wide variety of epithelial cells, mutations of which are responsible for hallmark defective Cl- and HCO3- secretion seen in cystic fibrosis (CF).	Bicarbonates	206-210	CF transmembrane conductance regulator	Homo sapiens	53-57	
16414184-4	2006	Our recent results show that endometrial epithelial cells possess a cAMP-activated HCO3- transport mechanism, which could be impaired with channel blockers known to block CFTR or antisense against CFTR.	Bicarbonates	83-87	CF transmembrane conductance regulator	Homo sapiens	171-175	
16414184-4	2006	Our recent results show that endometrial epithelial cells possess a cAMP-activated HCO3- transport mechanism, which could be impaired with channel blockers known to block CFTR or antisense against CFTR.	Bicarbonates	83-87	CF transmembrane conductance regulator	Homo sapiens	197-201	
16414184-7	2006	Immunostaining and Western blot revealed that CFTR is expressed in rodent sperm and intracellular measurement of pH during sperm capacitation indicated that the entry of HCO3- into sperm could be inhibited by CFTR inhibitor.	Bicarbonates	170-174	CF transmembrane conductance regulator	Homo sapiens	46-50	
16414184-7	2006	Immunostaining and Western blot revealed that CFTR is expressed in rodent sperm and intracellular measurement of pH during sperm capacitation indicated that the entry of HCO3- into sperm could be inhibited by CFTR inhibitor.	Bicarbonates	170-174	CF transmembrane conductance regulator	Homo sapiens	209-213	
16414184-8	2006	These results are consistent with a critical role of CFTR in controlling uterine HCO3- secretion and sperm fertilizing capacity, suggesting that CFTR may be a potential target for post-meiotic regulation of fertility.	Bicarbonates	81-85	CF transmembrane conductance regulator	Homo sapiens	53-57	
16414184-8	2006	These results are consistent with a critical role of CFTR in controlling uterine HCO3- secretion and sperm fertilizing capacity, suggesting that CFTR may be a potential target for post-meiotic regulation of fertility.	Bicarbonates	81-85	CF transmembrane conductance regulator	Homo sapiens	145-149	
15956032-2	2005	Previously, we demonstrated that in pancreatic duct CFPAC-1 cells, which express DeltaF508 CFTR (cystic fibrosis transmembrane conductance regulator), the intracellular trafficking of carbonic anhydrase IV (CA IV), a membrane protein involved in HCO(3)(-) secretion, was impaired.	Bicarbonates	246-252	CF transmembrane conductance regulator	Homo sapiens	91-95	
16543717-3	2006	To investigate CFTR-mediated HCO(3)(-) conductance and the role of HCO(3)(-) in regulating ASL pH we determined the pH of the fluid covering the apical surface of airway epithelial cells.	Bicarbonates	29-35	CF transmembrane conductance regulator	Homo sapiens	15-19	
16543717-12	2006	The pH measurements of the fluid covering the apical part of cell cultures support the notion that bicarbonate ions may be transported by CFTR, and that this can be inhibited by specific CFTR inhibitors.	Bicarbonates	99-110	CF transmembrane conductance regulator	Homo sapiens	138-142	
16543717-12	2006	The pH measurements of the fluid covering the apical part of cell cultures support the notion that bicarbonate ions may be transported by CFTR, and that this can be inhibited by specific CFTR inhibitors.	Bicarbonates	99-110	CF transmembrane conductance regulator	Homo sapiens	187-191	
17091214-6	2006	Advances resulted from research into the airway disease associated with cystic fibrosis (CF) after it was found that the CFTR Cl(-) channel conducts HCO (3) (-) and, therefore, may contribute to ASL pH.	Bicarbonates	149-156	CF transmembrane conductance regulator	Homo sapiens	121-125	
17120768-1	2006	Most epithelia that express CFTR secrete fluid rich in HCO3- and poor in Cl- that is generated by a CFTR-dependent Cl- absorption and HCO3- secretion process that when aberrant leads to human diseases such as cystic fibrosis and congenital chloride diarrhoea.	Bicarbonates	55-59	CF transmembrane conductance regulator	Homo sapiens	28-32	
17120768-1	2006	Most epithelia that express CFTR secrete fluid rich in HCO3- and poor in Cl- that is generated by a CFTR-dependent Cl- absorption and HCO3- secretion process that when aberrant leads to human diseases such as cystic fibrosis and congenital chloride diarrhoea.	Bicarbonates	55-59	CF transmembrane conductance regulator	Homo sapiens	100-104	
17120768-1	2006	Most epithelia that express CFTR secrete fluid rich in HCO3- and poor in Cl- that is generated by a CFTR-dependent Cl- absorption and HCO3- secretion process that when aberrant leads to human diseases such as cystic fibrosis and congenital chloride diarrhoea.	Bicarbonates	134-138	CF transmembrane conductance regulator	Homo sapiens	28-32	
17120768-1	2006	Most epithelia that express CFTR secrete fluid rich in HCO3- and poor in Cl- that is generated by a CFTR-dependent Cl- absorption and HCO3- secretion process that when aberrant leads to human diseases such as cystic fibrosis and congenital chloride diarrhoea.	Bicarbonates	134-138	CF transmembrane conductance regulator	Homo sapiens	100-104	
17120768-2	2006	Epithelial Cl- absorption and HCO3- secretion require expression of CFTR and other Cl- and HCO3- transporters in the luminal membrane of the secreting cells.	Bicarbonates	30-34	CF transmembrane conductance regulator	Homo sapiens	68-72	
15956032-2	2005	Previously, we demonstrated that in pancreatic duct CFPAC-1 cells, which express DeltaF508 CFTR (cystic fibrosis transmembrane conductance regulator), the intracellular trafficking of carbonic anhydrase IV (CA IV), a membrane protein involved in HCO(3)(-) secretion, was impaired.	Bicarbonates	246-252	CF transmembrane conductance regulator	Homo sapiens	97-148	
15958523-0	2005	Regulation of CFTR channels by HCO(3)--sensitive soluble adenylyl cyclase in human airway epithelial cells.	Bicarbonates	31-37	CF transmembrane conductance regulator	Homo sapiens	14-18	
15958523-1	2005	CFTR channels conduct HCO(3)(-) in addition to Cl(-) in airway epithelial cells.	Bicarbonates	22-28	CF transmembrane conductance regulator	Homo sapiens	0-4	
15958523-2	2005	A defective HCO(3)(-)-transporting function of CFTR may underlie the pathogenesis of cystic fibrosis.	Bicarbonates	12-18	CF transmembrane conductance regulator	Homo sapiens	47-51	
15958523-3	2005	In the present study, we have investigated whether a HCO(3)(-)-sensitive soluble adenylyl cyclase (sAC) is functionally coupled with CFTR and thus forms an autoregulatory mechanism for HCO(3)(-) transport in human airway epithelial Calu-3 cells.	Bicarbonates	53-62	CF transmembrane conductance regulator	Homo sapiens	133-137	
15958523-3	2005	In the present study, we have investigated whether a HCO(3)(-)-sensitive soluble adenylyl cyclase (sAC) is functionally coupled with CFTR and thus forms an autoregulatory mechanism for HCO(3)(-) transport in human airway epithelial Calu-3 cells.	Bicarbonates	185-194	CF transmembrane conductance regulator	Homo sapiens	133-137	
15958523-8	2005	Adding 25 mM HCO(3)(-) to the bath stimulated CFTR-mediated whole cell currents in the absence, but not in the presence, of 2-HE.	Bicarbonates	13-19	CF transmembrane conductance regulator	Homo sapiens	46-50	
15958523-10	2005	These findings demonstrate that sAC signaling pathway is involved in the regulation of CFTR function in human airway epithelium and thereby provides a link between the level of intracellular HCO(3)(-)/CO(2) and the modulation of HCO(3)(-)-conductive CFTR function by cAMP/PKA.	Bicarbonates	191-197	CF transmembrane conductance regulator	Homo sapiens	87-91	
15958523-10	2005	These findings demonstrate that sAC signaling pathway is involved in the regulation of CFTR function in human airway epithelium and thereby provides a link between the level of intracellular HCO(3)(-)/CO(2) and the modulation of HCO(3)(-)-conductive CFTR function by cAMP/PKA.	Bicarbonates	191-197	CF transmembrane conductance regulator	Homo sapiens	250-254	
15958523-10	2005	These findings demonstrate that sAC signaling pathway is involved in the regulation of CFTR function in human airway epithelium and thereby provides a link between the level of intracellular HCO(3)(-)/CO(2) and the modulation of HCO(3)(-)-conductive CFTR function by cAMP/PKA.	Bicarbonates	191-198	CF transmembrane conductance regulator	Homo sapiens	87-91	
15958523-10	2005	These findings demonstrate that sAC signaling pathway is involved in the regulation of CFTR function in human airway epithelium and thereby provides a link between the level of intracellular HCO(3)(-)/CO(2) and the modulation of HCO(3)(-)-conductive CFTR function by cAMP/PKA.	Bicarbonates	191-198	CF transmembrane conductance regulator	Homo sapiens	250-254	
15286085-1	2004	The cystic fibrosis transmembrane conductance regulator (CFTR) is vital for Cl(-) and HCO(3)(-) transport in many epithelia.	Bicarbonates	86-92	CF transmembrane conductance regulator	Homo sapiens	4-55	
15709963-3	2005	At the apical membrane, the secretion of moderate concentrations of HCO3- can be explained by the parallel activity of a Cl-/HCO3- exchanger and a Cl- conductance, either the cystic fibrosis transmembrane conductance regulator (CFTR) or a Ca2+-activated Cl- channel (CaCC).	Bicarbonates	68-72	CF transmembrane conductance regulator	Homo sapiens	175-226	
15709963-3	2005	At the apical membrane, the secretion of moderate concentrations of HCO3- can be explained by the parallel activity of a Cl-/HCO3- exchanger and a Cl- conductance, either the cystic fibrosis transmembrane conductance regulator (CFTR) or a Ca2+-activated Cl- channel (CaCC).	Bicarbonates	68-72	CF transmembrane conductance regulator	Homo sapiens	228-232	
15709963-5	2005	HCO3- efflux across the apical membrane is an electrogenic process that is facilitated by the depletion of intracellular Cl-, but it remains to be seen whether it is mediated predominantly by CFTR or by an electrogenic SLC26 anion exchanger.	Bicarbonates	0-4	CF transmembrane conductance regulator	Homo sapiens	192-196	
15645646-0	2004	Homozygous (TG)11 allele in intron 8 of the cystic fibrosis transmembrane conductance regulator (CFTR) gene has a protective role against bicarbonate decrease in pure pancreatic juice among Japanese male alcoholics.	Bicarbonates	138-149	CF transmembrane conductance regulator	Homo sapiens	44-95	
15645646-0	2004	Homozygous (TG)11 allele in intron 8 of the cystic fibrosis transmembrane conductance regulator (CFTR) gene has a protective role against bicarbonate decrease in pure pancreatic juice among Japanese male alcoholics.	Bicarbonates	138-149	CF transmembrane conductance regulator	Homo sapiens	97-101	
15645646-3	2004	AIM: To investigate in Japanese alcoholics the association between bicarbonate concentration in pure pancreatic juice and one of the polymorphisms of the CFTR gene, the (TG)m Tn tract length in intron 8.	Bicarbonates	67-78	CF transmembrane conductance regulator	Homo sapiens	154-158	
15286085-1	2004	The cystic fibrosis transmembrane conductance regulator (CFTR) is vital for Cl(-) and HCO(3)(-) transport in many epithelia.	Bicarbonates	86-92	CF transmembrane conductance regulator	Homo sapiens	57-61	
15286085-2	2004	As the HCO(3)(-) concentration in epithelial secretions varies and can reach as high as 140 mm, the lumen-facing domains of CFTR are exposed to large reciprocal variations in Cl(-) and HCO(3)(-) levels.	Bicarbonates	7-13	CF transmembrane conductance regulator	Homo sapiens	124-128	
15286085-2	2004	As the HCO(3)(-) concentration in epithelial secretions varies and can reach as high as 140 mm, the lumen-facing domains of CFTR are exposed to large reciprocal variations in Cl(-) and HCO(3)(-) levels.	Bicarbonates	185-191	CF transmembrane conductance regulator	Homo sapiens	124-128	
15257112-1	2004	OBJECTIVE: To develop a simple, physiologically based mathematical model of pancreatic duct cell secretion using experimentally derived parameters that generates pancreatic fluid bicarbonate concentrations of >140 mM after CFTR activation.	Bicarbonates	179-190	CF transmembrane conductance regulator	Homo sapiens	226-230	
15257112-5	2004	RESULTS: This model predicts robust, NaK pump-dependent bicarbonate secretion with opening of the CFTR, generates and maintains pancreatic fluid secretion with bicarbonate concentrations >140 mM, and returns to basal levels with CFTR closure.	Bicarbonates	160-171	CF transmembrane conductance regulator	Homo sapiens	98-102	
15257112-6	2004	Limiting CFTR permeability to bicarbonate, as seen in some CFTR mutations, markedly inhibited pancreatic bicarbonate and fluid secretion.	Bicarbonates	30-41	CF transmembrane conductance regulator	Homo sapiens	9-13	
15257112-6	2004	Limiting CFTR permeability to bicarbonate, as seen in some CFTR mutations, markedly inhibited pancreatic bicarbonate and fluid secretion.	Bicarbonates	30-41	CF transmembrane conductance regulator	Homo sapiens	59-63	
15257112-6	2004	Limiting CFTR permeability to bicarbonate, as seen in some CFTR mutations, markedly inhibited pancreatic bicarbonate and fluid secretion.	Bicarbonates	105-116	CF transmembrane conductance regulator	Homo sapiens	9-13	
15257112-6	2004	Limiting CFTR permeability to bicarbonate, as seen in some CFTR mutations, markedly inhibited pancreatic bicarbonate and fluid secretion.	Bicarbonates	105-116	CF transmembrane conductance regulator	Homo sapiens	59-63	
15257112-7	2004	CONCLUSIONS: A simple CFTR-dependent duct cell model can explain active, high-volume, high-concentration bicarbonate secretion in pancreatic juice that reproduces the experimental findings.	Bicarbonates	105-116	CF transmembrane conductance regulator	Homo sapiens	22-26	
15257112-8	2004	This model may also provide insight into why CFTR mutations that predominantly affect bicarbonate permeability predispose to pancreatic dysfunction in humans.	Bicarbonates	86-97	CF transmembrane conductance regulator	Homo sapiens	45-49	
15257112-5	2004	RESULTS: This model predicts robust, NaK pump-dependent bicarbonate secretion with opening of the CFTR, generates and maintains pancreatic fluid secretion with bicarbonate concentrations >140 mM, and returns to basal levels with CFTR closure.	Bicarbonates	56-67	CF transmembrane conductance regulator	Homo sapiens	98-102	
15257112-5	2004	RESULTS: This model predicts robust, NaK pump-dependent bicarbonate secretion with opening of the CFTR, generates and maintains pancreatic fluid secretion with bicarbonate concentrations >140 mM, and returns to basal levels with CFTR closure.	Bicarbonates	56-67	CF transmembrane conductance regulator	Homo sapiens	232-236	
15048129-2	2004	Many SLC26 transporters (SLC26T) are expressed in the luminal membrane together with CFTR, which activates electrogenic chloride-bicarbonate exchange by SLC26T.	Bicarbonates	129-140	CF transmembrane conductance regulator	Homo sapiens	85-89	
14660706-4	2004	Liquid secretion is driven by the active transepithelial secretion of both Cl(-) and HCO(3)(-) and at least a portion of this process is mediated by the cystic fibrosis transmembrane conductance regulator (CFTR), which is highly expressed in glands.	Bicarbonates	85-91	CF transmembrane conductance regulator	Homo sapiens	153-204	
12562898-9	2003	We conclude that: (1) normal, but not CF, nasal epithelia have a constitutively active DPC-sensitive HCO3- influx/efflux pathway across the apical membrane of cells, consistent with the movement of HCO3- via CFTR; and (2) both normal and CF nasal epithelia have Na+-independent, H2DIDS-sensitive AE at their basolateral domain.	Bicarbonates	101-105	CF transmembrane conductance regulator	Homo sapiens	208-212	
15658882-1	2004	The cystic fibrosis transmembrane regulator (CFTR) should no longer be viewed primarily as a "chloride channel" but recognized as a channel that also controls the efflux of other physiologically important anions, such as glutathione (GSH) and bicarbonate.	Bicarbonates	243-254	CF transmembrane conductance regulator	Homo sapiens	4-43	
15658882-1	2004	The cystic fibrosis transmembrane regulator (CFTR) should no longer be viewed primarily as a "chloride channel" but recognized as a channel that also controls the efflux of other physiologically important anions, such as glutathione (GSH) and bicarbonate.	Bicarbonates	243-254	CF transmembrane conductance regulator	Homo sapiens	45-49	
14515130-5	2003	These results are consistent with a critical role of CFTR in controlling uterine bicarbonate secretion and the fertilizing capacity of sperm, providing a link between defective CFTR and lower female fertility in CF.	Bicarbonates	81-92	CF transmembrane conductance regulator	Homo sapiens	177-181	
12802335-3	2003	Here we report phosphorylation- and ATP-independent activation of CFTR by cytoplasmic glutamate that exclusively elicits Cl-, but not HCO3-, conductance in the human sweat duct.	Bicarbonates	134-138	CF transmembrane conductance regulator	Homo sapiens	66-70	
12802335-4	2003	We also report that the anion selectivity of glutamate-activated CFTR is not intrinsically fixed, but can undergo a dynamic shift to conduct HCO3- by a process involving ATP hydrolysis.	Bicarbonates	141-145	CF transmembrane conductance regulator	Homo sapiens	65-69	
12802335-6	2003	In contrast, duct cells from heterozygous patients with R117H/DeltaF508 mutant CFTR also lost most of the Cl- conductance, yet retained significant HCO3- conductance.	Bicarbonates	148-152	CF transmembrane conductance regulator	Homo sapiens	79-83	
16113406-1	2004	The cystic fibrosis transmembrane conductance regulator (CFTR) is a channel/enzyme which mediates passive diffusion of chloride and bicarbonate through epithelial cell membranes.	Bicarbonates	132-143	CF transmembrane conductance regulator	Homo sapiens	4-55	
16113406-1	2004	The cystic fibrosis transmembrane conductance regulator (CFTR) is a channel/enzyme which mediates passive diffusion of chloride and bicarbonate through epithelial cell membranes.	Bicarbonates	132-143	CF transmembrane conductance regulator	Homo sapiens	57-61	
14668433-1	2003	Cystic fibrosis (CF) transmembrane conductance regulator (CFTR)-dependent airway epithelial bicarbonate transport is hypothesized to participate in airway surface liquid pH regulation and contribute to lung defense.	Bicarbonates	92-103	CF transmembrane conductance regulator	Homo sapiens	0-56	
14668433-1	2003	Cystic fibrosis (CF) transmembrane conductance regulator (CFTR)-dependent airway epithelial bicarbonate transport is hypothesized to participate in airway surface liquid pH regulation and contribute to lung defense.	Bicarbonates	92-103	CF transmembrane conductance regulator	Homo sapiens	58-62	
14668433-6	2003	We also detected the following evidence for a CFTR-dependent HCO3- secretory pathway that was defective in CF: (i).	Bicarbonates	61-65	CF transmembrane conductance regulator	Homo sapiens	46-50	
14668433-10	2003	We conclude that cultured human CF bronchial epithelial pHASL is abnormally regulated under basal conditions because of absent CFTR-dependent HCO3- secretion and that this defect can lead to an impaired capacity to respond to airway conditions associated with acidification of ASL.	Bicarbonates	142-146	CF transmembrane conductance regulator	Homo sapiens	127-131	
14515130-0	2003	Involvement of CFTR in uterine bicarbonate secretion and the fertilizing capacity of sperm.	Bicarbonates	31-42	CF transmembrane conductance regulator	Homo sapiens	15-19	
14515130-2	2003	Although CFTR has been implicated in bicarbonate secretion, its ability to directly mediate bicarbonate secretion of any physiological significance has not been shown.	Bicarbonates	37-48	CF transmembrane conductance regulator	Homo sapiens	9-13	
14515130-2	2003	Although CFTR has been implicated in bicarbonate secretion, its ability to directly mediate bicarbonate secretion of any physiological significance has not been shown.	Bicarbonates	92-103	CF transmembrane conductance regulator	Homo sapiens	9-13	
14515130-3	2003	We demonstrate here that endometrial epithelial cells possess a CFTR-mediated bicarbonate transport mechanism.	Bicarbonates	78-89	CF transmembrane conductance regulator	Homo sapiens	64-68	
14515130-5	2003	These results are consistent with a critical role of CFTR in controlling uterine bicarbonate secretion and the fertilizing capacity of sperm, providing a link between defective CFTR and lower female fertility in CF.	Bicarbonates	81-92	CF transmembrane conductance regulator	Homo sapiens	53-57	
12651923-9	2003	cAMP-insensitive Cl--HCO3- exchange mediated by hDRA gained modest cAMP sensitivity when co-expressed with cystic fibrosis transmembrane conductance regulator (CFTR).	Bicarbonates	21-25	CF transmembrane conductance regulator	Homo sapiens	107-158	
12651923-9	2003	cAMP-insensitive Cl--HCO3- exchange mediated by hDRA gained modest cAMP sensitivity when co-expressed with cystic fibrosis transmembrane conductance regulator (CFTR).	Bicarbonates	21-25	CF transmembrane conductance regulator	Homo sapiens	160-164	
12403779-1	2002	Cystic fibrosis transmembrane conductance regulator (CFTR) regulates both HCO(3)(-) secretion and HCO(3)(-) salvage in secretory epithelia.	Bicarbonates	74-80	CF transmembrane conductance regulator	Homo sapiens	0-51	
12531931-2	2003	Recently, impaired HCO(3)(-) secretion has been shown in most tissues known to express the cystic fibrosis transmembrane conductance regulator (CFTR).	Bicarbonates	19-25	CF transmembrane conductance regulator	Homo sapiens	91-142	
12531931-2	2003	Recently, impaired HCO(3)(-) secretion has been shown in most tissues known to express the cystic fibrosis transmembrane conductance regulator (CFTR).	Bicarbonates	19-25	CF transmembrane conductance regulator	Homo sapiens	144-148	
12531931-3	2003	New results suggest that CFTR plays an important role in the transcellular secretion of HCO(3)(-).	Bicarbonates	88-94	CF transmembrane conductance regulator	Homo sapiens	25-29	
12409301-2	2003	The bulk of bicarbonate secretion in the luminal membrane of duct cells is mediated by a Cl(-)-dependent mechanism (Cl(-)/HCO(3)(-) exchange), and we previously reported that the mechanism is CFTR-dependent and cAMP-activated (Lee, M. G., Choi, J. Y., Luo, X., Strickland, E., Thomas, P. J., and Muallem, S. (1999) J. Biol.	Bicarbonates	12-23	CF transmembrane conductance regulator	Homo sapiens	192-196	
12409301-5	2003	In the present study, we provide comprehensive evidence that calcium signaling also activates the same CFTR- and Cl(-)-dependent HCO(3)(-) transport.	Bicarbonates	129-135	CF transmembrane conductance regulator	Homo sapiens	103-107	
12409301-11	2003	These results provide a molecular basis for calcium-induced bicarbonate secretion in pancreatic duct cells and highlight the importance of CFTR in epithelial bicarbonate secretion induced by various stimuli.	Bicarbonates	158-169	CF transmembrane conductance regulator	Homo sapiens	139-143	
12570106-1	2003	The cystic fibrosis (CF) transmembrane conductance regulator protein can transport bicarbonate and may therefore regulate airway surface (AS) pH.	Bicarbonates	83-94	CF transmembrane conductance regulator	Homo sapiens	4-60	
12403779-14	2002	We conclude that CFTR and NBC3 reside in the same HCO(3)(-)-transporting complex with the aid of PDZ domain-containing scaffolds, and this interaction is essential for regulation of NBC3 activity by CFTR.	Bicarbonates	50-57	CF transmembrane conductance regulator	Homo sapiens	17-21	
12403779-14	2002	We conclude that CFTR and NBC3 reside in the same HCO(3)(-)-transporting complex with the aid of PDZ domain-containing scaffolds, and this interaction is essential for regulation of NBC3 activity by CFTR.	Bicarbonates	50-57	CF transmembrane conductance regulator	Homo sapiens	199-203	
12403779-15	2002	Furthermore, these findings add additional evidence for the suggestion that CFTR regulates the overall trans-cellular HCO(3)(-) transport by regulating the activity of all luminal HCO(3)(-) secretion and salvage mechanisms of secretory epithelial cells.	Bicarbonates	118-124	CF transmembrane conductance regulator	Homo sapiens	76-80	
12403779-15	2002	Furthermore, these findings add additional evidence for the suggestion that CFTR regulates the overall trans-cellular HCO(3)(-) transport by regulating the activity of all luminal HCO(3)(-) secretion and salvage mechanisms of secretory epithelial cells.	Bicarbonates	180-186	CF transmembrane conductance regulator	Homo sapiens	76-80	
12403779-1	2002	Cystic fibrosis transmembrane conductance regulator (CFTR) regulates both HCO(3)(-) secretion and HCO(3)(-) salvage in secretory epithelia.	Bicarbonates	74-80	CF transmembrane conductance regulator	Homo sapiens	53-57	
12403779-1	2002	Cystic fibrosis transmembrane conductance regulator (CFTR) regulates both HCO(3)(-) secretion and HCO(3)(-) salvage in secretory epithelia.	Bicarbonates	98-104	CF transmembrane conductance regulator	Homo sapiens	0-51	
12403779-1	2002	Cystic fibrosis transmembrane conductance regulator (CFTR) regulates both HCO(3)(-) secretion and HCO(3)(-) salvage in secretory epithelia.	Bicarbonates	98-104	CF transmembrane conductance regulator	Homo sapiens	53-57	
12388101-2	2002	These peptides elicit chloride and bicarbonate secretion via the cystic fibrosis transmembrane conductance regulator.	Bicarbonates	35-46	CF transmembrane conductance regulator	Homo sapiens	65-116	
12403872-2	2002	Bicarbonate (HCO(3)(-)) secretion is also impaired in CFTR expressing tissues and CFTR is thought to regulate HCO(3)(-) secretion at the apical membrane of epithelial cells.	Bicarbonates	0-11	CF transmembrane conductance regulator	Homo sapiens	54-58	
12403872-2	2002	Bicarbonate (HCO(3)(-)) secretion is also impaired in CFTR expressing tissues and CFTR is thought to regulate HCO(3)(-) secretion at the apical membrane of epithelial cells.	Bicarbonates	13-19	CF transmembrane conductance regulator	Homo sapiens	54-58	
12403872-2	2002	Bicarbonate (HCO(3)(-)) secretion is also impaired in CFTR expressing tissues and CFTR is thought to regulate HCO(3)(-) secretion at the apical membrane of epithelial cells.	Bicarbonates	110-116	CF transmembrane conductance regulator	Homo sapiens	54-58	
12403872-2	2002	Bicarbonate (HCO(3)(-)) secretion is also impaired in CFTR expressing tissues and CFTR is thought to regulate HCO(3)(-) secretion at the apical membrane of epithelial cells.	Bicarbonates	110-116	CF transmembrane conductance regulator	Homo sapiens	82-86	
12234015-3	2002	In CF cells homozygous for the deltaF508 mutation, the defect in targeting of CFTR to plasma membranes leads to a disruption in the secretion of Cl- and HCO3 ions along with a defective targeting of other proteins.	Bicarbonates	153-157	CF transmembrane conductance regulator	Homo sapiens	78-82	
12234015-12	2002	On the basis of these observations, we propose that the absence of CA IV in apical plasma membranes due to the impairment in targeting in cells expressing a deltaAF508 CFTR largely contributes to the disruption in HCO3- secretion in CF epithelia.	Bicarbonates	214-218	CF transmembrane conductance regulator	Homo sapiens	168-172	
12079272-4	2002	In the exocrine pancreas the CFTR plays a key role in the apical Cl(-), HCO(3)(-), and water transport in duct cells.	Bicarbonates	72-78	CF transmembrane conductance regulator	Homo sapiens	29-33	
11875266-0	2001	Cl(-)-dependent HCO3- transport by cystic fibrosis transmembrane conductance regulator.	Bicarbonates	16-20	CF transmembrane conductance regulator	Homo sapiens	35-86	
11786964-1	2002	In view of the occurrence of hepatobiliary disorders in cystic fibrosis (CF) this study addresses the role of the cystic fibrosis transmembrane conductance regulator (CFTR) and of Ca(2+)-activated Cl(-) channels in promoting HCO3- secretion in bile ductular cells.	Bicarbonates	225-229	CF transmembrane conductance regulator	Homo sapiens	114-165	
11786964-9	2002	The observation that activation of Ca(2+)-dependent Cl(-) channels can substitute for cystic fibrosis transmembrane conductance regulator (CFTR) in supporting HCO3- secretion and the efficacy of gentamicin in restoring CFTR function and HCO3- secretion in class I mutations are of potential clinical interest.	Bicarbonates	159-163	CF transmembrane conductance regulator	Homo sapiens	86-137	
11786964-9	2002	The observation that activation of Ca(2+)-dependent Cl(-) channels can substitute for cystic fibrosis transmembrane conductance regulator (CFTR) in supporting HCO3- secretion and the efficacy of gentamicin in restoring CFTR function and HCO3- secretion in class I mutations are of potential clinical interest.	Bicarbonates	159-163	CF transmembrane conductance regulator	Homo sapiens	139-143	
11875261-0	2001	Functional interactions of HCO3- with cystic fibrosis transmembrane conductance regulator.	Bicarbonates	27-31	CF transmembrane conductance regulator	Homo sapiens	38-89	
11875261-2	2001	CFTR is also required for HCO(3)(-) transport in many tissues such as the lungs, gastro-intestinal tract, and pancreas, although the exact role CFTR plays is uncertain.	Bicarbonates	26-32	CF transmembrane conductance regulator	Homo sapiens	0-4	
11875261-5	2001	Ion selectivity studies shows that CFTR is between 3-5 times more selective for Cl(-) over HCO(3)(-).	Bicarbonates	91-97	CF transmembrane conductance regulator	Homo sapiens	35-39	
11875261-6	2001	In addition, extracellular HCO(3)(-) has a novel inhibitory effect on cAMP-stimulated CFTR currents carried by Cl(-).	Bicarbonates	27-33	CF transmembrane conductance regulator	Homo sapiens	86-90	
11875261-8	2001	These data show that luminal HCO(3)(-) acts as a potent regulator of CFTR, and suggests that inhibition involves an external anion-binding site on the channel.	Bicarbonates	29-35	CF transmembrane conductance regulator	Homo sapiens	69-73	
11875262-0	2001	Selective activation of cystic fibrosis transmembrane conductance regulator Cl- and HCO3- conductances.	Bicarbonates	84-88	CF transmembrane conductance regulator	Homo sapiens	24-75	
11875262-1	2001	While cystic fibrosis transmembrane conductance regulator (CFTR) is well known to function as a Cl(-) channel, some mutations in the channel protein causing cystic fibrosis (CF) disrupt another vital physiological function, HCO(3)(-) transport.	Bicarbonates	224-230	CF transmembrane conductance regulator	Homo sapiens	6-57	
11875262-1	2001	While cystic fibrosis transmembrane conductance regulator (CFTR) is well known to function as a Cl(-) channel, some mutations in the channel protein causing cystic fibrosis (CF) disrupt another vital physiological function, HCO(3)(-) transport.	Bicarbonates	224-230	CF transmembrane conductance regulator	Homo sapiens	59-63	
11875262-7	2001	Further, the HCO(3)(-)/Cl(-) selectivity of CFTR appears to be dependent on the conditions of stimulating CFTR.	Bicarbonates	13-19	CF transmembrane conductance regulator	Homo sapiens	44-48	
11875262-7	2001	Further, the HCO(3)(-)/Cl(-) selectivity of CFTR appears to be dependent on the conditions of stimulating CFTR.	Bicarbonates	13-19	CF transmembrane conductance regulator	Homo sapiens	106-110	
11875262-8	2001	That is, CFTR activated by cAMP + ATP appears to conduct both HCO(3)(-) and Cl(-) (with an estimated selectivity ratio of 0.2 to 0.5).	Bicarbonates	62-69	CF transmembrane conductance regulator	Homo sapiens	9-13	
11875262-10	2001	Glutamate activated CFTR can be induced to conduct HCO(3)(-) by the addition of ATP without cAMP.	Bicarbonates	51-57	CF transmembrane conductance regulator	Homo sapiens	20-24	
11875262-12	2001	We also found that a heterozygous R117H/DeltaF508 CFTR sweat duct retained significant HCO(3)(-) conductance while a homozygous DeltaF508 CFTR duct showed virtually no HCO(3)(-) conductance.	Bicarbonates	87-93	CF transmembrane conductance regulator	Homo sapiens	50-54	
11875262-12	2001	We also found that a heterozygous R117H/DeltaF508 CFTR sweat duct retained significant HCO(3)(-) conductance while a homozygous DeltaF508 CFTR duct showed virtually no HCO(3)(-) conductance.	Bicarbonates	87-92	CF transmembrane conductance regulator	Homo sapiens	50-54	
11875262-14	2001	That is physiologically, CFTR may exhibit Cl(-) conductance with and/or without HCO(3)(-) conductance.	Bicarbonates	80-86	CF transmembrane conductance regulator	Homo sapiens	25-29	
11875262-15	2001	We also surmise that the severity of the pathogenesis in CF is closely related to the phenotypic ability of a mutant CFTR to express a HCO(3)(-) conductance.	Bicarbonates	135-141	CF transmembrane conductance regulator	Homo sapiens	117-121	
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).	Bicarbonates	32-38	CF transmembrane conductance regulator	Homo sapiens	138-142	
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).	Bicarbonates	20-26	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).	Bicarbonates	20-26	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).	Bicarbonates	20-25	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).	Bicarbonates	20-25	CF transmembrane conductance regulator	Homo sapiens	108-112	
11875272-14	2001	By analogy with organ-specific CFTR effects on Cl(-) transport, it seems likely that the relative importance of CFTR in HCO(3)(-) transport will also vary across organs.	Bicarbonates	120-126	CF transmembrane conductance regulator	Homo sapiens	112-116	
11875272-17	2001	CFTR is highly expressed in serous cells of submucosal glands and the Calu-3 serous cell model secretes HCO(3)(-).	Bicarbonates	104-110	CF transmembrane conductance regulator	Homo sapiens	0-4	
11875274-6	2001	These data suggest that cAMP agonists can stimulate HCO(3)(-) secretion across airway epithelia and that CFTR may provide a conductive pathway for HCO(3)(-) movement across the apical membrane.	Bicarbonates	147-153	CF transmembrane conductance regulator	Homo sapiens	105-109	
11875275-1	2001	In gastrointestinal tissues, cumulative evidence from both in vivo and in vitro studies suggests a role for the cystic fibrosis transmembrane conductance regulator (CFTR) in apical epithelial bicarbonate conductance.	Bicarbonates	192-203	CF transmembrane conductance regulator	Homo sapiens	112-163	
11875275-1	2001	In gastrointestinal tissues, cumulative evidence from both in vivo and in vitro studies suggests a role for the cystic fibrosis transmembrane conductance regulator (CFTR) in apical epithelial bicarbonate conductance.	Bicarbonates	192-203	CF transmembrane conductance regulator	Homo sapiens	165-169	
11875266-6	2001	The mechanism of HCO(3)(-) secretion by cystic fibrosis transmembrane conductance regulator (CFTR) expressing cells is not well understood.	Bicarbonates	17-23	CF transmembrane conductance regulator	Homo sapiens	40-91	
11875266-6	2001	The mechanism of HCO(3)(-) secretion by cystic fibrosis transmembrane conductance regulator (CFTR) expressing cells is not well understood.	Bicarbonates	17-23	CF transmembrane conductance regulator	Homo sapiens	93-97	
11875266-7	2001	In the present communication we discuss results suggesting that CFTR itself can transport large amounts of HCO(3)(-) and that HCO(3)(-) transport by CFTR is mediated by a coupled, Cl(-)-dependent process that is different from a simple HCO(3)(-) conductance.	Bicarbonates	107-113	CF transmembrane conductance regulator	Homo sapiens	64-68	
11875266-7	2001	In the present communication we discuss results suggesting that CFTR itself can transport large amounts of HCO(3)(-) and that HCO(3)(-) transport by CFTR is mediated by a coupled, Cl(-)-dependent process that is different from a simple HCO(3)(-) conductance.	Bicarbonates	126-132	CF transmembrane conductance regulator	Homo sapiens	149-153	
11875266-7	2001	In the present communication we discuss results suggesting that CFTR itself can transport large amounts of HCO(3)(-) and that HCO(3)(-) transport by CFTR is mediated by a coupled, Cl(-)-dependent process that is different from a simple HCO(3)(-) conductance.	Bicarbonates	126-132	CF transmembrane conductance regulator	Homo sapiens	149-153	
11116277-8	2001	The role of CFTR in bicarbonate secretion has not yet been established with certainty, but correction of the defect in bicarbonate secretion may be important in clinical treatment of the disease.	Bicarbonates	20-31	CF transmembrane conductance regulator	Homo sapiens	12-16	
11242048-0	2001	Aberrant CFTR-dependent HCO3- transport in mutations associated with cystic fibrosis.	Bicarbonates	24-28	CF transmembrane conductance regulator	Homo sapiens	9-13	
11242048-5	2001	Indeed, CFTR regulates other transporters, including Cl(-)-coupled HCO3- transport.	Bicarbonates	67-71	CF transmembrane conductance regulator	Homo sapiens	8-12	
11242048-8	2001	We have examined Cl(-)-coupled HCO3- transport by CFTR mutants that retain substantial or normal Cl- channel activity.	Bicarbonates	31-35	CF transmembrane conductance regulator	Homo sapiens	50-54	
10833480-1	2000	BACKGROUND & AIMS: The duodenum is a cystic fibrosis transmembrane conductance regulator (CFTR)-expressing epithelium with high bicarbonate secretory capacity.	Bicarbonates	132-143	CF transmembrane conductance regulator	Homo sapiens	41-92	
11053257-0	2000	Ca2+-activated Cl- channels can substitute for CFTR in stimulation of pancreatic duct bicarbonate secretion.	Bicarbonates	86-97	CF transmembrane conductance regulator	Homo sapiens	47-51	
11053257-1	2000	This study addresses the mechanisms by which a defect in CFTR impairs pancreatic duct bicarbonate secretion in cystic fibrosis.	Bicarbonates	86-97	CF transmembrane conductance regulator	Homo sapiens	57-61	
10898717-0	2000	CFTR induces the expression of DRA along with Cl(-)/HCO(3)(-) exchange activity in tracheal epithelial cells.	Bicarbonates	52-58	CF transmembrane conductance regulator	Homo sapiens	0-4	
10998665-2	2000	In the field of intestinal secretion, research on the secretion of bicarbonate by pancreatic ducts and duodenal epithelia in cystic fibrosis revealed the crucial role of chloride channel (CFTR) in the control of activity of other transporters involved in bicarbonate secretion.	Bicarbonates	67-78	CF transmembrane conductance regulator	Homo sapiens	188-192	
10998665-2	2000	In the field of intestinal secretion, research on the secretion of bicarbonate by pancreatic ducts and duodenal epithelia in cystic fibrosis revealed the crucial role of chloride channel (CFTR) in the control of activity of other transporters involved in bicarbonate secretion.	Bicarbonates	255-266	CF transmembrane conductance regulator	Homo sapiens	188-192	
10898755-1	2000	The loss of cystic fibrosis transmembrane conductance regulator (CFTR)-mediated transepithelial HCO(3)(-) secretion contributes to the pathogenesis of pancreatic and biliary disease in cystic fibrosis (CF) patients.	Bicarbonates	96-101	CF transmembrane conductance regulator	Homo sapiens	12-63	
10898755-1	2000	The loss of cystic fibrosis transmembrane conductance regulator (CFTR)-mediated transepithelial HCO(3)(-) secretion contributes to the pathogenesis of pancreatic and biliary disease in cystic fibrosis (CF) patients.	Bicarbonates	96-101	CF transmembrane conductance regulator	Homo sapiens	65-69	
10833480-1	2000	BACKGROUND & AIMS: The duodenum is a cystic fibrosis transmembrane conductance regulator (CFTR)-expressing epithelium with high bicarbonate secretory capacity.	Bicarbonates	132-143	CF transmembrane conductance regulator	Homo sapiens	94-98	
10833480-2	2000	We aimed to define the role of CFTR in human duodenal epithelial bicarbonate secretion in normal (NL) subjects and patients with cystic fibrosis (CF).	Bicarbonates	65-76	CF transmembrane conductance regulator	Homo sapiens	31-35	
10718446-4	2000	This disease is characterized by abnormalities in the cystic fibrosis transmembrane conductance regulator, which normally conducts bicarbonate and chloride exchange.	Bicarbonates	131-142	CF transmembrane conductance regulator	Homo sapiens	54-105	
9142951-0	1997	cAMP and genistein stimulate HCO3- conductance through CFTR in human airway epithelia.	Bicarbonates	29-33	CF transmembrane conductance regulator	Homo sapiens	55-59	
9142951-3	1997	CFTR as the current carrier for HCO3- was identified by 1) stimulation by cAMP, 2) ATP dependence, 3) blocker sensitivity, 4) stimulation by genistein, and 5) lack of stimulation in CF epithelia bearing mutated delta F508 CFTR.	Bicarbonates	32-36	CF transmembrane conductance regulator	Homo sapiens	0-4	
9142951-3	1997	CFTR as the current carrier for HCO3- was identified by 1) stimulation by cAMP, 2) ATP dependence, 3) blocker sensitivity, 4) stimulation by genistein, and 5) lack of stimulation in CF epithelia bearing mutated delta F508 CFTR.	Bicarbonates	32-36	CF transmembrane conductance regulator	Homo sapiens	222-226	
8766016-9	1996	Thus, the HCO3-dependent, Na- and Cl-independent, DPC-blockable pHi recovery may be largely due to an influx of HCO3 via CFTR Cl channels.	Bicarbonates	10-14	CF transmembrane conductance regulator	Homo sapiens	121-125	
8766016-9	1996	Thus, the HCO3-dependent, Na- and Cl-independent, DPC-blockable pHi recovery may be largely due to an influx of HCO3 via CFTR Cl channels.	Bicarbonates	112-116	CF transmembrane conductance regulator	Homo sapiens	121-125	
8766016-10	1996	Under physiological conditions, when the electrochemical gradient for HCO3 is likely to be outwardly rather than inwardly directed, the CFTR (or another HCO3-permeable channel) may mediate HCO3 secretion and contribute to regulation of pH of the periciliary fluid.	Bicarbonates	70-74	CF transmembrane conductance regulator	Homo sapiens	136-140	
8766016-10	1996	Under physiological conditions, when the electrochemical gradient for HCO3 is likely to be outwardly rather than inwardly directed, the CFTR (or another HCO3-permeable channel) may mediate HCO3 secretion and contribute to regulation of pH of the periciliary fluid.	Bicarbonates	153-157	CF transmembrane conductance regulator	Homo sapiens	136-140	
8766016-10	1996	Under physiological conditions, when the electrochemical gradient for HCO3 is likely to be outwardly rather than inwardly directed, the CFTR (or another HCO3-permeable channel) may mediate HCO3 secretion and contribute to regulation of pH of the periciliary fluid.	Bicarbonates	153-157	CF transmembrane conductance regulator	Homo sapiens	136-140	
10652014-7	2000	NBC is activated by cystic fibrosis transmembrane conductance regulator (CFTR) and plays an important role in HCO3- secretion in the agonist-stimulated state in pancreatic duct cells.	Bicarbonates	110-114	CF transmembrane conductance regulator	Homo sapiens	73-77	
10845107-6	2000	The result is activation of CFTR and/or C1C-2 channel proteins to enhance the electrogenic secretion of chloride and bicarbonate.	Bicarbonates	117-128	CF transmembrane conductance regulator	Homo sapiens	28-32	
10516209-0	1999	CFTR involvement in chloride, bicarbonate, and liquid secretion by airway submucosal glands.	Bicarbonates	30-41	CF transmembrane conductance regulator	Homo sapiens	0-4	
10491290-2	1999	In the CF pancreatic duct, mutations in CFTR cause a reduction in bicarbonate secretion.	Bicarbonates	66-77	CF transmembrane conductance regulator	Homo sapiens	40-44	
9920885-1	1999	A central function of cystic fibrosis transmembrane conductance regulator (CFTR)-expressing tissues is the secretion of fluid containing 100-140 mM HCO3-.	Bicarbonates	148-152	CF transmembrane conductance regulator	Homo sapiens	22-73	
9920885-1	1999	A central function of cystic fibrosis transmembrane conductance regulator (CFTR)-expressing tissues is the secretion of fluid containing 100-140 mM HCO3-.	Bicarbonates	148-152	CF transmembrane conductance regulator	Homo sapiens	75-79	
9920885-3	1999	HCO3- secretion is impaired in CF in all CFTR-expressing, HCO3--secreting tissues examined.	Bicarbonates	0-4	CF transmembrane conductance regulator	Homo sapiens	41-45	
9920885-10	1999	The novel finding of regulation of Cl-/HCO3- exchange by CFTR reported here may have important physiological implications and explain, at least in part, the impaired HCO3- secretion in CF.	Bicarbonates	39-43	CF transmembrane conductance regulator	Homo sapiens	57-61	
9920885-10	1999	The novel finding of regulation of Cl-/HCO3- exchange by CFTR reported here may have important physiological implications and explain, at least in part, the impaired HCO3- secretion in CF.	Bicarbonates	166-170	CF transmembrane conductance regulator	Homo sapiens	57-61	
9886916-4	1999	We propose that the defect in agonist-stimulated ductal HCO-3 secretion in patients with CF is predominantly due to decreased NBC-driven HCO-3 entry at the basolateral membrane, secondary to the lack of sufficient electrogenic driving force in the absence of functional CFTR.	Bicarbonates	56-61	CF transmembrane conductance regulator	Homo sapiens	270-274	
9843756-2	1998	Regulation of CFTR by small molecules including HCO3-.	Bicarbonates	48-52	CF transmembrane conductance regulator	Homo sapiens	14-18	
9843756-8	1998	It is likely that there are complicated interactions between Cl- and HCO-3 in the secretion of both ions through the CFTR and the anion exchanger in intestinal cells, and these may yield a role of CFTR in regulation of intestinal HCO-3 secretion as well as of intra- and extracellular pH.	Bicarbonates	69-74	CF transmembrane conductance regulator	Homo sapiens	117-121	
9843756-8	1998	It is likely that there are complicated interactions between Cl- and HCO-3 in the secretion of both ions through the CFTR and the anion exchanger in intestinal cells, and these may yield a role of CFTR in regulation of intestinal HCO-3 secretion as well as of intra- and extracellular pH.	Bicarbonates	69-74	CF transmembrane conductance regulator	Homo sapiens	197-201	
9843756-8	1998	It is likely that there are complicated interactions between Cl- and HCO-3 in the secretion of both ions through the CFTR and the anion exchanger in intestinal cells, and these may yield a role of CFTR in regulation of intestinal HCO-3 secretion as well as of intra- and extracellular pH.	Bicarbonates	230-235	CF transmembrane conductance regulator	Homo sapiens	117-121	
9843756-8	1998	It is likely that there are complicated interactions between Cl- and HCO-3 in the secretion of both ions through the CFTR and the anion exchanger in intestinal cells, and these may yield a role of CFTR in regulation of intestinal HCO-3 secretion as well as of intra- and extracellular pH.	Bicarbonates	230-235	CF transmembrane conductance regulator	Homo sapiens	197-201	
9530182-4	1998	Because Isc could be partially inhibited by basolateral 4,4"-dinitrostilbene-2,2"-disulfonic acid and because the only known apical exit pathway for anions is the cystic fibrosis transmembrane conductance regulator, which has a relatively poor conductance for HCO3-, it was concluded that most basal Isc is HCO3(-)-dependent Cl- secretion [M. Singh, M. Krouse, S. Moon, and J. J.	Bicarbonates	260-264	CF transmembrane conductance regulator	Homo sapiens	163-214	
9530182-4	1998	Because Isc could be partially inhibited by basolateral 4,4"-dinitrostilbene-2,2"-disulfonic acid and because the only known apical exit pathway for anions is the cystic fibrosis transmembrane conductance regulator, which has a relatively poor conductance for HCO3-, it was concluded that most basal Isc is HCO3(-)-dependent Cl- secretion [M. Singh, M. Krouse, S. Moon, and J. J.	Bicarbonates	307-311	CF transmembrane conductance regulator	Homo sapiens	163-214	
9461126-1	1998	Guanylin is a mammalian peptide ligand that binds to the enterocyte receptor guanylyl cyclase C and mediates Cl- and HCO3- efflux via the cystic fibrosis transmembrane conductance regulator.	Bicarbonates	117-121	CF transmembrane conductance regulator	Homo sapiens	138-189	
9626762-4	1997	Secretin induces a bicarbonate rich choleresis by stimulating the activity of the Cl-/HCO3- exchanger by cAMP and protein kinase A mediated phosphorylation of CFTR regulatory domain.	Bicarbonates	19-30	CF transmembrane conductance regulator	Homo sapiens	159-163	
9142951-10	1997	Blocker effects were absent in human CF tracheal cells homozygous for the delta F508 mutation of CFTR (CFT1); Cl- and HCO3- currents were rescued in CFT1 cells recombinantly expressing wild-type CFTR.	Bicarbonates	118-122	CF transmembrane conductance regulator	Homo sapiens	97-101	
9142951-11	1997	Thus CFTR functions as a HCO3- and Cl- conductor, and genistein and bromotetramisole maximize CFTR activity in airway epithelial cells.	Bicarbonates	25-29	CF transmembrane conductance regulator	Homo sapiens	5-9	
8663158-13	1996	In Calu-3 cells, which natively express CFTR, trans-Golgi pH was (in 25 mM HCO3-) 6.19 +/- 0.05 (n = 25) and 6.17 +/- 0.08 (n = 23, CPT-cAMP).	Bicarbonates	75-79	CF transmembrane conductance regulator	Homo sapiens	40-44