PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 11875266-0 2001 Cl(-)-dependent HCO3- transport by cystic fibrosis transmembrane conductance regulator. Bicarbonates 16-20 CF transmembrane conductance regulator Homo sapiens 35-86 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 9142951-0 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 15-71 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 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 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 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 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 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 0-51 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 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 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 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 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 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 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 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 33376814-1 2021 : Regulation of HCO3 -Transport and extracellular pH by CFTR. Bicarbonates 16-20 CF transmembrane conductance regulator Homo sapiens 56-60 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 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 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 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 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 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 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 31561038-6 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 29845767-0 2018 Editorial Focus: CFTR-dependent bicarbonate secretion by Calu-3 cells. Bicarbonates 32-43 CF transmembrane conductance regulator Homo sapiens 17-21 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 140-144 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 78-82 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 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 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 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 67-71 CF transmembrane conductance regulator Homo sapiens 34-38 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 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 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 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 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 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 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 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 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 22515107-7 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 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 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 21893120-0 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 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 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 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 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 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 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 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 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 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 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 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 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 21145458-6 2010 CFTR-(/)- epithelia showed markedly reduced Cl- and HCO3- transport. Bicarbonates 52-56 CF transmembrane conductance regulator Homo sapiens 0-4 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 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 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 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 20406739-0 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 20406739-2 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 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 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 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 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 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 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 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 19019741-0 2009 Mechanism of direct bicarbonate transport by the CFTR anion channel. Bicarbonates 20-31 CF transmembrane conductance regulator Homo sapiens 49-53 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 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 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 19019741-1 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 4-55 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