ライフサイエンスコーパス: HCO3-

1 HCO3 (-) is a key factor in the regulation of sperm moti

2 HCO3 (-) is crucial for pH regulation and is transported

3 HCO3- efflux across the apical membrane is an electrogen

4 .g. Na-H exchangers) by accelerating CO(2) / HCO3- -mediated buffering of acid-base equivalents, they

5 cted with bCA and clamped to -40 mV, CO(2) / HCO3- exposures markedly decrease E(rev) , producing lar

6 In oocytes not expressing NBCe1-A, CO(2) / HCO3- triggers rapid increases in [Na(+) ](i) that both

7 carbonate, including As(OH)2CO3- and As(OH)3(HCO3-)2.

8 We therefore propose that Best2 is a HCO3- channel that works in concert with a Cl:HCO3- exch

9 ribe the first cloning and localization of a HCO3- transporter from sperm of the sea urchin, Strongyl

10 that ZIP8 is a Mn2+/HCO3- symporter, that a HCO3- gradient across the plasma membrane acts as the dr

11 ine, where endogenous pNBC1 functions with a HCO3-:Na+ stoichiometry of 2:1, 8-Br-cAMP increased GDS

12 , supporting the conclusion that an NBCe1-A- HCO3- metabolon does not exist in oocytes.

13 unctionally polarized, and 4) can accumulate HCO3 (-)ions from the basolateral side and secrete them

14 Administering HCO3 (-) after FPI prevented the acidosis and reduced th

15 e subsequent export of carbonate alkalinity (HCO3- + CO3-2) from soils to rivers account for signific

16 e investigation of PEPc kinetics, suggest an HCO3 (-) limitation imposed by CA, and show similarities

17 In addition to an HCO3--dependent activation, the cyclase endogenous to hu

18 s thought to facilitate Cl(-) absorption and HCO3 (-) secretion.

19 eans to examine the role of eCA activity and HCO3 (-) /CO2 uptake in the functioning of the CCM.

20 ghts a differential sensitivity of Cl(-) and HCO3 (-) transporters to raised CO2 in Calu-3 cells.

21 inc metalloenzymes that interconvert CO2 and HCO3 (-) In plants, both alpha- and beta-type CAs are pr

22 amma deletion in mice eliminated the CO2 and HCO3 (-) sensitivities of JHCO3 as well as the normal de

23 red with a smaller increase in bile flow and HCO3 (-) biliary output, as well as altered biliary comp

24 y carbonic anhydrase in epithelial fluid and HCO3 (-) secretion and works by activating the ductal Cl

25 Aberrant epithelial fluid and HCO3 (-) secretion is associated with many diseases.

26 Fluid and HCO3 (-) secretion is essential for all epithelia; aberr

27 ne and kidney plays a major role in NaCl and HCO3 (-) absorption that is closely linked to fluid abso

28 (-) exchange with SCN(-), I(-), NO3 (-), and HCO3 (-) with drug concentration causing 50% inhibition

29 Intracellular pH regulation and HCO3 (-)transport were assessed by microfluorometry.

30 reduced sperm motility, swimming speed, and HCO3 (-)-enhanced beat frequency.

31 hich H+ is neutralized, CO2 is absorbed, and HCO3- is secreted.

32 CFTR activities, luminal Cl- absorption and HCO3- secretion, and the associated fluid secretion.

33 In mammals, Ca2+ and HCO3- ions play a critical role in the regulation of spe

34 Similarly, both Ca2+ and HCO3- stimulate cAMP accumulation in human spermatozoa.

35 rodes to measure fluid secretion and Cl- and HCO3- concentrations in cultured murine sealed intralobu

36 lamiloride, which respectively block Cl- and HCO3- secretion in porcine airways, induced the formatio

37 out the complexity of the intestinal Cl- and HCO3- transport in health and disease.

38 In Ringer solution containing both Cl- and HCO3-, the magnitude of cAMP-stimulated anion secretion

39 role of this regulatory gene in both CO2 and HCO3- acquisition of the cyanobacterium.

40 ion of overall HCO3- reabsorption by CO2 and HCO3- sensors at the basolateral membrane.

41 ion of genes encoding both inducible CO2 and HCO3- uptake systems.

42 ith similar inorganic carbon (Ci; as CO2 and HCO3-) transporter systems.

43 es the reversible interconversion of CO2 and HCO3-.

44 l as HCO3- secretion by pancreatic ducts and HCO3- reabsorption by renal proximal tubules.

45 as a key coordinator of epithelial fluid and HCO3- secretion and may have implications to all CFTR-ex

46 Fluid and HCO3- secretion are vital functions of secretory epithel

47 and the luminal CFTR to coordinate fluid and HCO3- secretion by the pancreatic duct.

48 se the reversible hydration of CO2 to H+ and HCO3- ions.

49 ation mixtures containing hSOD1WT, H2O2, and HCO3-.

50 t basolateral NHE1 regulates apical NHE3 and HCO3- absorption in the MTAL by controlling the organiza

51 facilitated CO2 uptake, CO2 scavenging, and HCO3- transport with varying external pH.

52 ) in response to changes in blood [CO2] and [HCO3 (-)].

53 in causing changes in intracellular pH and [HCO3 (-)], but was not obligatory for the pH-dependent c

54 - > NO2- > Br- > Cl- > SO4(2-) approximately HCO3- approximately gluconate- approximately aspartate-

55 intracellular pH (pHi) regulation as well as HCO3- secretion by pancreatic ducts and HCO3- reabsorpti

56 pathway that was defective in CF: (i). ASL [HCO3-] was higher in NL than CF ASL; (ii). activating CF

57 n B, which disrupts F-actin, decreased basal HCO3- absorption by 30% and prevented the inhibition by

58 CAs augments the apparent rate of net basal HCO3- secretion.

59 ne CO2 permeability and vigorous basolateral HCO3 (-)uptake, which was sensitive to Na(+)withdrawal,

60 Chloride (Cl(-) ) and bicarbonate (HCO3 (-) ) are two major anions and their permeation thr

61 ion of carbon dioxide (CO2) and bicarbonate (HCO3 (-)).

62 Bicarbonate (HCO3-) transporters play crucial roles in cell-signaling

63 dismutase (hSOD1WT) induced by bicarbonate (HCO3-)-mediated peroxidase activity.

64 egulator (CFTR) is required for bicarbonate (HCO3-) transport and that HCO3- is critical for normal m

65 A biliary HCO3- umbrella protects human cholangiocytes against dam

66 recently hypothesized that an apical biliary HCO3- umbrella might prevent the protonation of biliary

67 Defects of the biliary HCO3- umbrella may lead to the development of chronic ch

68 bile acids, and that defects in this biliary HCO3- umbrella might predispose to chronic cholangiopath

69 ACZ led to lower arterial and venous blood [HCO3-], pH and lactate levels (P < 0.05), and increased

70 Both HCO3 (-) administration and loss of ASIC1a also reduced

71 cate that in normal colon NHE3 mediates both HCO3 (-)-dependent and butyrate-dependent Na(+) absorpti

72 conditions in controls demonstrate that both HCO3 (-)-dependent and butyrate-dependent Na(+) absorpti

73 zymogen granules is significantly blunted by HCO3 (-) buffer in comparison with HEPES, and that this

74 tons that must be neutralized, presumably by HCO3 (-)ions transported from ameloblasts into the devel

75 ut mutant mice show responses to stimulus by HCO3 (-) or CO2 that were delayed in onset and reduced i

76 hat most of the Best2 current was carried by HCO3-.

77 the cAMP-mediated activation of motility by HCO3-, and the protein phosphorylation cascade of sperm

78 ates of NBCe1 or other transporters carrying HCO3- , CO3= , or NaCO3- ion pairs.

79 gans to reveal a novel mechanism of cellular HCO3 (-) uptake.

80 the major HCO3 (-) supplier of ductal Cl(-) -HCO3 (-) exchanger AE2, but not of NBCe1-B.

81 on and works by activating the ductal Cl(-) -HCO3 (-) exchanger AE2.

82 ) /HCO3 (-) (apex) anion exchanger 2 (Cl(-) /HCO3 (-) AE2), and adenylyl cyclase (AC)8 (proteins regu

83 rosis transmembrane regulator (CFTR), Cl(-) /HCO3 (-) (apex) anion exchanger 2 (Cl(-) /HCO3 (-) AE2),

84 features, and the expression of CFTR, Cl(-) /HCO3 (-) AE2, AC8, and secretin-stimulated cAMP levels.

85 Cl(-) /HCO3- anion exchanger 2 (AE2) participates in intracellu

86 fferent anion exchangers that exchange Cl(-)/HCO3 (-), including Slc26a3/Dra, Slc26a6/Pat-1, and Slc2

87 the involvement of pendrin-facilitated Cl(-)/HCO3 (-) in the regulation of ASL volume and suggest the

88 brane conductance regulator results in Cl(-)/HCO3 (-) hyposecretion and triggers Na(+) hyperabsorptio

89 drin up-regulation, strongly increased Cl(-)/HCO3 (-) exchange and the increase was blocked by pendri

90 mbinant HEK293 cells revealed that the Cl(-)/HCO3 (-) exchange activity of a kAE1 protein mutated on

91 shift from a predominantly electroneutral Cl-HCO3- exchange in normal mice, to a predominantly electr

92 changer AE1 (band 3) is an electroneutral Cl-HCO3- exchanger with 12-14 transmembrane spans (TMs).

93 onductive pathways intrinsic to two other Cl-HCO3- exchangers, trout AE1 and mammalian SLC26A7.

94 cytes mediated bidirectional Cl--Cl- and Cl--HCO3- exchange.

95 cAMP-insensitive Cl--HCO3- exchange mediated by hDRA gained modest cAMP sensi

96 Cl-/HCO3- exchange activity mediated by the AE1 anion exchan

97 explained by the parallel activity of a Cl-/HCO3- exchanger and a Cl- conductance, either the cystic

98 The AE2 Cl-/HCO3- exchanger is expressed in numerous cell types, inc

99 ich may normally be coupled with the AE2 Cl-/HCO3- exchanger, is important for normal levels of gastr

100 Xenopus oocytes, we compared Cl-/Cl- and Cl-/HCO3- exchange activities of AE1 polypeptides with trunc

101 1 901X mutant exhibited both Cl-/Cl- and Cl-/HCO3- exchange activities.

102 in the CA2 binding site were inactive as Cl-/HCO3- exchangers despite exhibiting normal Cl-/Cl- excha

103 luid cannot be explained by conventional Cl-/HCO3- exchange.

104 ort via conductive versus electroneutral Cl-/HCO3- exchange (anion exchange, AE) pathways, nasal cell

105 y in AE1 mutants selectively impaired in Cl-/HCO3- exchange.

106 CFTR results in a double hit of reduced Cl-/HCO3- and H2O secretion as well as ENaC hyperactivity an

107 CA2 co-expression could not rescue Cl-/HCO3- exchange activity in AE1 mutants selectively impai

108 incompetent AE1 mutants failed to rescue Cl-/HCO3- exchange by the AE1 truncation mutant 896X, despit

109 act CA2 binding sites completely rescued Cl-/HCO3- exchange by an AE1 missense mutant devoid of CA2 b

110 CO3- channel that works in concert with a Cl:HCO3- exchanger in the apical membrane to affect transce

111 fixation, carbonic anhydrase activity, CO2 /HCO3 (-) uptake, delta(13) Corg ) in natural phytoplankt

112 transporter currents in the presence of CO2-HCO3-.

113 The stimulating effect of CrCAH3 and CO2/HCO3 (-) on PSII activity was demonstrated by comparing

114 HCO3 (-) facilitate monitoring of blood CO2/HCO3 (-) concentrations.

115 amma appears to be a novel extracellular CO2/HCO3 (-) sensor critical for pH homeostasis.

116 llular Ci limitation in the slow-growing CO2/HCO3 (-)-uptake mutant DeltandhD3 (for NADH dehydrogenas

117 Yet CO2/HCO3 (-) sensing mechanisms remain poorly characterized.

118 In 5% CO2/HCO3--buffered conditions, in the presence of 30 microM

119 27 degrees C was similar in Hepes- or 5% CO2/HCO3--buffered superfusates but, in both cases, was appr

120 a major role for carbonic anhydrase and CO2/HCO3- in this developmental cascade leading to the produ

121 luous, most likely because extracellular CO2/HCO3- buffer is clamped at equilibrium.

122 ng different intracellular [H(+)] and [CO2]/[HCO3 (-)].

123 hat normal mucus release requires concurrent HCO3- secretion and that the characteristically aggregat

124 , but can undergo a dynamic shift to conduct HCO3- by a process involving ATP hydrolysis.

125 A speeds transport by regenerating/consuming HCO3- .

126 10 microM amiloride or 0.7 nM NGF decreased HCO3- absorption by 27-32%.

127 ls with CF may be a consequence of defective HCO3- transport.

128 iven that neither a change in CFTR-dependent HCO3 (-) efflux nor Na(+) /HCO3 (-) cotransporter-depend

129 and fluid secretion, but not CFTR-dependent HCO3 (-) secretion, which highlights a differential sens

130 nor Na(+) /HCO3 (-) cotransporter-dependent HCO3 (-) influx were CO2 -sensitive.

131 brane conductance regulator (CFTR)-dependent HCO3- secretion also demonstrated apparently normal gobl

132 conditions because of absent CFTR-dependent HCO3- secretion and that this defect can lead to an impa

133 the following evidence for a CFTR-dependent HCO3- secretory pathway that was defective in CF: (i). A

134 Basal Cl--dependent HCO3- secretion, measured using a pH stat technique, was

135 n independent cAMP-mediated, CFTR-dependent, HCO3- secretion that appears to mainly enhance the extra

136 CFTR) is associated with diminished duodenal HCO3- secretion, despite a reported lack of clinical duo

137 In most epithelia, this entails HCO3- entry at the basolateral membrane, mediated by the

138 logical implications ranging from epithelial HCO3 (-) secretion to neuronal excitation.

139 the major anions I-, Br-, Cl-, SO4(2-), F-, HCO3-, and B(OH)4 on the response for mercury showed tha

140 eabsorbing approximately 80% of the filtered HCO3- as well as generating new HCO3- for regulating blo

141 icant pathway in pancreatic acinar cells for HCO3 (-) secretion into the lumen.

142 to date, there is no functional evidence for HCO3 (-)transport in these cells.

143 ion, the amount of CFTR is rate-limiting for HCO3 (-) secretion and for correcting host defense abnor

144 genes encoding the essential components for HCO3- and CO2 uptake.

145 here it may be the predominant mechanism for HCO3- efflux and Cl- influx across the basolateral membr

146 component of the basolateral mechanisms for HCO3- uptake during cAMP-stimulated anion secretion in t

147 Molecular oxygen was needed for HCO3-/H2O2-dependent aggregation of hSOD1WT, implicating

148 ties of sAC and that Ca2+ can substitute for HCO3- in the stimulation of this enzyme, underscoring an

149 To test for HCO3- transport via conductive versus electroneutral Cl-

150 se (GST) fusion proteins, to form functional HCO3- metabolons.

151 nd is mainly known to catalyze the CO(2) <-> HCO3- equilibrium.

152 When (bi)carbonate (CO2, H2CO3, HCO3- and CO3(-2)) was added to the reaction mixture, it

153 rminal cytoplasmic domains compared to human HCO3- transporters.

154 ingle knockout animals display an imbalanced HCO3 (-) homeostasis, resulting in substantially reduced

155 talysed) protonation and removal of imported HCO3- ions.

156 anion secretion was not due to a decrease in HCO3 (-) transport given that neither a change in CFTR-d

157 porters and channels known to be involved in HCO3 (-)transport in other epithelia.

158 s not explained by pH-independent changes in HCO3- concentration, altered glycosylation, additional p

159 pecific role for the intracellular enzyme in HCO3- transport, and hence pHi regulation in the heart.

160 either an increase in Isc nor an increase in HCO3- secretion, confirming the role for Cftr protein in

161 onsistent with the known function of NBC1 in HCO3- absorption in the kidney and demonstrate that NBC1

162 events that underlie four major processes in HCO3- reabsorption.

163 dosis in humans, consistent with its role in HCO3- absorption in the kidney.

164 n which goblet cells play a critical role in HCO3- homeostasis.

165 antly electrogenic anion secretion including HCO3- that occurs via functional Cftr during anti-CD3-me

166 Overexpressing CFTR increased HCO3 (-) secretion to rates greater than wild type, but

167 h a simultaneous increase in Cl--independent HCO3- secretion that was also inhibited by glibenclamide

168 Vasopressin, which inhibits HCO3- absorption by an amount similar to that observed w

169 lic channeling of HCO3- to the intracellular HCO3- binding site of AE1.

170 acellular [H(+)] or a rise in intracellular [HCO3 (-)], or by both, in mammalian astrocytes.

171 a concomitant rise or fall in intracellular [HCO3 (-)].

172 mulated by an increase in the intracellular [HCO3 (-)].

173 n (1) pH, (2) adequate expression of the key HCO3- exporter, anion exchanger 2 (AE2), and (3) an inta

174 edly increases the activity and is the major HCO3 (-) supplier of ductal Cl(-) -HCO3 (-) exchanger AE

175 scoveries focused attention on CFTR-mediated HCO3 (-) secretion and airway surface liquid (ASL) pH as

176 by increased GABA receptor (GABAR)-mediated HCO3- efflux, alkalinizing the cleft and disinhibiting c

177 ant rod-cone dystrophy disrupt NBC1-mediated HCO3- transport.

178 is highly permeable to HCO3 (-) and mediates HCO3 (-) uptake into amphid sheath glia.

179 fluence of intrinsic CA activity on membrane HCO3- or H+ transport via the native acid-extruding prot

180 treatment with acidic medium (pH 6.9, 10 mm HCO3-).

181 t in Xenopus oocytes exposed to 5% CO2-26 mm HCO3- (pH 7.40).

182 It is likely that ZIP8 is a Mn2+/HCO3- symporter, that a HCO3- gradient across the plasma

183 al barrier consists of a preepithelial mucus HCO3- layer, intercellular tight junctions connecting th

184 in CFTR-dependent HCO3 (-) efflux nor Na(+) /HCO3 (-) cotransporter-dependent HCO3 (-) influx were CO

185 events and mediated by an electrogenic Na(+)/HCO3 (-) cotransporter.

186 mechanism of HCO3 (-) uptake involves Na(+)/HCO3 (-) cotransporters, here we demonstrate that the C.

187 ivity, are mediated by an electrogenic Na(+)/HCO3- cotransporter, and are more tightly coupled to net

188 o novel variants of the electroneutral Na(+)/HCO3- cotransporter NBCn1, one full-length starting with

189 rise from operation of the electrogenic Na+ -HCO3- cotransporter NBCe1.

190 via the native acid-extruding proteins, Na+ -HCO3- cotransport (NBC) and Na+ / H+ exchange (NHE), exp

191 sion proteins, Na+-H+ exchange (NHE) and Na+-HCO3- co-transport (NBC) in guinea-pig isolated ventricu

192 the basolateral membrane is achieved by Na+-HCO3- cotransport and also by a H+-ATPase and Na+/H+ exc

193 The electrogenic Na+-HCO3- cotransporter (NBCe1) plays a central role in intr

194 m that is characteristic of electrogenic Na+-HCO3- cotransporters.

195 The Na+-HCO3- cotransporter NBC1 is located exclusively on the b

196 he basolateral membrane, mediated by the Na+-HCO3- cotransporter, pNBC1, and exit at the luminal memb

197 gesting that the sea urchin protein is a Na+/HCO3- cotransporter.

198 SLC4A7 encodes the electroneutral Na+/HCO3- co-transporter NBCn1 which regulates intracellular

199 This is characteristic for Na+/HCO3- cotransporters, but not for anion exchangers, sugg

200 The NBC1 Na+/HCO3- cotransporter is expressed in many tissues, includ

201 The most similar human protein is the Na+/HCO3- cotransporter-2 (NBC2), which has 53% identity and

202 hed net perfusate CO2 loss and increased net HCO3- gain, whereas all CA inhibitors inhibited PV acidi

203 the filtered HCO3- as well as generating new HCO3- for regulating blood pH.

204 show that, although CAs could stimulate non- HCO3- transporters (e.g. Na-H exchangers) by acceleratin

205 DSS-induced inflammation, butyrate-, but not HCO3 (-)-dependent Na(+) absorption is present and is in

206 , which mediates butyrate-dependent (but not HCO3 (-)-dependent) Na(+) absorption.

207 tamate that exclusively elicits Cl-, but not HCO3-, conductance in the human sweat duct.

208 The activity of HCO3 (-) transporters depends of HCO3 (-) availability t

209 High concentrations of HCO3 (-) in the female genital tract induce an increase

210 ers of size-exclusion and ion dehydration of HCO3 (-) permeation.

211 activity of HCO3 (-) transporters depends of HCO3 (-) availability that is determined by carbonic anh

212 While the classical mechanism of HCO3 (-) uptake involves Na(+)/HCO3 (-) cotransporters,

213 +) secretion (nearly the same as the rate of HCO3 (-) reabsorption, JHCO3 ) in response to changes in

214 from PSII, possibly by rapid reformation of HCO3 (-) from CO2.

215 Transport of HCO3 (-) into and out of astrocytes by the electrogenic

216 me is necessary, whereas selective uptake of HCO3 (-) into the carboxysome would not appreciably enha

217 However, neither absence of HCO3- nor inhibition of HCO3- transport affected fluid s

218 mucus release in the presence or absence of HCO3- were similar.

219 In addition, in the absence of HCO3-, cholinergic-activated current was identical in co

220 However, in the absence of HCO3-, mucus release stimulated by either PGE2 or 5-hydr

221 r PGE2 or 5-HT in the presence or absence of HCO3-.

222 to represent reduced metabolic channeling of HCO3- to the intracellular HCO3- binding site of AE1.

223 the secretion of moderate concentrations of HCO3- can be explained by the parallel activity of a Cl-

224 Net intestinal fluid secretion consists of HCO3--rich plasma-like fluid.

225 The polarized distribution of HCO3- transport was investigated in human nasal epitheli

226 cretion rates, indicating that the effect of HCO3- removal on mucus release was not due to decreased

227 The third process is the basolateral exit of HCO3- via the electrogenic Na/HCO3 co-transporter, which

228 tein shares the major structural features of HCO3- transporters, including 13 transmembrane segments,

229 Implications of HCO3--dependent SOD1 peroxidase activity in amyotrophic

230 normal, but not CF, cells induced influx of HCO3- across the apical membrane that was reversibly blo

231 latrunculin B did not prevent inhibition of HCO3- absorption by vasopressin or stimulation by hyposm

232 Inhibition of HCO3- and fluid transport markedly reduced stimulated mu

233 , neither absence of HCO3- nor inhibition of HCO3- transport affected fluid secretion rates, indicati

234 However, the regulation and mechanisms of HCO3- secretion in normal and acutely inflamed ileum are

235 ne of cells, consistent with the movement of HCO3- via CFTR; and (2) both normal and CF nasal epithel

236 ctive intestinal peptide) in the presence of HCO3- both normal exocytosis and normal discharge was ob

237 own, but we observed that in the presence of HCO3-, stimulating dissected segments of native mouse in

238 eover, we found that even in the presence of HCO3-, when WT intestines were stimulated only with a Ca

239 ulated by these molecules in the presence of HCO3-.

240 cetazolamide could be mimicked by removal of HCO3-/CO2 from the bathing medium, and furthermore showe

241 The inter-protomeric rescue of HCO3- transport within the AE1 dimer shows functional pr

242 We therefore investigated the role of HCO3- in mucus secretion using mouse small intestine seg

243 However, the sustained secretion of HCO3- into a HCO- -rich luminal fluid cannot be explaine

244 ic CAs cooperatively facilitate secretion of HCO3- into the lumen and CO2 diffusion into duodenal muc

245 iderations argue against a CA stimulation of HCO3- transport, supporting the conclusion that an NBCe1

246 ranches closer to the electroneutral type of HCO3- transporters.

247 intestinal apical anion exchanger Cl(-)/OH- (HCO3-).

248 Jasplakinolide had no effect on HCO3- absorption in tubules bathed with amiloride or a N

249 sistent with binding of extracellular CO2 or HCO3 (-) facilitate monitoring of blood CO2/HCO3 (-) con

250 oquinoline and inhibited by acetazolamide or HCO3-/CO2 removal can be said to represent bicarbonate-d

251 FTR showed no glutamate/ATP activated Cl- or HCO3- conductance.

252 d by the changes in intracellular [H(+)] or [HCO3 (-)].

253 The uptake of CO2 over HCO3 - was found to support the majority of carbon fixat

254 e final process is the regulation of overall HCO3- reabsorption by CO2 and HCO3- sensors at the basol

255 Recent studies show that in higher plants, HCO3 (-) increases PSII activity by acting as a mobile a

256 ic anhydrase (CA) binds to NBCe1-A, promotes HCO3- replenishment/consumption, and enhances transport.

257 tion by hyposmolality, factors that regulate HCO3- absorption through primary effects on apical Na(+)

258 The loss of this uniquely regulated HCO3- conductance is most probably responsible for the m

259 factor, the role of serotonin in regulating HCO3- secretion, the role of mechanisms in ulcer healing

260 In terms of pH regulation, HCO3 (-) buffering has been shown to be important in bot

261 or CFTR(+/F508)) expressed CFTR and secreted HCO3 (-) at approximately 50% of wild-type values.

262 Epithelia with a 50:50 mix secreted HCO3 (-) at half the rate of wild-type epithelia.

263 massive amounts of gastric H+ with secreted HCO3-, generating CO2 and H2O accompanied by the neutral

264 cies the pancreatic duct epithelium secretes HCO3- ions at a concentration of around 140 mM by a mech

265 in inner ear epithelial cells that secretes HCO3- into endolymph.

266 a have a constitutively active DPC-sensitive HCO3- influx/efflux pathway across the apical membrane o

267 he Cl- conductance, yet retained significant HCO3- conductance.

268 led a sharp decrease in both cAMP-stimulated HCO3- secretion and SITS-sensitive current in NBC1-/- pr

269 In in vivo loop studies HCO3 (-)-Ringer and butyrate-Ringer exhibit similar rate

270 Michaelis-Menten constant for its substrate HCO3 (-), and there is little information on the tempera

271 nge in channel selectivity and evidence that HCO3 (-) permeability can be significant.

272 d for bicarbonate (HCO3-) transport and that HCO3- is critical for normal mucus formation.

273 F) and recent results in vitro indicate that HCO3- is required for gel-forming mucins to form the muc

274 We know that HCO3- uptake at the basolateral membrane is achieved by

275 otential candidates in the regulation of the HCO3 (-) homeostasis in sperm and the composition of the

276 ecretion over 24 h, yet had no effect on the HCO3 (-) content of the secreted fluid.

277 The HCO3- metabolon hypothesis predicts that cytosolic carbo

278 The HCO3-:Na+ stoichiometry of these cotransporters is an im

279 ental observations, taken as support for the HCO3- metabolon hypothesis.

280 According to the HCO3- metabolon hypothesis, direct association of cytoso

281 shift in inorganic carbon uptake from CO2 to HCO3 (-) .

282 catalyze the reversible hydration of CO2 to HCO3 (-), represent potential candidates in the regulati

283 C Cl(-) channel CLH-1 is highly permeable to HCO3 (-) and mediates HCO3 (-) uptake into amphid sheath

284 To address questions related to HCO3 (-)export from ameloblasts, we have developed a pol

285 kout animals, show an even lower response to HCO3 (-).

286 alpha-CA catalyzes the conversion of CO2 to HCO3-, the role of CO2 in periplasmic buffering was stud

287 sepithelial anion conductance was limited to HCO3- revealed a sharp decrease in both cAMP-stimulated

288 he conversion of CO2, produced by urease, to HCO3- by the periplasmic alpha-CA.

289 the apical membrane to affect transcellular HCO3- transport.

290 Measurements of transepithelial HCO3 (-)transport showed a marked increase in response t

291 xchanger, thereby decreasing transepithelial HCO3- absorption.

292 is that NBC1 plays a role in transepithelial HCO3- secretion in the intestinal tract, null mutant (NB

293 ver, A20 was also able to indirectly utilize HCO3 - by first converting it to CO2 via external carbon

294 85%) with most species capable of utilizing HCO3 (-) ; however, most are not saturated at current oc

295 id sheath glia regulate intracellular pH via HCO3 (-) flux through the voltage-gated ClC channel CLH-

296 e involved in maintenance of synaptic pH via HCO3 (-) flux.

297 Exactly where HCO3- becomes crucial in these processes is unknown, but

298 inger reversed water secretion observed with HCO3 (-)-Ringer to fluid absorption.

299 as also observed when sAC was activated with HCO3-, was independent of calmodulin, and was associated

300 icated that As(OH)3 could be associated with HCO3- through a hydrogen bond.