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 s of (mM) U, 0.0055; Ca, 2.98; NO3(-), 0.11; HCO3(-), 5.07; and SO4(2-), 1.23.

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 , O2 saturation, Na(+), K(+), Cl(-), Ca(2+), HCO3(-), glucose, lactate) were measured.

8 t the apical membrane were able to support a HCO3(-) -rich secretion.

9 whereas LCIA appears to be associated with a HCO3(-) transport system.

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

11 defective bacterial killing due to aberrant HCO3(-) transport and acidic ASL, make the CF airways su

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

13 The activator HCO3(-) binds adjacent to Arg176, which acts as a switch

14 queous solutions saturated in CO2 with added HCO3(-).

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

16 out CO2 recovery mechanisms or high-affinity HCO3(-) transporters.

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

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

19 Type B cells mediate Cl(-) absorption and HCO3(-) secretion primarily through pendrin-mediated Cl(

20 yze the conversion of substrates acetone and HCO3(-) to form the product acetoacetate.

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

22 extracted from the molalities of CO2(aq) and HCO3(-).

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

24 teral K(+) permeability and apical Cl(-) and HCO3(-) permeabilities (CFTR), and reducing the activity

25 ers or channels that mediate K(+), Cl(-) and HCO3(-) transport.

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

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

28 that catalyze the interconversion of CO2 and HCO3(-) and are ubiquitous in nature.

29 on requires rapid conversion between CO2 and HCO3(-) Carbonic anhydrase II facilitates this reversibl

30 ation, rapid interconversion between CO2 and HCO3(-) catalyzed by carbonic anhydrases (CAs), and acti

31 of the downstream metabolic products CO2 and HCO3(-), which otherwise are near the detection limit, b

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

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

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

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

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

37 Fluid and HCO3(-) secretion is a vital function of secretory epith

38 us in the regulation of epithelial fluid and HCO3(-) secretion.

39 fatty acids inhibited secretion of fluid and HCO3(-), as well as CFTR activity, in pancreatic ductal

40 esters on secretion of pancreatic fluid and HCO3(-), levels and function of CFTR, and exchange of Cl

41 nce by catalyzing CO2 hydration (to H(+) and HCO3(-)), thereby changing the gradient for CO2 venting.

42 Acid-dependent changes in H+ and HCO3 secretion were largely blunted by AMD3100, which se

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

44 the H2O-rich phase, scCO2, aqueous H2O, and HCO3(-).

45 nical IC forms: acid-secreting alpha-ICs and HCO3-secreting beta-ICs.

46 elevated terrestrial export of [Ca + Mg] and HCO3(-) resulted from increased weathering caused by acc

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

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

49 ctate concentrations, and blood pH, PCO2 and HCO3(-) concentration.

50 prostaglandin E2, prostaglandin F2, pH, and HCO3 were measured.

51 t (NBC) regulates intracellular pH (pHi) and HCO3 secretion in rat colon.

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

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

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

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

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

57 dissolved inorganic carbon species CO2(aq), HCO3(-), and CO3(2-) of alkaline solutions under high CO

58 to a seemingly maladaptive persistent base (HCO3(-)) loss that incurs an energetic expense at the ti

59 f secretory epithelia, involving basolateral HCO3(-) entry through the Na(+)-HCO3(-) cotransporter (N

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

61 firmed by a significant relationship between HCO3(-)/Na(+) and DSi/Na(+), and DSi:HCO3(-) ratio can r

62 Bicarbonate (HCO3(-)) is an abundant anion that regulates extracellul

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

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

65 ), carbamic acid (RnNCOOH), and bicarbonate (HCO3(-)) moieties.

66 ly sAC is directly activated by bicarbonate (HCO3(-)); it thereby serves as a cellular sensor for HCO

67 gas (CO2) or its hydrated form, bicarbonate (HCO3(-)), into target molecules.

68 Removal of bicarbonate (HCO3(-)) shifts the Em from approximately -145 mV to -70

69 entrations (1, 3, and 10 mM) of bicarbonate (HCO3(-)) under light and dark conditions.

70 elevated terrestrial export of bicarbonate (HCO3(-); 3.6 mueq L(-1) yr(-1)).

71 - tromethamine (THAM) or sodium bicarbonate (HCO3) +/- AC probes in a micropuncture model of AEC inju

72 consistent with the presence of bicarbonate, HCO3(-), since it is commonly observed at approximately

73 ng to the active site entrance, which blocks HCO3(-) activation through steric hindrance and trapping

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

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

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

77 ive macroalgal species capable of using both HCO3(-) and CO2 had greater CO2 use as concentrations in

78 of the redox state of QA and the binding by HCO3(-) regulates and protects PSII.

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

80 ppocampal CA3 pyramidal cell excitability by HCO3(-) in acute brain slices from C57BL/6 mice.

81 om a highly alkaline pHi was rate-limited by HCO3(-) supply from spontaneous CO2 hydration.

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

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

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

85 lar mechanism for sAC catalysis and cellular HCO3(-) sensing and a basis for targeting this system wi

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

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

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

89 paB, which reduced expression of the Cl(-) / HCO3(-) exchanger DRA (SLC26A3), via direct binding to t

90 O3(-) cotransporter (NBC1) and apical Cl(-) /HCO3(-) exchanger (solute carrier family 26 member A6; S

91 ucing the activity of the basolateral Cl(-) /HCO3(-) exchanger (anion exchanger 2; AE2).

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

93 ative 1:2 and 1:1 stoichiometries for Cl(-) /HCO3(-) exchange via SLC26A6 at the apical membrane were

94 f background electrolyte composition (Cl(-), HCO3(-), and NH4(+)) on the formation and fate of electr

95 Pendrin is a Cl(-)/HCO3(-) exchanger expressed in type B and non-A, non-B i

96 Loss of the AE3 Cl(-)/HCO3(-) exchanger (Slc4a3) in mice causes an impaired ca

97 sults support a model in which the AE3 Cl(-)/HCO3(-) exchanger, coupled with parallel Cl(-) and H(+)-

98 cts in tandem with the Na(+)-dependent Cl(-)/HCO3(-) exchanger (NDCBE) encoded by Slc4a8 to mediate N

99 how that Slc26a6 mediates electrogenic Cl(-)/HCO3(-) exchange activities in cardiomyocytes, suggestin

100 Slc26a6, a unique cardiac electrogenic Cl(-)/HCO3(-) transporter in ventricular myocytes, linking the

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

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

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

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

105 Pendrin is a Na(+)-independent Cl(-)/HCO3(-) exchanger that localizes to type B and non-A, no

106 The pendrin-mediated Cl(-)/HCO3(-) exchange process is greatly upregulated in model

107 ion primarily through pendrin-mediated Cl(-)/HCO3(-) exchange.

108 Anion exchanger 1 (AE1) mediates Cl(-)/HCO3(-) exchange in erythrocytes and kidney intercalated

109 ) and solute carrier family 26 (SLC26) Cl(-)/HCO3(-) exchangers.

110 -pendrin and restored its cell-surface Cl(-)/HCO3(-) exchange activity.

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

112 ular alkalization, consistent with the Cl(-)/HCO3(-) exchange activities of Slc26a6.

113 ing from the parallel operation of the Cl(-)/HCO3(-) exchanger pendrin and the Na(+)-driven Cl(-)/2HC

114 iew summarizes the contribution of the Cl(-)/HCO3(-) exchanger pendrin in distal nephron function.

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

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

117 talyze the chemical equilibration among CO2, HCO3(-) and H(+).

118 pressure (pCO2) that disturb cytoplasmic CO2-HCO3(-)-H(+) equilibrium.

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

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

121 le that H(+) diffusion is facilitated by CO2/HCO3(-) buffer and thus provides a read-out of DCO2.

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

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

124 Intracellular H2O is necessary for CO2/HCO3(-) conversion.

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

126 lated to its function in band 3-mediated CO2/HCO3(-) exchange.

127 even by residual HCO3(-) in a nominally CO2/HCO3(-)-free saline solution.

128 The effect of CO2/HCO3(-) was ablated by connexin43 inhibition or knockdow

129 t the core was halved in the presence of CO2/HCO3(-), but this process requires a restorative HCO3(-)

130 activity, even in the nominal absence of CO2/HCO3(-).

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

132 essed abundance patterns and a proxy for CO2:HCO3(-) use (delta(13)C values) of macroalgae along a gr

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

134 The experimentally determined [CO2]/[HCO3(-)] ratios agree well with the predicted values for

135 oscopy allows the concentration ratio [CO2]/[HCO3(-)] to be experimentally determined.

136 A speeds transport by regenerating/consuming HCO3- .

137 s large volumes of alkaline fluid containing HCO3(-) concentrations as high as 140 mm during hormonal

138 8 media increased H+ secretion and decreased HCO3 secretion in isolated perfused rabbit CCDs.

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

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

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

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

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

144 is uniquely associated with a depolarizing, HCO3(-) independent, Cl(-) -conductance in oocytes that

145 between HCO3(-)/Na(+) and DSi/Na(+), and DSi:HCO3(-) ratio can reflect the mineral source of chemical

146 hich luminal SCFA perfusion affects duodenal HCO3(-) secretion (DBS), a measure of mucosal neurohumor

147 ellular pH acidification as part of duodenal HCO3(-) secretion appears to require cystic fibrosis tra

148 (FFA1) and presumed FFA3 stimulates duodenal HCO3(-) secretion via a glucagon-like peptide (GLP)-2 pa

149 rt-term plant cellular responses to elevated HCO3(-) concentrations as a result of ambient increases

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

151 ly increased intracellular and extracellular HCO3(-) concentrations and elevated brain pHi compared t

152 uld only be mimicked in non-CF HBE following HCO3(-) removal.

153 e rely to a greater degree upon V-ATPase for HCO3(-)-independent pHi regulation than do cultured astr

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

155 function of CFTR, and exchange of Cl(-) for HCO3(-) in pancreatic cell lines as well as in tissues f

156 DRA-mediated exchange of Cl(-) for HCO3(-) was measured by uptake of (125)I.

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

158 ions from ingested seawater in exchange for HCO3(-) to maintain water balance.

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

160 on exchanger 1 (AE1)] provides a passage for HCO3(-) flux across the cell membrane.

161 ; it thereby serves as a cellular sensor for HCO3(-), carbon dioxide (CO2), and pH in physiological f

162 )) over hard, stongly hydrated anions (e.g., HCO3(-) and SO4(2-)).

163 ence of a local depolarizing Cl(-) gradient, HCO3(-) efflux through GABAA receptors may ensure the in

164 ronal cells due to changes in ion gradients (HCO3(-) and/or Cl(-)) that occur in the body following c

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

166 that the main requirement for secreting high HCO3(-) concentrations is to minimize the secretion of C

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

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

169 used enteroid intracellular acidification in HCO3(-)-free buffer.

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

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

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

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

174 anions of environmental concerns, including HCO3(-), HCO2(-), CH3CO2(-), SO4(2-), NO3(-), NO2(-), Br

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

176 We found that increasing HCO3(-) levels enhances action potential (AP) generation

177 )-2 pathway, whereas FFA2 activation induces HCO3(-) secretion via muscarinic and 5-HT4 receptor acti

178 exposure causes a 13% increase of intestinal HCO3(-) secretion that the animal does not appear to reg

179 Conversely, decreasing intracellular HCO3(-) leads to attenuation of AP firing.

180 nge of extracellular Cl(-) for intracellular HCO3(-) .

181 nge of extracellular Cl(-) for intracellular HCO3(-) .

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

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

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

185 unction at least in part by altering luminal HCO3(-) and ATP concentrations.

186 (-) cotransporter (NBC) NBCe1-B, and luminal HCO3(-) exit mediated by cystic fibrosis transmembrane c

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

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

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

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

191 ippocampal neurons, not astrocytes; mediates HCO3(-) efflux) enhances intracellular pH (pHi ) recover

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

193 ted in flow-through columns at pH 7.9 (10 mM HCO3(-)) and pH 3.4 (10 mM CH3COOH) to evaluate the effe

194 is the main requirement for secreting 140 mm HCO3(-) .

195 The model was readily able to secrete 140 mm HCO3(-) .

196 ons, the model secreted approximately 140 mm HCO3(-) at a rate of approximately 3 nl min(-1) mm(-2) ,

197 Interestingly, 3 mM HCO3(-) concentration treatment induced more significant

198 Adding 0.1-3 mm HCO3(-) to an O2-gassed, HEPES-buffered saline solution

199 oocytes could be activated by adding 1-3 mm HCO3(-), and even by residual HCO3(-) in a nominally CO2

200 ular H(+) concentration with a Km of 0.65 mm HCO3(-) in WT astrocytes, but slowly raised [H(+)]i in N

201 S was partially inhibited by monocarboxylate/HCO3(-) exchanger inhibition without affecting GLP-2 rel

202 ing the activities of the basolateral Na(+) -HCO3(-) cotransporter (NBC1) and apical Cl(-) /HCO3(-) e

203 retain a close-to-normal per molecule Na(+) /HCO3(-) cotransport activity in Xenopus oocytes, suggest

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

205 1 molecules exhibit apparently normal Na(+) /HCO3(-) cotransport activity but that Q913R is associate

206 Activation of Na(+),HCO3(-) cotransport in vascular smooth muscle cells (VSM

207 nd functional interactions between the Na(+),HCO3(-) cotransporter NBCn1 (slc4a7) and the Ca(2+)/calm

208 sion by Na(+)/H(+) exchange (NHE1) and Na(+)-HCO3(-) co-transport (NBC) is essential for maintaining

209 In the electrogenic Na(+)-HCO3(-) cotransporter NBCe1-A, EL-3 is the largest extra

210 basolateral HCO3(-) entry through the Na(+)-HCO3(-) cotransporter (NBC) NBCe1-B, and luminal HCO3(-)

211 tem astrocytes acidification activates Na(+)/HCO3(-) cotransport, which brings Na(+) inside the cell.

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

213 nteroid model showed that electrogenic Na(+)/HCO3(-) cotransporter 1 might be a target in the intesti

214 conductance regulator and electrogenic Na(+)/HCO3(-) cotransporter 1.

215 of mice deficient in the electrogenic Na(+)/HCO3(-) cotransporter NBCe1.

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

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

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

219 try, markedly reduced by inhibition of Na(+)/HCO3(-) cotransport (NBC) or Na(+)/Ca(2+) exchange (NCX)

220 ed by compensatory upregulation of the Na(+)/HCO3(-) cotransporter NBCn1.

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

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

223 Na-HCO3 cotransport (NBC) regulates intracellular pH (pHi)

224 gulates HCO3-dependent HOE694-insensitive Na-HCO3 cotransport and plays a critical role in pHi regula

225 codes electrogenic, amiloride-insensitive Na-HCO3 cotransport in proximal colon.

226 ply hypoxic neighbors with acid-neutralizing HCO3(-) ions.

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

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

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

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

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

232 bromide; however, elevated concentrations of HCO3(-) often altered transformation rates due to format

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

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

235 influence of the kinetics of dissociation of HCO3(-) formed after the C-H activation step in actually

236 the potential to extrude CO2 in the form of HCO3(-), impairs O2/CO2 balance in cardiac myocytes.

237 lation of the CCM based on the inhibition of HCO3(-) transporters by moderate to high levels of CO2.

238 lbenedisulfonic acid (DIDS), an inhibitor of HCO3(-) uptake, had no effect on cytoplasmic [H(+)] in t

239 ported earlier are attributed to the loss of HCO3(-) during the titrations (pH 6.5, stirred under arg

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

241 The mechanisms of HCO3(-)-independent intracellular pH (pHi) regulation we

242 fficient, transporting only two molecules of HCO3(-) per molecule of CO2 fixed.

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

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

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

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

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

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

249 supporting acid extrusion by H(+) efflux or HCO3(-) influx, nor for maintaining intracellular pH (pH

250 d to low CO2 rather than to changes in pH or HCO3(-), and the rates of eCA activity are nearly optima

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

252 main of the NBC that may be present in other HCO3(-) transporters and thus in the regulation of epith

253 ify the mechanism responsible for pancreatic HCO3(-) secretion, a vital process that prevents the for

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

255 through an unprecedented increase in plasma [HCO3(-)] (>75 mM) in exchange for [Cl(-)].

256 CO3; (ii) monodeprotonated cryptand with PPN[HCO3]; and (iii) free cryptand with TBA[OH] and atmosphe

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

258 ron transfer and the upshift in the Em of QA HCO3(-)-depleted PSII also showed diminished light-induc

259 We also conclude that NBCn1C/D regulates HCO3-dependent HOE694-insensitive Na-HCO3 cotransport an

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

261 adding 1-3 mm HCO3(-), and even by residual HCO3(-) in a nominally CO2/HCO3(-)-free saline solution.

262 (-), but this process requires a restorative HCO3(-) flux.

263 SCFA/HCO3(-) exchange also appears to be present in the duode

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

265 lular Cl(-) and resulted in a lower secreted HCO3(-) concentration, as is characteristic of those spe

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

267 0 had little impact upon either the secreted HCO3(-) concentration or the volume flow.

268 mulation and thereby maximizing the secreted HCO3(-) concentration.

269 e for MCT-driven H(+) secretion by secreting HCO3(-), a process which is dysfunctional in CF airway e

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

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

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

273 Results indicate that HCO3(-) treatment responsive metabolomic changes depend

274 creased upon DIDS treatment, indicating that HCO3(-) ions are taken up actively by peripheral cells a

275 These findings mean that HCO3(-) binds less strongly when QA(-*) is present.

276 We show that HCO3(-) interferes with Kv7/KCNQ channel activation by p

277 The HCO3- metabolon hypothesis predicts that cytosolic carbo

278 s, an observation that probably explains the HCO3(-) transport deficit in the individual.

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

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

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

282 responsive metabolomic changes depend on the HCO3(-) concentration, time of treatment, and light/dark

283 Raising the HCO3(-) /Cl(-) permeability ratio of CFTR from 0.4 to 1.

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

285 space promotes the hydrolysis of CO3(2-) to HCO3(-) and OH(-).

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

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

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

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

290 ssociated with increased CO2 use relative to HCO3(-).

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

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

293 ments, which show the oxyanion binding trend HCO3(-) > H2PO4(-) > HSO4(-), whereas no binding with NO

294 Light-induced QA(-*) formation triggered HCO3(-) loss as manifest by the slowed electron transfer

295 hey have a simple CCM composed of one or two HCO3(-) pumps and a carboxysome, but its functionality h

296 but that Q913R is associated with an unusual HCO3(-) independent anion-leak.

297 These species (and one unable to use HCO3(-)) increased in abundance with elevated CO2 wherea

298 Using HCO3(-) measurements from the damselfish, the reversal p

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

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

301 o determine the transport mechanism by which HCO3(-) ions are secreted at concentrations in excess of

302 e, and suggests it is mainly associated with HCO3(-) transport in very low CO2 concentrations, condit

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