ライフサイエンスコーパス: HCO

1 ays important roles in heme-copper oxidases (HCO).

2 ipotent stem cell-derived cardiac organoids (hCOs).

3 emistry carried out in heme-copper oxidases (HCOs).

4 roton-pumping heme-copper oxygen reductases (HCOs).

5 d direct hPSC-derived gut tube cultures into HCOs.

6 L = mu(2):eta(1)-OH(-) (17) and mu(2):eta(2)-HCO(2)(-) (18) and -CN(-) (19).

7 hyl formate and CO(2) to form unidentate L = HCO(2)(-) (5) and HCO(3)(-) (6) products.

8 h direct mass-spectrometric detection of the HCO(2)(-) product.

9 nversion of C(n) fatty aldehydes to formate (HCO(2)(-)) and the corresponding C(n-1) alk(a/e)nes.

10 nic-organic framework material: Ce(C(2)O(4))(HCO(2)), 1.

11 ormylation of (-)-menthone (11) with LDA and HCO(2)CH(2)CF(3) avoids loss of configurational integrit

12 uring formylation of menthone with NaOMe and HCO(2)Et led, by a similar strategy, to syntheses of 7-e

13 DMN and DEN were also oxidized to HCO(2)H and CH(3)CO(2)H, respectively.

14 be cleaved efficiently when treated with 10% HCO(2)H for 0.5 h.

15 These same features (no lag phase for HCO(2)H formation and a lack of equilibration in pulse-c

16 (3)Cl(2) in combination with (i)Pr(2)NEt and HCO(2)H or Hantzsch ester as the hydrogen atom donor.

17 50 mM Na(2)S(2)O(4), 2% HOCH(2)CH(2)SH, 10% HCO(2)H, 95% CF(3)CO(2)H, or irradiation at 365 nm.

18 dation of C(3)H(6)(OCO(2)Li)(2), Li(2)CO(3), HCO(2)Li, CH(3)CO(2)Li accompanied by CO(2) and H(2)O ev

19 Li(2)CO(3), HCO(2)Li, CH(3)CO(2)Li, and C(3)H(6)(OCO(2)Li)(2) accumu

20 mation of C(3)H(6)(OCO(2)Li)(2), Li(2)CO(3), HCO(2)Li, CH(3)CO(2)Li, CO(2), and H(2)O at the cathode,

21 hode on discharge are Li(2)O(2), Li(2)CO(3), HCO(2)Li, CH(3)CO(2)Li, NO, H(2)O, and CO(2).

22 atalyzes the reversible hydration of CO 2 to HCO 3 (-).

23 rate and expression of SR, CFTR, and Cl(-) /HCO 3- AE2 and ablated secretin-stimulated biliary secre

24 iferation and increased SR, CFTR, and Cl(-) /HCO 3- AE2 expression.

25 nate anion exchanger 2 (cAMP-->CFTR-->Cl(-) /HCO 3- AE2) signaling that is elevated by biliary hyperp

26 nal role in the adaptive regulation of renal HCO(3(-)) secretion and salt reabsorption.

27 dissolve proteins in reagents, such as NH(4)HCO(3) and urea, with high efficiency and with an added

28 l types: the beta-intercalated cell secretes HCO(3) by an apical Cl:HCO(3) named pendrin and a basola

29 rename NCBE as the second electroneutral Na/HCO(3) cotransporter, NBCn2.

30 data are not consistent with Na(+)-driven Cl-HCO(3) exchange activity.

31 has an apical V-ATPase and a basolateral Cl:HCO(3) exchanger (kAE1).

32 One NCBT, the Na-driven Cl-HCO(3) exchanger (SLC4A8 or NDCBE), appears to be the ma

33 udy, we examined whether the Na(+)-driven Cl/HCO(3) exchanger NDCBE (Slc4a8) is also upregulated by s

34 se data demonstrate that the Na(+)-driven Cl/HCO(3) exchanger NDCBE is upregulated by chronic acid lo

35 unlike both human and squid Na(+)-driven Cl-HCO(3) exchangers, human NCBE does not normally couple t

36 calated cell secretes HCO(3) by an apical Cl:HCO(3) named pendrin and a basolateral vacuolar (V)-ATPa

37 rate that this differentiation proceeds from HCO(3) secreting to acid secreting phenotypes, a process

38 ns, that are conserved among electrogenic Na/HCO(3) transporters but are substituted with residues at

39 corresponding site of all electroneutral Na/HCO(3) transporters.

40 (2) to form unidentate L = HCO(2)(-) (5) and HCO(3)(-) (6) products.

41 nic anhydrase-like activities, the non-CO(2)/HCO(3)(-) (intrinsic) intracellular buffering power, or

42 g the cell to extracellular 1.5% CO(2)/10 mM HCO(3)(-) (pH 7.50) causes pH(i) to fall and pH(S) to ri

43 solved inorganic carbon (DIC) (DIC = CO(2) + HCO(3)(-) + CO(3)(-2)) availability with a carbon-concen

44 Inhibition of HCO(3)(-) absorption by LPS did not require CD14.

45 In contrast, inhibition of HCO(3)(-) absorption by lumen LPS was preserved in TLR2(

46 Inhibition of HCO(3)(-) absorption by TLR2-specific ligands was preser

47 S (ultrapure Escherichia coli K12) decreased HCO(3)(-) absorption in isolated, perfused MTALs from wi

48 These findings indicate that NGF inhibits HCO(3)(-) absorption in the medullary thick ascending li

49 hat the effect of basolateral LPS to inhibit HCO(3)(-) absorption in the MTAL through MyD88-dependent

50 e demonstrated that basolateral LPS inhibits HCO(3)(-) absorption in the renal medullary thick ascend

51 e1-A electrogenically cotransports Na(+) and HCO(3)(-) across the basolateral membrane of renal proxi

52 impaired CO(2)-induced stomatal closing and HCO(3)(-) activation of anion channels.

53 Ringer solutions with/without B(OH)(4)(-) or HCO(3)(-) after overexpressing or small interfering RNA

54 CAs) catalyze the hydration of CO(2) forming HCO(3)(-) and a proton, an important reaction for many p

55 n perfused CE in the presence and absence of HCO(3)(-) and acetazolamide (ACTZ) using tissue treated

56 he slow parallel reversible reaction between HCO(3)(-) and amine has also been determined for a numbe

57 ble adenylyl cyclase (dfsAC) is activated by HCO(3)(-) and can be inhibited by two structurally and m

58 n HEK293 cells, and relative conductances of HCO(3)(-) and Cl(-) were measured.

59 ission intensity of the dimer is quenched by HCO(3)(-) and H(2)PO(4)(-) but not by Cl(-) and NO(3)(-)

60 stic fibrosis transmembrane regulator, Cl(-)/HCO(3)(-) anion exchanger 2 and AC8, and responded to se

61 o the negatively charged CO(2) moiety of the HCO(3)(-) anion.

62 suggest that prestin can act as a weak Cl(-)/HCO(3)(-) antiporter and it is proposed that, in additio

63 For cells in the nominal absence of CO(2)/HCO(3)(-) at an extracellular pH of 7.40 (37 degrees C),

64 enable it to contribute to the secretion of HCO(3)(-) at high concentrations.

65 y absorbing and secreting protons (H(+)) and HCO(3)(-) at its gills.

66 ate (HCO(3)(-)) and a multitude of non-CO(2)/HCO(3)(-) buffers.

67 was significantly greater in the presence of HCO(3)(-) but was reduced by ACTZ.

68 upon acidification in the presence of CO(2)/HCO(3)(-) by 2',7'-bis(carboxyethyl)-5,6-carboxyfluoresc

69 e did not fully recover, showing lower blood HCO(3)(-) concentration and more alkaline urine.

70 CO(3) plus acetazolamide to increase luminal HCO(3)(-) concentration, [HCO(3)(-)], independent of pen

71 ward 1,1,1,2-TeCA depended upon NO(3)(-) and HCO(3)(-) concentration, with complete reactivity loss o

72 onductance regulator channel (Cftr)-mediated HCO(3)(-) conductance.

73 ne conductance regulator (CFTR), a Cl(-) and HCO(3)(-) conducting ion channel known to be associated

74 3)(-) in secretory glands is fueled by Na(+)/HCO(3)(-) cotransport mediated by basolateral solute car

75 The renal electrogenic Na(+)/HCO(3)(-) cotransporter (NBCe1-A) contributes to the bas

76 The electrogenic Na(+)/HCO(3)(-) cotransporter (NBCe1-A) transports sodium and

77 on 555 with a glutamate) produced decreasing HCO(3)(-) currents at more positive membrane voltages.

78 Here, a CO(2) and HCO(3)(-) diffusion-reaction model is developed to exami

79 This was mediated via membrane Cl(-)/HCO(3)(-) exchange (the AE1 gene product), irrespective

80 currents with only a modest affect on nCl(-)-HCO(3)(-) exchange activity.

81 ies in applying the model suggest that Cl(-)/HCO(3)(-) exchange also contributes to cAMP-stimulated s

82 enopus oocytes, both Slc26a9-mediated nCl(-)-HCO(3)(-) exchange and Cl(-) currents are almost fully i

83 es Cl(-) absorption mediated by apical Cl(-)/HCO(3)(-) exchange as well as generates more favorable e

84 Furthermore, silencing of CFTR altered Cl(-)/HCO(3)(-) exchange by Slc26a6, but had no effect on I(-)

85 Because apical HCO(3)(-) exchange depends on cystic fibrosis transmembr

86 h anion exchangers (AEs) to facilitate Cl(-)-HCO(3)(-) exchange in cotransfected cells.

87 ild-type mice, suggesting little or no Cl(-)-HCO(3)(-) exchange in the absence of AE3.

88 In murine duodenum, Dra Cl(-)/HCO(3)(-) exchange is concentrated in the lower crypt-vi

89 ier family 4 member 4 (NBCe1-B) and by Cl(-)/HCO(3)(-) exchange mediated by luminal solute carrier fa

90 Dra Cl(-)/HCO(3)(-) exchange should be considered in efforts to no

91 Apical membrane Cl(-)/HCO(3)(-) exchange was measured by microfluorometry of i

92 en under these conditions, in which no Cl(-)-HCO(3)(-) exchange was possible.

93 oses that basal secretion results from Cl(-)/HCO(3)(-) exchange, whereas cyclic adenosine monophospha

94 neurons, by facilitating AE3-mediated Cl(-)-HCO(3)(-) exchange.

95 recently showed that Slc26a9 has both nCl(-)-HCO(3)(-) exchanger and Cl(-) channel function.

96 The Cl(-)/HCO(3)(-) exchanger at the apical membrane of pancreatic

97 ctional evidence that Dra is the major Cl(-)/HCO(3)(-) exchanger coupled with Nhe3 for electroneutral

98 demonstrated that Dra is the dominant Cl(-)/HCO(3)(-) exchanger in the lower villous epithelium.

99 malian cells encodes a Na(+)-dependent Cl(-)/HCO(3)(-) exchanger in which four specific charged amino

100 ed mutations in ABTS-1, a Na(+)-driven Cl(-)-HCO(3)(-) exchanger that extrudes chloride from cells, l

101 ember 3), which functions as a coupled Cl(-)/HCO(3)(-) exchanger, cause CLD.

102 pithelial Na(+) channel, ENaC, and the Cl(-)/HCO(3)(-) exchanger, pendrin, mediate NaCl absorption wi

103 important of which is pendrin, a luminal Cl/HCO(3)(-) exchanger.

104 Our results show that Na(+)-driven Cl(-)-HCO(3)(-) exchangers function with KCCs in generating th

105 that NHE, probably in combination with Cl(-)-HCO(3)(-) exchangers, contributes to RVI in choroid plex

106 Of 2 candidate Cl(-)/HCO(3)(-) exchangers, studies of putative anion transpor

107 tosol, which is mitigated by Cl(-) entry and HCO(3)(-) exit.

108 ting CO(2) flux, HCO(3)(-) permeability, and HCO(3)(-) flux across the apical membrane.

109 Basolateral to apical (B-to-A) HCO(3)(-) flux was determined by measuring the pH of a w

110 changes in response to altering the CO(2) or HCO(3)(-) gradient across the apical membrane.

111 ne encodes an electroneutral Na(+)-dependent HCO(3)(-) importer for which the precise mode of action

112 Secretion of ductal fluid and HCO(3)(-) in secretory glands is fueled by Na(+)/HCO(3)(

113 th the maintenance of a low concentration of HCO(3)(-) in the cytoplasm.

114 r 10 microM PIP(2) (diC8) in the presence of HCO(3)(-) induced an inward current in 54% of macropatch

115 um is remarkable for its capacity to secrete HCO(3)(-) ions at concentrations as high as 140 mmol/l.

116 Binding of a water to the hydroxyl group of HCO(3)(-) is particularly disfavored and apparently does

117 es in which the interconversion of CO(2) and HCO(3)(-) is separate from intermolecular proton transfe

118 ic Ci affinity, especially at pH 9, at which HCO(3)(-) is the predominant form of available Ci.

119 is essential for maintaining systemic pH and HCO(3)(-) levels in the whole organism.

120 ransport Na(+) and are expected to move more HCO(3)(-) molecules/turnover were targeted by site-direc

121 It remains unclear whether CO(2), HCO(3)(-) or a combination activates downstream signalli

122 not significantly greater in the presence of HCO(3)(-) or reduced by ACTZ.

123 CFTR channels also appear to have sufficient HCO(3)(-) permeability to contribute directly to HCO(3)(

124 Apical CO(2) fluxes and HCO(3)(-) permeability were determined by measuring pH(i

125 ydrase IV (CAIV) in facilitating CO(2) flux, HCO(3)(-) permeability, and HCO(3)(-) flux across the ap

126 oplasmic N termini play roles in controlling HCO(3)(-) permeation.

127 Geochemical modeling indicated that HCO(3)(-) promoted dissolution accelerated brucite carbo

128 sis (pRTA; usually associated with defective HCO(3)(-) reabsorption in proximal tubule cells) and hyp

129 s to the basolateral step of transepithelial HCO(3)(-) reabsorption in proximal tubule epithelia, con

130 tubule showed that flow-dependent Na(+) and HCO(3)(-) reabsorption is due to a modulation of both NH

131 Dra activity contributes most basal HCO(3)(-) secretion and approximately 50% of cAMP-stimul

132 ar lumen strongly stimulated Cl(-)-dependent HCO(3)(-) secretion and electroneutral transepithelial N

133 R1 is involved in the adaptive regulation of HCO(3)(-) secretion and NaCl reabsorption in the CNT/CCD

134 ivotal role of IRBIT in epithelial fluid and HCO(3)(-) secretion and provide a molecular mechanism by

135 Fluid and HCO(3)(-) secretion are fundamental functions of epithel

136 f the key transporters involved in Cl(-) and HCO(3)(-) secretion have now been identified and charact

137 should be considered in efforts to normalize HCO(3)(-) secretion in duodenal disorders such as ulcer

138 Thus, because HCO(3)(-) secretion is defective in cystic fibrosis, muc

139 Without CFTR, airway epithelial HCO(3)(-) secretion is defective, the ASL pH falls and i

140 The current model of duodenal HCO(3)(-) secretion proposes that basal secretion result

141 down-regulated in adenoma (Dra) in duodenal HCO(3)(-) secretion was investigated using DraKO mice.

142 Duodenal HCO(3)(-) secretion was measured by pH stat in Ussing ch

143 cAMP-stimulated HCO(3)(-) secretion was reduced approximately 50%, but s

144 Basal HCO(3)(-) secretion was reduced approximately 55%-60% in

145 e and NaHCO(3) to increase pendrin-dependent HCO(3)(-) secretion within the connecting tubule and cor

146 Because pendrin mediates HCO(3)(-) secretion, we asked if increasing distal deliv

147 3)(-) permeability to contribute directly to HCO(3)(-) secretion.

148 ion and approximately 50% of cAMP-stimulated HCO(3)(-) secretion.

149 We conclude that Asp(555) plays a role in HCO(3)(-) selectivity.

150 tor mutants slowed but did not abolish CO(2)/HCO(3)(-) signalling, redefining the convergence point o

151 inside-out macropatches to a 5% CO(2)/33 mM HCO(3)(-) solution elicited a mean inward current of 14

152 The estimated Na(+):HCO(3)(-) stoichiometry was 1:2.

153 ate hydroxide formation limits reactivity in HCO(3)(-) suspensions.

154 n, we asked if increasing distal delivery of HCO(3)(-) through a pendrin-independent mechanism "rescu

155 E does not normally couple the net influx of HCO(3)(-) to a net efflux of Cl(-).

156 ting a role for LCIA in chloroplast envelope HCO(3)(-) transport and a role for LCIB in chloroplast C

157 (+) flux is facilitated by active transport, HCO(3)(-) transport and CA activity, disruption of which

158 llular pH (pH(i)) probe, pHluorin, to report HCO(3)(-) transport and to monitor the small pH(i) chang

159 Transcellular Cl(-) and HCO(3)(-) transport is a vital function of secretory epi

160 Over the past few years, that HCO(3)(-) transport is also defective in patients with c

161 t HLA3 is directly or indirectly involved in HCO(3)(-) transport, along with additional evidence supp

162 capacity through the presence of HCO(3)(-), HCO(3)(-) transport, NHE and CA activity.

163 hibited in the absence of serosal HCO(3)(-), HCO(3)(-) transport, or functional cystic fibrosis trans

164 I(-) secretion with minimal role in luminal HCO(3)(-) transport.

165 s of CFTR, an anion channel that facilitates HCO(3)(-) transport.

166 BC-type transporter HLA3 might function as a HCO(3)(-) transporter by evaluating the effect of pH on

167 NBCe1-A and AE1 both belong to the SLC4 HCO(3)(-) transporter family.

168 ition of HCO(3)(-) transporters, as a single HCO(3)(-) transporter increased modeled A(sat) by 9%.

169 that the best first step is the addition of HCO(3)(-) transporters, as a single HCO(3)(-) transporte

170 Subsequent removal of CO(2)/HCO(3)(-) with HEPES buffer caused rapid alkalinization

171 id/carbamate from the reactions of CO(2) and HCO(3)(-) with the amines are reported.

172 as able to exchange halides for SO(4)(2-) or HCO(3)(-) yet previous analyses of mammalian prestin hav

173 photon dissociation spectra are reported for HCO(3)(-)(H(2)O)(1-10) clusters in the spectral range of

174 among carbonic acid (H(2)CO(3))/bicarbonate (HCO(3)(-)) and a multitude of non-CO(2)/HCO(3)(-) buffer

175 rtial pressure of CO(2) (or concentration of HCO(3)(-)) and the electron flux through nitrogenase.

176 pon addition of an exogenous proton carrier (HCO(3)(-)) provides evidence that proton-transfer pathwa

177 astid envelope protein reported to transport HCO(3)(-)) resulted in dramatic decreases in growth, Ci

178 tically depends upon concurrent bicarbonate (HCO(3)(-)) secretion.

179 ification of inorganic carbon (Ci; CO(2) and HCO(3)(-)) transporters; however, specific knowledge of

180 senger cAMP in response to bicarbonate ions (HCO(3)(-)).

181 Thus, in the nominal absence of CO(2)/HCO(3)(-), acute hypoxia has little effect on steady-sta

182 When used together, NO(3)(-), HCO(3)(-), and DOM closely simulated the photolysis beha

183 r buffering capacity through the presence of HCO(3)(-), HCO(3)(-) transport, NHE and CA activity.

184 severely inhibited in the absence of serosal HCO(3)(-), HCO(3)(-) transport, or functional cystic fib

185 In the presence of CO(2)/HCO(3)(-), however, the outward current produced by D555

186 Second, NHE3-dependent absorption of HCO(3)(-), measured by single tubule perfusion, was redu

187 d for M(H(2)O)(35-37), with M = I(-), Cl(-), HCO(3)(-), OH(-), tetrabutyl-, tetrapropyl-, and tetrame

188 In the presence of extracellular HCO(3)(-), pH(i) recovered from an acid load 4 times fas

189 This was highly dependent on Na(+) and HCO(3)(-), suggesting a bicarbonate buffer mechanism inv

190 was significantly faster in the presence of HCO(3)(-), was greater on the apical surface, was reduce

191 Mean pH(i) was 7.25 in CO(2)/HCO(3)(-)-buffered medium and 7.15 in Hepes-buffered med

192 nit mutant caused increased acidification of HCO(3)(-)-containing culture medium compared with cells

193 ulfonic acid (DIDS)-sensitive and Na(+)- and HCO(3)(-)-dependent (36)Cl(-)-efflux during pH(i) recove

194 PIP(2)-induced currents were HCO(3)(-)-dependent and somewhat larger following more N

195 hibit unusual outward rectification in their HCO(3)(-)-dependent conductance and A(A799G) exhibits re

196 Intrinsic (non-CO(2)/HCO(3)(-)-dependent) buffering power, estimated in the i

197 The RVI was HCO(3)(-)-dependent, that is it was not observed in hepe

198 in HEK-293T cells expressing WT A subunit in HCO(3)(-)-free buffer.

199 efflux and/or pH(i) were measured in BCEC in HCO(3)(-)-free or HCO(3)(-)-rich Ringer, with and withou

200 ly rectifying current in the nominally CO(2)/HCO(3)(-)-free solution that was abolished by Cl(-) remo

201 = -60 mV) containing a low-Na(+), nominally HCO(3)(-)-free solution.

202 9V) expression is associated with an unusual HCO(3)(-)-independent conductance that, if associated wi

203 ysine, and neomycin all reduced the baseline HCO(3)(-)-induced inward currents by as much as 85%.

204 age-clamped oocytes stimulated NBC-mediated, HCO(3)(-)-induced outward currents by >100% for the B an

205 ly 70%) did not alter pHi responses to CO(2)/HCO(3)(-)-rich Ringer, Na(+)-free induced acidification,

206 ) were measured in BCEC in HCO(3)(-)-free or HCO(3)(-)-rich Ringer, with and without niflumic acid (M

207 wth of the GSBs, in the presence of CO(2) or HCO(3)(-).

208 mily which, like CFTR, are also permeable to HCO(3)(-).

209 nt decreased by 70% in the presence of CO(2)/HCO(3)(-).

210 sport, but does not transport B(OH)(4)(-) or HCO(3)(-).

211 and significantly reduced in the presence of HCO(3)(-).

212 ting the normal physiological buffers (24 mm HCO(3)(-)/5%CO(2)) with 10 mm HEPES similarly diminished

213 n CF than normal cells upon increased apical HCO(3)(-)/CO(2) exposure in part because of greater intr

214 racellular Cl(-), as H(2)DIDS and removal of HCO(3)(-)/CO(2) inhibited the negative E(gly) shift.

215 ic promoter) in response to increased apical HCO(3)(-)/CO(2) perfusion was higher in normal compared

216 rmeabilization and subsequent perfusion with HCO(3)(-)/CO(2) rescued CBF and FRET changes in CF cells

217 enylyl cyclase (sAC) that produces cAMP upon HCO(3)(-)/CO(2) stimulation to increase ciliary beat fre

218 se of gradual acidification after removal of HCO(3)(-)/CO(2) was inhibited by DIDS, acetazolamide, me

219 gradual alkalinization after the addition of HCO(3)(-)/CO(2) was inhibited by sodium-free conditions,

220 after stimulation with secretin, forskolin, HCO(3)(-)/CO(2), cholinergic agonists, and beta-adrenerg

221 akly basic aqueous buffer solutions of CO(2)/HCO(3)(-)/CO(3)(2-) or HPO(4)(2-)/PO(4)(3-).

222 Cd(2+) uptake is dependent on extracellular HCO(3)(-); 5) like ZIP8, ZIP14 transporters are localize

223 lpha(1,2)(-/-) mice exhibited a lower blood [HCO(3)(-)] and less Na(+) and K(+) retention than either

224 ion, at least in part by increasing luminal [HCO(3)(-)] and/or pH.

225 pendrin-null mice had lower urinary pH and [HCO(3)(-)] as well as lower renal ENaC abundance and fun

226 We explored whether [HCO(3)(-)] directly alters ENaC abundance and function i

227 Moreover, increasing [HCO(3)(-)] on the apical and basolateral side of Xenopus

228 rent and ENaC abundance rose with increased [HCO(3)(-)] on the apical or the basolateral side, indepe

229 ever, ENaC was more sensitive to changes in [HCO(3)(-)] on the basolateral side of the monolayer.

230 ctivated S-type anion currents, whereas low [HCO(3)(-)](i) at high [CO(2)] and [H(+)] did not.

231 ecretion stimulated by isohydric changes in [HCO(3)(-)](i) was cAMP-dependent and inhibited by sAC in

232 Elevated intracellular [HCO(3)(-)](i) with low [CO(2)] and [H(+)] activated S-ty

233 in, beta-adrenergic agonists, or changes in [HCO(3)(-)](i), respectively; and (3) AC gene expression

234 o increase luminal HCO(3)(-) concentration, [HCO(3)(-)], independent of pendrin.

235 l(-)], and an increase in blood [Na(+)] and [HCO(3)(-)].

236 tially neutralized by addition of NaHCO(3) ([HCO(3)(-)]/[Fe(3+)] < 3).

237 When [HCO(3)(-)]/[Fe(3+)] = 0.5 and 0.6 (initial pH approximat

238 When [HCO(3)(-)]/[Fe(3+)] = 1 (initial pH approximately 2.5),

239 In contrast, when [HCO(3)(-)]/[Fe(3+)] = 2 (initial pH approximately 2.7),

240 process involving apical membrane Na-H, SCFA-HCO(3), and Cl-SCFA exchanges.

241 lc26a4 functions as an electroneutral Cl-/I-/HCO(3)- exchanger.

242 D555E induced Na/HCO(3)-dependent pH recovery from a CO(2)-induced acidif

243 cells secrete acid, while beta cells secrete HCO(3).

244 3 times higher than those of their [NHC(H)][HCO(3)] counterparts 4.

245 mass spectrometry (TGA-MS) of most [NHC(H)][HCO(3)] precursors 4 showed a degradation profile in sta

246 The generation of NHCs from [NHC(H)][HCO(3)] precursors occurred via the formal loss of H(2)C

247 ee NHCs (2), while the synthesis of [NHC(H)][HCO(3)] precursors was directly achieved by anion metath

248 In addition, such [NHC(H)][HCO(3)] precursors were successfully investigated as pre

249 solution, NHC generation from both [NHC(H)][HCO(3)] salts and NHC-CO(2) adducts could be achieved at

250 The [NHC(H)][HCO(3)] salts were next shown to behave as masked NHCs,

251 contrast, upon CID, both [M + F](-) and [M + HCO(3)](-) precursor adducts gave structurally informati

252 nz)imidazolium hydrogen carbonates ([NHC(H)][HCO(3)], 4) were independently employed as organic preca

253 ium hydrogen carbonates, denoted as [NHC(H)][HCO(3)].

254 The duodenal epithelial brush border IAP-P2Y-HCO(3-) surface microclimate pH regulatory system effect

255 Regulation of Cl-/Cl- and Cl-/HCO(-)3 exchange by intracellular pH (pHi) or extracellu

256 g the extracellular buffer to 5% CO(2)/22 mM HCO(-)(3) also alkali shifted the phi(E)-pH(i) plot (upp

257 the plasma membrane, orthologs of the Cl(-)/HCO(-)(3) antiporters ae1 and pendrin, and two isoforms

258 id loading, whereas in the presence of CO(2)/HCO(-)(3), hypoxia stimulates the SITS-insensitive but i

259 can bind to the same nonheme site and confer HCO activity in a heme-nonheme biosynthetic model in myo

260 as been found to vary >500 mV, its impact on HCO activity remains poorly understood.

261 anism in which one H atom moves far from the HCO, almost to dissociation, and then returns to abstrac

262 or the two primary channel products, CH(3) + HCO and H + CH(2)CHO.

263 radical channel C(7)H(15)CHO --> C(7)H(15) + HCO and the molecular channel C(7)H(15)CHO --> C(6)H(12)

264 rt study among 1.25 million adults from 4 US HCOs and included persons with >/=1 clinical encounter d

265 ork suggests that fine-tuning E degrees ' in HCOs and other heme enzymes can modulate their substrate

266 Heme-copper oxidases (HCOs) are key enzymes in prokaryotes and eukaryotes for

267 essive PMF is known to limit the turnover of HCOs, but the molecular mechanism of this regulatory fee

268 Haem-copper oxidase (HCO) catalyses the natural reduction of oxygen to water

269 Heme-copper oxidases (HCOs) catalyze efficient reduction of oxygen to water in

270 (2)CHO, H + CH(3)CO, H(2) + CH(2)CO, CH(3) + HCO, CH(2) + CH(2)O) and branching ratios (BRs) are dete

271 hat cytochrome bo3 from Escherichia coli, an HCO closely homologous to Complex IV in human mitochondr

272 vious studies have established that C-family HCOs contain a single channel for uptake from the bacter

273 barrier imposed by fatty acid metabolism in hCOs could be rescued by simultaneous activation of both

274 The HCO couples with residual methoxy on the surface to yiel

275 educed oxy-F33Y-CuBMb, a functional model of HCOs engineered in myoglobin (Mb).

276 firm support for the tyrosyl radical in the HCO enzymatic mechanism.

277 In vitro, HCOs express colonic markers and contained colon-specifi

278 differentiation of human colonic organoids (HCOs) from hPSCs.

279 groups of burster instances but not for the HCO groups.

280 the oat fractions were 5-CH(3)-H(4)folate, 5-HCO-H(4)folate, and 5,10-CH(+)-H(4)folate.

281 insights to predict and demonstrate that the HCo(I) (dmpe)2 catalyst system, previously described for

282 Here, we use a biosynthetic model of HCO in myoglobin that selectively binds different non-ha

283 predominant transcellular pathway for Cl and HCO in porcine airway epithelia, and reduced anion perme

284 persons in private healthcare organizations (HCOs) in the United States.

285 Visualizations of HCO instances in a reduced space suggested that there mi

286 Next, transient HCO is made photochemically from formaldehyde.

287 Heme-copper oxidase (HCO) is a class of respiratory enzymes that use a heme-c

288 in the oxidase activity of Cu- and Fe-bound HCO mimics, respectively, as compared with Zn-bound mimi

289 existing database of half-center oscillator (HCO) model instances of the leech heartbeat CPG.

290 , we use a set of myoglobin-based functional HCO models to investigate the mechanism by which heme E

291 al translational energy distributions of H + HCO products from S(0) and T(1) are also reported as wel

292 copper and iron, in the heme-copper oxidase (HCO) superfamily is critical to the enzymatic activity o

293 are discussed in relation to O-O cleavage in HCOs, supporting a model in which a peroxo intermediate

294 r from the titration of metabolic acids with HCO taken up from the extracellular milieu.

295 Despite decades of research on HCOs, the role of non-haem metal and the reason for natu

296 ay enable cytochrome bo3, and possibly other HCOs, to maintain a suitable DeltapH under extreme redox

297 (/) epithelia showed markedly reduced Cl and HCO transport.

298 duction potential (E degrees ') of different HCO types has been found to vary >500 mV, its impact on

299 Following transplantation into mice, HCOs undergo morphogenesis and maturation to form tissue

300 P-dependent patterning of human hindgut into HCOs, which will be valuable for studying diseases inclu