ライフサイエンスコーパス: H ATPase

1 or and is an essential component of vacuolar H+ ATPase.

2 of H+ generated by the action of the V-type H+-ATPase.

3 or bafilomycin A1, an inhibitor of vacuolar H+-ATPase.

4 rate a requirement for a functional vacuolar H+-ATPase.

5 not only included these SNAREs but also the H+-ATPase.

6 ate the transport of H+ by a plasma membrane H+-ATPase.

7 re regulated by the activity of the vacuolar H+-ATPase.

8 to facilitating endosomal acidification by (H+)ATPases.

9 ion transport protein is the plasma membrane H(+)-ATPase.

10 sed by the inhibitors of lysosomal fusion or H(+)-ATPase.

11 cal gradient maintained by the vacuolar-type H(+)-ATPase.

12 mediates glucose-dependent activation of the H(+)-ATPase.

13 een the G3 subunit and the a4 subunit of the H(+)-ATPase.

14 owth via localization of the plasma membrane H(+)-ATPase.

15 the phytotoxin fusicoccin, in analogy to the H(+)-ATPase.

16 sequent activation of the plasmalemma Ca(2+)-H(+)-ATPase.

17 he latter identified by co-localization with H(+)-ATPase.

18 ted with the activity of the plasma membrane H(+)-ATPase.

19 on gradient generated by the plasma membrane H(+)-ATPase.

20 e intracellular localization and activity of H(+)-ATPases.

21 ilt-in counter ion, as has been proposed for H(+)-ATPases.

22 2 is conserved in all P-type plasma membrane H(+)-ATPases.

23 t bafilomycin A(1), an inhibitor of vacuolar H(+)-ATPases, abolished resensitization.

24 V1 H(+)-ATPase accumulation and activity on cell membranes

25 -bound (V(O)) complex of eukaryotic vacuolar H(+)-ATPase acidification machinery.

26 elongation growth and play a key role in PM H(+)-ATPase activation by inhibiting PP2C.D family prote

27 mulated slowly into puncta based on vacuolar H(+)-ATPase activity and dispersed rapidly upon dissipat

28 uoles from crd1Delta show decreased vacuolar H(+)-ATPase activity and proton pumping, which may contr

29 We find that SAUR19 stimulates PM H(+)-ATPase activity by promoting phosphorylation of the

30 eased distal nephron Na(+)/H(+) exchange and H(+)-ATPase activity in HiPro.

31 ntion ability are (1) an intrinsically lower H(+)-ATPase activity in the root apex, (2) greater salt-

32 t that under conditions in which increased V-H(+)-ATPase activity is required, a4 is regulated by tra

33 k/early endosome (TGN/EE)-localized vacuolar H(+)-ATPase activity nor the function of the brefeldin A

34 This may allow for the rapid adaptation of V-H(+)-ATPase activity to altered acid-base intake to achi

35 esulting from loss of Vma-dependent vacuolar H(+)-ATPase activity was not the cause of vma mutants' n

36 ediated by augmented Na(+)/H(+) exchange and H(+)-ATPase activity without augmented H(+),K(+)-ATPase

37 SAUR19 fusion proteins exhibit increased PM H(+)-ATPase activity, and the increased growth phenotype

38 AtGCN4 overexpression plants have reduced H(+)-ATPase activity, stomata that are less responsive t

39 Steady-state water exchange correlates with H(+)-ATPase activity.

40 ensitive increase in Na(+)/H(+) exchange and H(+)-ATPase activity.

41 atal apertures, and enhanced plasma membrane H(+)-ATPase activity.

42 ly through the inhibition of plasma membrane H(+)-ATPase activity.

43 PM H(+)-ATPases, and negatively regulate PM H(+)-ATPase activity.

44 s as a result of reduced Na+/H+ exchange and H+-ATPase activity as shown previously by the authors' l

45 l/mm per min; P < 0.05) as a result of lower H+-ATPase activity without differences in Na+/H+ exchang

46 omyces cerevisiae strain deficient in P-type H+-ATPase activity, providing genetic evidence for their

47 vidence was found of an intracellular P-type H+-ATPase activity.

48 lar H+/Ca2+ transport, and a 47% decrease in H+-ATPase activity.

49 d also displayed a 22% reduction in vacuolar H+-ATPase activity.

50 mulated aldosterone secretion that increases H+-ATPase activity.

51 g each of the 11 isoforms in the Arabidopsis H(+)-ATPase (AHA) gene family, we found that one member,

52 The plasma membrane H(+)-ATPase AHA1 is highly expressed in guard cells, and

53 interacts with the plasma membrane-localized H(+)-ATPases AHA1 and AHA2 and with the BRI-associated r

54 tes in related proteins, as found for the PM H(+)-ATPases AHA1, 2 and 3.

55 ent phosphorylation sites in plasma membrane H(+)-ATPases AHA1, AHA2, AHA3, and AHA4/11, five of whic

56 the conserved Vo domain of the vacuolar-type H(+)-ATPase and causes deacidification of the lysosomes

57 dies against the B subunit of the malarial V-H(+)-ATPase and erythrocyte (spectrins) and parasite (me

58 minimally affected by inhibition of vacuolar H(+)-ATPase and phosphatases but was markedly suppressed

59 racts with almost all components of vacuolar H(+)-ATPase and the Ragulator complex and with the small

60 with the plasma membrane anion channels and H(+)-ATPase and with the tonoplast TPK K(+) channel.

61 etween PIB-type Zn(2+)-ATPases and PIII-type H(+)-ATPases and at the same time show structural featur

62 hosphatases to activate plasma membrane (PM) H(+)-ATPases and promote cell expansion.

63 translocating V0a1 subunit of the vacuolar (H+)-ATPase and targeting to the lysosome.

64 ne is mediated by an interaction between the H+-ATPase and a specific t-SNARE.

65 ieved by Na+-HCO3- cotransport and also by a H+-ATPase and Na+/H+ exchanger operating together with c

66 absorption occurs by stimulation of apical K/H-ATPase and inhibition of K recycling across the apical

67 URs in vivo, can physically interact with PM H(+)-ATPases, and negatively regulate PM H(+)-ATPase act

68 , but only non-H3-truncated syntaxin-1 bound H+-ATPase, and synt-1ADeltaC expression by intact IMCD c

69 across type B intercalated cells (IC) via an H(+)-ATPase-and pendrin-dependent mechanism.

70 but it could not be inhibited by a lysosomal H+-ATPase antagonist, bafilomycin A1.

71 The inhibitors of both lysosomal fusion and H(+)-ATPase apparently attenuated FasL-caused pH decreas

72 Co-localization with calbindin-D28k, H(+)-ATPase, aquaporin-2, and pendrin showed that distal

73 pecifically activate a plant plasma membrane H(+)-ATPase (Arabidopsis thaliana AHA2) by a mechanism t

74 The vacuolar (H(+))-ATPases are ATP-dependent proton pumps that acidif

75 In addition, V-H(+)-ATPases are involved in HCO(3)(-) reabsorption in t

76 Eukaryotic P-type plasma membrane H(+)-ATPases are primary active transport systems that a

77 These results establish that T. brucei H+-ATPases are plasma membrane enzymes essential for par

78 V-ATPases (H(+) ATPases) are multisubunit, ATP-dependent proton pum

79 Vacuolar-type H(+)-ATPases (V-H(+)-ATPases) are the major H(+)-secreting protein in th

80 icrobial activity, and identify the vacuolar H(+)-ATPase as a potential target for host-directed ther

81 found to be a more general feature of human H(+)-ATPases, as similar G1/a1, G3/a1, and G1/a4 interac

82 ns in man, which is known to be required for H(+)-ATPase assembly and regulation.

83 adigm by showing coupling of NHA2 and V-type H(+)-ATPase at the plasma membrane of kidney-derived MDC

84 and autoinhibited Ca2+-ATPase, P2A and P2B), H+-ATPases (autoinhibited H+-ATPase, P3A), putative amin

85 Two isoforms of the H(+)-ATPase B-subunit exist in humans; we have shown tha

86 c HXK1 unconventional partners: the vacuolar H(+)-ATPase B1 (VHA-B1) and the 19S regulatory particle

87 Mutations in the vacuolar-type H(+)-ATPase B1 subunit gene ATP6V1B1 cause autosomal-rec

88 at recurrent stone formers with the vacuolar H(+)-ATPase B1 subunit p.E161K SNP exhibit a urinary aci

89 on is conserved between the murine and human H(+)-ATPase B1-subunits, and Atp6v1b1 maps to a region o

90 ibitors of Na+/H+ exchange (EIPA, 10(-5) M), H+-ATPase (bafilomycin, 10(-7) M), and H+-K+-ATPase (Sch

91 H+-ATPase exocytosis, it is likely that the H+-ATPase binds directly to the H3 domain of syntaxin-1

92 nce of the entire C-terminal domain to yeast H+-ATPase biogenesis and defines a sequence element of 2

93 pport that higher Na+/H+ exchange and higher H+-ATPase but not higher H+-K+-ATPase activity mediated

94 e ATPases, inhibition of the plasma membrane H(+)-ATPase by metal fluorides was partly reversible, an

95 Inhibition of vacuolar H(+)-ATPases by use of the specific inhibitor bafilomyci

96 reduces the activity of the plasma membrane H(+)-ATPase complex, thus reducing proton pump activity

97 V-H(+)-ATPases consist of at least 13 subunits, the functi

98 ictate its preference for host vacuolar-type H(+)-ATPase-containing membranes, indicating that its po

99 ng that the rapid H(+) efflux mediated by PM H(+) -ATPases could function upstream of the Ca(2+) flux

100 rect evidence that translocated lysosomal V1 H(+)-ATPase critically contributes to the formation of l

101 influx into vesicles driven by H(+)-PPase or H(+)-ATPase decreased exponentially as the intravesicula

102 oluble proteins, requires both vacuolar-type H(+) ATPase-dependent acidification as well as proton ef

103 regulated by the vacuole-specific Rab32a and H(+)-ATPase-dependent acidification.

104 cin A1, a specific inhibitor of the vacuolar H+-ATPase, did not alter the fusion protein mobility, al

105 In chromaffin cells, inhibition of H(+)-ATPase diverted CHGA from regulated to constitutive

106 ient (Deltamu(H+)) generated by the vacuolar H(+)-ATPase drives the accumulation of classical transmi

107 rized human gene, ATP6V0E2, encoding a novel H(+)-ATPase e-subunit designated e2.

108 p6v1b1(-/-) medulla and colocalizes with the H(+)ATPase E-subunit; however, the greater severity of m

109 al acidification by inhibiting vacuolar-type H(+)-ATPase enabled macrophages to elicit cytokine respo

110 ts in transporters (pmr1, pdr5, and vacuolar H+-ATPase), ergosterol biosynthesis (erg3, erg6, and erg

111 ese data indicate that plant plasma membrane H(+)-ATPases evolved as specific receptors for lysophosp

112 aC expression by intact IMCD cells inhibited H+-ATPase exocytosis, it is likely that the H+-ATPase bi

113 nt-1ADeltaC, but not synt-4DeltaC, inhibited H+-ATPase exocytosis.

114 isoforms of the Arabidopsis plasma membrane H(+)-ATPase family, have been isolated and characterized

115 function for a member of the plasma membrane H+-ATPase family.

116 d concanamycin A, inhibitors of the vacuolar H(+)-ATPase, for its dependence on Rag GTPase in suppres

117 Plasma membrane H(+)-ATPases form a subfamily of P-type ATPases responsi

118 selen or a yeast genetic strain with reduced H(+)-ATPase found reduced tau(i)(-1), notwithstanding hi

119 The specialized H(+)-ATPases found in the inner ear and acid-handling ce

120 weak homology to a component of the vacuolar H+-ATPase found in organisms as diverse as insect and co

121 The plasma membrane proton pump (H(+)-ATPase) found in plants and fungi is a P-type ATPas

122 This mouse model recapitulates the loss of H(+)-ATPase function seen in human disease and can provi

123 overexpression are dependent upon normal PM H(+)-ATPase function.

124 Vacuolar H(+)-ATPase functions as a vacuolar proton pump and is r

125 Previous studies showed that the H(+)-ATPase gene HA1 is expressed specifically in arbusc

126 T. brucei H+-ATPase genes were functionally characterized using do

127 In this study, yeast Pma1 H+-ATPase has served as a model to examine the role of t

128 nit (VPP-c, the 16-kDa subunit c of vacuolar H+-ATPase) has been identified as an interacting partner

129 eral of the 13 subunits comprising mammalian H(+)-ATPases have multiple alternative forms, encoded by

130 low pH by stretch-activated plasma membrane H(+)-ATPases, hence a substantial source of cytosolic Ca

131 es (i) apical proton secretion by a vacuolar H(+)-ATPase, (ii) actin cytoskeleton reorganization into

132 ncorporates into functional, plasma membrane H(+)ATPases in intercalated cells of the cortical collec

133 n auxin and plasma membrane H(+)-ATPases (PM H(+)-ATPases) in Arabidopsis thaliana.

134 usicoccin, a fungal toxin that activates the H(+)-ATPase, indicates that depolarization did not resul

135 '-diindolylmethane is a strong mitochondrial H(+)-ATPase inhibitor (IC(50) approximately 20 micromol/

136 , lysosomotropic agents such as the vacuolar H(+)-ATPase inhibitor bafilomycin A1 blocked the deliver

137 the NAADP antagonist Ned-19 or the vacuolar H(+)-ATPase inhibitor bafilomycin A1, indicating Ca(2+)

138 Studies using the H(+)-ATPase inhibitor ebselen or a yeast genetic strain

139 In the presence of a vacuolar H(+)-ATPase inhibitor, concanamycin A, oxidized proteins

140 itors (SM-19712, PD-069185) and the vacuolar H(+)ATPase inhibitor bafilomycin A(1), which prevent end

141 decrease after treatment with the selective H(+)ATPase inhibitor concanamycin.

142 Bafilomycin A1, the vacuolar H+-ATPase inhibitor, inhibited degradation of LDL and ca

143 ncentrations of the vacuolar H(+) -ATPase (V-H(+) -ATPase) inhibitor bafilomycin A1 , suggesting that

144 turally similar to more potent vacuolar-type H(+)-ATPase inhibitors, which all inhibited LGR5 interna

145 endent manner by treatment with the vacuolar H+-ATPase inhibitors concanamycin A and bafilomycin A1 o

146 Insertion of the H(+)-ATPase into nanodiscs has the potential to enable s

147 Proton pumping of the vacuolar-type H(+)-ATPase into the lumen of the central plant organell

148 that the exocytic insertion of proton pumps (H+-ATPase) into the apical membrane of rat IMCD cells, i

149 ansporter for lactate secretion and a V type H(+) -ATPase involved in cytosolic pH homeostasis.

150 The plasma membrane H(+)-ATPase is a P-type ATPase responsible for establish

151 tional malaria parasite-encoded vacuolar (V)-H(+)-ATPase is exported to the erythrocyte and localized

152 that although the pH(i) maintained by the V-H(+)-ATPase is important for maximum uptake of small met

153 A P-type H(+)-ATPase is the primary transporter that converts ATP

154 te bond of the phosphoenzyme intermediate of H(+)-ATPases is labile in the basal state, which may pro

155 However, a functional vacuolar (H+) ATPase is required for early steps of TeNT HC traffi

156 Interaction between the syntaxin-1A and H+-ATPase is important in the targeted exocytosis of the

157 The vacuolar H+-ATPase is inhibited with high specificity and potency

158 In Deltacwh36 cells, the vacuolar H+-ATPase is not assembled and there are reduced levels

159 uminal acidic pH, maintained by the vacuolar H+-ATPase, is one of the critical factors for secretory

160 Arabidopsis thaliana P-type plasma membrane H(+)-ATPase isoform 2 (AHA2) consists of an aspartate re

161 psis (Arabidopsis thaliana) plant expressing H(+)-ATPase isoform 2 (AHA2) that is translationally fus

162 of the Arabidopsis thaliana plasma membrane H(+)-ATPase isoform 2 into soluble nanoscale lipid bilay

163 Auto-inhibited H+-ATPase isoform 10 (AHA10) is expressed primarily in d

164 These results suggest that H(+)-ATPase, known to transfer cytosolic H(+) into prefu

165 cells is regulated by exocytic insertion of H+-ATPase-laden vesicles into the apical membrane.

166 The multisubunit vacuolar-type H(+)ATPases mediate acidification of various intracellul

167 vacuolar-type proton-translocating ATPases (H(+)-ATPases) mediate the acidification of various intra

168 INSENSITIVE1 (COI1) mutant coi1-1 and the PM H(+) -ATPase mutants aha1-6 and aha1-7, using a non-inva

169 ductance of the slac1 Cl(-) channel and ost2 H(+)-ATPase mutants, which we verified experimentally.

170 was impaired by vanadate pre-treatment or PM H(+) -ATPase mutation, suggesting that the rapid H(+) ef

171 The activity of a Ca2+/H+-ATPase named TgA1 may be important for the accumulati

172 The RAVE complex (regulator of the H(+)-ATPase of vacuolar and endosomal membranes) is requ

173 1 genes (abbreviated as AHA, for Arabidopsis H(+)-ATPase), of which AHA1 and AHA2 are the two most pr

174 shed across the tonoplast by either vacuolar H(+)-ATPase or vacuolar H(+)-pyrophosphatase.

175 Proton translocation by the vacuolar (H+)-ATPase (or V-ATPase) has been shown by mutagenesis t

176 The vacuolar (H+)-ATPase (or V-ATPase) is an ATP-dependent proton pump

177 ase, P2A and P2B), H+-ATPases (autoinhibited H+-ATPase, P3A), putative aminophospholipid ATPases (ALA

178 atory mechanism by which SAUR19 modulates PM H(+)-ATPase phosphorylation status.

179 Subunit a of the vacuolar H(+)-ATPases plays an important role in proton transport

180 , these findings indicate that the vacuolar (H+ ATPase plays a specific role in early sorting events

181 istic link between auxin and plasma membrane H(+)-ATPases (PM H(+)-ATPases) in Arabidopsis thaliana.

182 n the 1970s, auxin activates plasma membrane H(+)-ATPases (PM H(+)-ATPases) to facilitate cell expans

183 lgi compartment, whereas the plasma membrane H(+) ATPase Pma1, which is transported in the same class

184 roteins tagged to the C terminus (CT) of the H(+)-ATPase PMA2.

185 mical localization of the plasmalemma Ca(2+)-H(+)-ATPase (PMCA pump) revealed intense labelling withi

186 inant wild-type HvCDPK1 activated the V-type H(+)-ATPase present in isolated aleurone vacuoles.

187 etch-activated Ca(2+) channels and activates H(+) -ATPase proton pump efflux that dissociates peripla

188 onsistent with the augmented plasma membrane H(+)-ATPase proton transport values, and ATP hydrolytic

189 nt, consistent with a role for the vacuolar (H+)-ATPase proton pump in copper assembly of laccase in

190 n exchanger 1, and different subunits of the H+-ATPase proton pump.

191 present study hypothesized that lysosomal V1 H(+)-ATPase provides a hospitable acid microenvironment

192 scopy of prokaryotic and eukaryotic vacuolar H(+)-ATPases, respectively, clarifying their orientation

193 ng, then the activity of the plasma membrane H(+)-ATPase should be reduced at this time.

194 Interestingly, the inhibition of vacuolar H(+)-ATPases significantly increased the levels of TMEM1

195 vacuole/lysosome, and contained the vacuolar H(+)-ATPase subunit a3, alias TCIRG1, a known antimycoba

196 slocalization of the Golgi-enriched vacuolar H(+)-ATPase subunit isoform a2.

197 that mutants and morphants involving other V-H(+)-ATPase subunits also demonstrated developmental bil

198 a9), carbonic anhydrase isoforms, and V-type H(+)-ATPase subunits in pendrin-positive intercalated ce

199 H+-ATPase (subunits E, a, and c) bound to syntaxin-1A an

200 pH homeostasis is affected by inhibitors of H+-ATPases, suggesting a major role for these pumps in t

201 gesting that either TgVP1 or the T. gondii V-H(+) -ATPase (TgVATPase) are sufficient to support CPL p

202 PH4, we silenced PH5, a tonoplast-localized H(+) -ATPase that maintains vacuolar pH homeostasis.

203 in A1, a specific inhibitor of vacuolar-type H(+)-ATPase that blocks lysosomal degradation, prevented

204 sa cells were also found to possess a V-type H(+)-ATPase that drives partial acidosis recovery when N

205 yldiphyllin, a selective blocker of vacuolar H(+)-ATPase that increases the pH of intracellular vesic

206 Mutations in the B1-subunit of the apical H(+)ATPase that secretes protons in the distal nephron c

207 ystal structure of the plant plasma membrane H(+)-ATPase, this residue is located in the putative lig

208 specific interaction with the V1A subunit of H(+) ATPase; this interaction may be important both for

209 tio of apical plasma membrane to cytoplasmic H(+)-ATPase three-fold.

210 erminal regulatory domain of plasma membrane H(+)-ATPase to protein kinase action.

211 n-mediated expansion growth by activating PM H(+)-ATPases to facilitate apoplast acidification and me

212 to nitro-drug action, plasma membrane P-type H(+)-ATPases to pentamidine action, and trypanothione an

213 n activates plasma membrane H(+)-ATPases (PM H(+)-ATPases) to facilitate cell expansion by both loose

214 ery of the K(+) channel, but not of the PMA2 H(+)-ATPase, to the plasma membrane is suppressed by Sp2

215 BE, bis-enoxacin; V-ATPase, vacuolar H(+)-ATPase; TRAP, tartrate-resistant acid phosphatase;

216 Accordingly, inhibition of the vacuolar (H+) ATPase under conditions that completely abolish the

217 tissue-restricted a4 and B1 subunits of the H(+)-ATPase underlie this syndrome.

218 esence of low concentrations of the vacuolar H(+) -ATPase (V-H(+) -ATPase) inhibitor bafilomycin A1 ,

219 The vacuolar H(+) ATPase (V-ATPase) is a complex multisubunit machine

220 The vacuolar H(+) ATPases (V-ATPases) are ATP-driven proton pumps tha

221 Defects of the V-type proton (H(+)) ATPase (V-ATPase) impair acidification and intrace

222 one of which is the d2 isoform of vacuolar (H(+)) ATPase (v-ATPase) V(0) domain (Atp6v0d2).

223 The vacuolar (H(+))-ATPase (V-ATPase) is crucial for maintenance of th

224 of extrinsic V(1) subunits of the vacuolar (H(+))-ATPase (V-ATPase) to rat liver endosomes.

225 in alterations in vacuolar pH and vacuolar (H(+))-ATPase (V-ATPase)-dependent H(+) transport and ATP

226 The vacuolar (H(+))-ATPases (V-ATPases) are a family of ATP-driven pro

227 The vacuolar (H(+))-ATPases (V-ATPases) are ATP-driven proton pumps co

228 e show that Rab5a colocalizes with vacuolar (H(+))-ATPases (V-ATPases) on transport vesicles.

229 The integral V(0) domain of the vacuolar (H(+))-ATPases (V-ATPases) provides the pathway by which

230 highly specific inhibitors of the vacuolar (H(+))-ATPases (V-ATPases), typically inhibiting at nanom

231 Plasma membrane vacuolar H(+)-ATPase (V-ATPase) activity of tumor cells is a majo

232 ue to a modulation of both NHE3 and vacuolar H(+)-ATPase (V-ATPase) activity.

233 The vacuolar H(+)-ATPase (V-ATPase) along with ion channels and trans

234 ls (ICs) express the proton pumping vacuolar H(+)-ATPase (V-ATPase) and are extensively involved in a

235 teraction between the B2 subunit of vacuolar H(+)-ATPase (V-ATPase) and microfilaments is required fo

236 ts binding between the B-subunit of vacuolar H(+)-ATPase (V-ATPase) and microfilaments, and also betw

237 Vacuolar H(+)-ATPase (V-ATPase) binds microfilaments, and that in

238 The function of the vacuolar H(+)-ATPase (V-ATPase) enzyme complex is to acidify orga

239 s to the V(o) domain of the conserved V-type H(+)-ATPase (V-ATPase) found on acidic compartments such

240 lized on the mechanisms suppressing vacuolar H(+)-ATPase (V-ATPase) in pfk2Delta to gain new knowledg

241 The vacuolar H(+)-ATPase (V-ATPase) is a major contributor to luminal

242 The yeast Saccharomyces cerevisiae vacuolar H(+)-ATPase (V-ATPase) is a multisubunit complex respons

243 Eukaryotic vacuolar H(+)-ATPase (V-ATPase) is a multisubunit enzyme complex

244 The vacuolar H(+)-ATPase (V-ATPase) is a rotary motor enzyme that aci

245 The vacuolar H(+)-ATPase (V-ATPase) is an ATP-dependent proton pump c

246 The vacuolar H(+)-ATPase (V-ATPase) is an ATP-driven proton pump esse

247 -dependent localization of the vacuolar-type H(+)-ATPase (V-ATPase) mediate the impact of the lipid p

248 olin plays a key role in regulating vacuolar H(+)-ATPase (V-ATPase) recycling.

249 ein and an accessory subunit of the vacuolar H(+)-ATPase (V-ATPase) that may also function within the

250 endent interaction of the endosomal vacuolar H(+)-ATPase (V-ATPase) with cytohesin-2, a GDP/GTP excha

251 The vacuolar H(+)-ATPase (V-ATPase), a multisubunit proton pump, has

252 is restoration is activation of the vacuolar H(+)-ATPase (V-ATPase), a proton pump that acidifies lys

253 fus-1 encodes the e subunit of the vacuolar H(+)-ATPase (V-ATPase), and loss of other V-ATPase subun

254 over, ZnT2 directly interacted with vacuolar H(+)-ATPase (V-ATPase), and ZnT2 deletion impaired vesic

255 otent and specific inhibitor of the vacuolar H(+)-ATPase (V-ATPase), binding to the V(0) membrane dom

256 The screen also revealed the vacuolar H(+)-ATPase (V-ATPase), which acidifies the lysosome-lik

257 afilomycin-A1, an inhibitor of vacuolar-type H(+)-ATPase (v-ATPase), which actively pumps H(+) into t

258 of proton pumping activity of vacuolar-type H(+)-ATPase (v-ATPase).

259 -stimulated reassembly of the yeast vacuolar H(+)-ATPase (V-ATPase).

260 )-pyrophosphatase (V-PPase) and the vacuolar H(+)-ATPase (V-ATPase).

261 rane fusion and have implicated the vacuolar H(+)-ATPase (V-ATPase).

262 atp6ap2 encodes a subunit of the vacuolar H(+)-ATPase (V-H(+)-ATPase), which modulates pH in intra

263 alated cells (A-ICs), which contain vacuolar H(+)-ATPase (V-type ATPase)-rich vesicles that fuse with

264 Vacuolar H(+)-ATPases (V-ATPases) acidify intracellular organelle

265 Vacuolar H(+)-ATPases (V-ATPases) are a family of highly conserve

266 Vacuolar H(+)-ATPases (V-ATPases) drive organelle acidification i

267 Vacuolar-type H(+)-ATPases (V-H(+)-ATPases) are the major H(+)-secreti

268 iport and, like cax1 mutants, reduced V-type H+ -ATPase (V-ATPase) activity.

269 tify that genetic disruption of the Vacuolar H+ ATPase (V-ATPase), the key proton pump for endo-lysos

270 The vacuolar (H+) ATPases (V-ATPases) are large, multimeric proton pum

271 The vacuolar (H+)-ATPases (V-ATPases) are ATP-dependent proton pumps t

272 The vacuolar (H+)-ATPases (V-ATPases) are multisubunit complexes respo

273 Vacuolar (H+)-ATPases (V-ATPases) are ubiquitous, ATP-driven proto

274 f binding between the B2-subunit of vacuolar H+-ATPase (V-ATPase) and microfilaments.

275 The effect of selective vacuolar H+-ATPase (V-ATPase) inhibitor bafilomycin A1 on the pH

276 The Saccharomyces cerevisiae vacuolar H+-ATPase (V-ATPase) is a multisubunit complex composed

277 The vacuolar H+-ATPase (V-ATPase) is an ATP-driven rotary molecular m

278 eripheral cytoplasmic domain of the vacuolar H+-ATPase (V-ATPase) were present in a SOS2-containing p

279 ely associated with a multi-subunit vacuolar H+-ATPase (V-ATPase).

280 Vacuolar H+-ATPases (V-ATPases) are a family of ATP-driven proton

281 lly occurring class of inhibitor of vacuolar H+-ATPases (V-ATPases) isolated from vacuolar membranes

282 luble adenylyl cyclase (sAC) to the vacuolar H+ATPase (V-ATPase).

283 olecules, such as the d2 isoform of vacuolar H(+)-ATPase V0 domain and the dendritic cell-specific tr

284 ding the algae abundantly expresses vacuolar H(+)-ATPase (VHA), which acidifies the symbiosome space

285 racellular compartments by the vacuolar-type H(+)-ATPases (VHA) is known to energize ion and metaboli

286 ated that a 16-kDa subunit (16K) of vacuolar H(+)-ATPase via one of its transmembrane domains, TMD4,

287 Loss of function of the vacuolar H(+)-ATPase (vma1) or a defect in the biosynthesis of th

288 ment, indicating that the activity of the PM H(+) -ATPase was reduced.

289 However, when activity of the vacuolar H+-ATPase was also inhibited, disulfide reduction decrea

290 lular trafficking regulates both pendrin and H(+)-ATPase, we hypothesized that AngII induces the subc

291 subcellular distributions of pendrin and the H(+)-ATPase were quantified using immunogold cytochemist

292 des a subunit of the vacuolar H(+)-ATPase (V-H(+)-ATPase), which modulates pH in intracellular compar

293 Yeast Pma1 H(+)-ATPase, which belongs to the P-type family of catio

294 Pma1 H(+)-ATPase, which is responsible for H(+)-dependent nut

295 acidification occurs by local activation of H(+)-ATPases, which in the context of gravity response i

296 to a differential targeting of the vacuolar (H+) ATPase, which is not present on moving TeNT HC compa

297 +) acts as an affinity cleavage agent of the H(+)-ATPase with backbone cleavage occurring in conserve

298 Blocking H(+) pumping by vesicular H(+)-ATPase (with folimycin or bafilomycin) suppresses s

299 id not change the distribution of pendrin or H(+)-ATPase within type B IC but within type A IC increa

300 role in the structure, site and function of H(+)-ATPases within the cell.