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

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

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

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

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

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

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

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

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

13 tem, and work as a component of the vacuolar H(+) -ATPase.

14 ugh a mechanism other than activation of the H(+) -ATPase.

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

16 2 is conserved in all P-type plasma membrane H(+)-ATPases.

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

18 e ACA8, noncanonical Galpha protein XLG2 and H(+) -ATPases.

19 g mutant analyses, we identified Arabidopsis H(+)-ATPase 1 (AHA1) as a SWP regulator.

20 h-30 mutant worms, and knockdown of vacuolar H+-ATPase 12 (vha-12) and its upstream regulator, nuclea

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

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

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

24 n rapid auxin effects, their relationship to H(+)-ATPase activation and other transporters, and depen

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

26 acid growth theory invoking plasma membrane H(+)-ATPase activation is still useful.

27 ting cell expansion via plasma membrane (PM) H(+)-ATPase activation, which facilitates cell wall loos

28 s in the involvement of PRR for the vacuolar H(+) -ATPase activity.

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

30 ulators of autophagy by controlling vacuolar H(+)-ATPase activity and mTOR signalling.

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

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

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

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

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

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

37 the hypothesis that wounding inhibits P-type H(+)-ATPase activity, leading to apoplastic alkalization

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

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

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

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

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

43 ation of cell expansion via modulation of PM H(+)-ATPase activity.

44 ins regulate protein phosphatases to control H(+)-ATPase activity.

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

46 We show that vacuolar H+-ATPase activity regulates sorting of O-glycosylated p

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

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

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

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

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

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

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

54 s), or constitutive activation of the P-type H(+)-ATPase AHA1.

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

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

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

58 Autoinhibited plasma membrane proton (H(+)) ATPases (AHAs) have been proposed to energize poll

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

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

61 vels of the V0a/V100 subunit of the vacuolar H(+)-ATPase and lysosomal pH.

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

63 , we show strong evidence that vacuolar-type H(+)-ATPase and plasma-accessible carbonic anhydrase in

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

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

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

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

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

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

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

71 phototropin photoreceptors, plasma membrane H(+)-ATPases, and multiple members of the 14-3-3 protein

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

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

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

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

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

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

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

79 We hypothesized that ClC-5 and H(+)-ATPase are functionally coupled during H(+)-ATPase-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 5 phenotypes, demonstrating that impaired PM H(+)-ATPase function is largely responsible for the redu

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

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

119 In contrast, a PM H(+)-ATPase gain-of-function mutation that results in a

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

121 One of these mutants, affecting the vacuolar H+-ATPase gene atp6ap1b, revealed specific requirements

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

123 onstrate that plant plasma membrane AHA-type H(+)-ATPase governs the gross repolarization process.

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

125 However, no defined H(+)-ATPases have been shown to modulate these electrica

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

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

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

129 ATASE (PP2C.D) activity, thereby trapping PM H(+)-ATPases in the phosphorylated, activated state, but

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 H(+)-ATPase are functionally coupled during H(+)-ATPase-mediated endosomal acidification, crucial fo

160 s, but shunt conductance facilitated further H(+)-ATPase-mediated endosomal acidification.

161 H(+)-ATPase-mediated proton pumping orchestrates cellula

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

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

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

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

166 The plasma membrane proton (H(+))-ATPases of plants generate steep electrochemical g

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

168 s intervention of the conserved regulator of H(+)-ATPase of vacuoles and endosomes (RAVE) complex, wh

169 1 genes (abbreviated as AHA, for Arabidopsis H(+)-ATPase), of which AHA1 and AHA2 are the two most pr

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

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

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

173 orresponding constitutively low levels of PM H(+)-ATPase phosphorylation.

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

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

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

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

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

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

180 raffic and activation of the plasma membrane H(+)-ATPase proteins already present at the membrane.

181 All evidence suggests that the population of H(+)-ATPase proteins at the plasma membrane reflects a b

182 nted SYP132 expression reduces the amount of H(+)-ATPase proteins at the plasma membrane.

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

184 eation, because inhibition of the macrophage H(+)-ATPase proton pump significantly decreased O(2) (*-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 nexpected and vital roles in auxin-regulated H(+)-ATPase traffic and associated functions at the plas

210 2 (Syntaxin of Plants132) as a key factor in H(+)-ATPase traffic and demonstrate its association with

211 Even so, H(+)-ATPase traffic, its relationship with SNAREs, and i

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

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

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

215 mps, H(+) -pyrophosphatase (V-PPase) and the H(+) -ATPase (V-ATPase), establish the proton gradient t

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

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

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

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

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

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

222 Vacuolar (H(+))-ATPase (V-ATPase) is fundamental in inflammatory c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

239 Here we report that vacuolar H(+)-ATPase (V-ATPase) inhibition differentially affects

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

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

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

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

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

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

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 The yeast vacuolar H(+)-ATPase (V-ATPase) of budding yeast (Saccharomyces c

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

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

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

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

262 The vacuolar H(+)-ATPase (V-ATPase; V(1)V(o)-ATPase) is an ATP-depend

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

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

265 The vacuolar-type H(+)-ATPases (V-ATPase) hydrolyze ATP to pump protons ac

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

267 d for full assembly and activity of vacuolar H(+)-ATPases (V-ATPases) containing the vacuolar a-subun

268 Vacuolar-type H(+)-ATPases (V-ATPases) contribute to pH regulation and

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

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

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

272 one particular subunit of the vacuolar-type H+ ATPase (V-ATPase), which is responsible for proper ly

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

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

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

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

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

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

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

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

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

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

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

284 he silica deposition vesicle (SDV) by V-type H(+) ATPase (VHA).

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

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 s, whereas activation of the plasma membrane H(+) -ATPase was not.

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

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

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

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

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

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

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

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

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

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.