ライフサイエンスコーパス: V-ATPase

1 V-ATPase activation through V1-V(o) assembly in response

2 V-ATPase activity is regulated by a unique mechanism ref

3 V-ATPase activity, vacuolar physiology, and in vitro vir

4 V-ATPase assembly increases upon amino acid starvation,

5 V-ATPase consists of soluble V1-ATPase and membrane-inte

6 V-ATPase subunit a of the Vo domain (Voa) is present as

7 V-ATPases (H(+) ATPases) are multisubunit, ATP-dependent

8 V-ATPases are conserved ATP-driven proton pumps that aci

9 V-ATPases are rotary molecular motors that generally fun

10 Our screen identified 14 V-ATPase subunits and all 4 adaptin-3 subunits, implicat

11 V-ATPase associated proteins and construct a V-ATPase interactome.

12 ngst the differentially expressed proteins a V-ATPase and a 14-3-3 protein were down-regulated.

13 nce pH assay showed that adenosine activates V-ATPase in isolated medullary ICs.

14 the endolysosomal lipid PI(3,5)P2 activates V-ATPases containing the vacuolar a-subunit isoform in S

15 regulated in the vma2Delta mutant, and acute V-ATPase inhibition with concanamycin A induced coordina

16 umulation in the kinetoplast continued after V-ATPase subunit depletion, acriflavine-induced kinetopl

17 ular pH homeostasis, and inactivation of all V-ATPase function has been shown to prevent infectivity

18 ferase (pap) in polyphosphate metabolism and V-ATPase in orthophosphate transport were absent from CA

19 1;2, H(+)-pyrophosphatase AVP1 [SlAVP1] and V-ATPase [SlVHA-A1]) supported a reduced capacity to acc

20 d that V-ATPase activity at steady state and V-ATPase reassembly after readdition of glucose to gluco

21 summary, our findings indicate that ZnT2 and V-ATPase interact and that this interaction critically m

22 ocalizes to the V1-Vo interface in assembled V-ATPase complexes and is important in regulated disasse

23 These results establish the Golgi-associated V-ATPase activity as the molecular link between actin an

24 components of the vacuolar H(+)-ATP ATPase (V-ATPase) known to be necessary for amino acid-induced a

25 The vacuolar H(+) ATPase (V-ATPase) is a complex multisubunit machine that regulat

26 Defects of the V-type proton (H(+)) ATPase (V-ATPase) impair acidification and intracellular traffic

27 Plasma membrane vacuolar H(+)-ATPase (V-ATPase) activity of tumor cells is a major factor in c

28 ess the proton pumping vacuolar H(+)-ATPase (V-ATPase) and are extensively involved in acid-base home

29 tween the B-subunit of vacuolar H(+)-ATPase (V-ATPase) and microfilaments, and also between osteoclas

30 domain of the conserved V-type H(+)-ATPase (V-ATPase) found on acidic compartments such as the yeast

31 mechanisms suppressing vacuolar H(+)-ATPase (V-ATPase) in pfk2Delta to gain new knowledge of the mech

32 Eukaryotic vacuolar H(+)-ATPase (V-ATPase) is a multisubunit enzyme complex that acidifie

33 The vacuolar H(+)-ATPase (V-ATPase) is a rotary motor enzyme that acidifies intrac

34 The vacuolar H(+)-ATPase (V-ATPase) is an ATP-dependent proton pump composed of a

35 The vacuolar H(+)-ATPase (V-ATPase) is an ATP-driven proton pump essential to the

36 calization of the vacuolar-type H(+)-ATPase (V-ATPase) mediate the impact of the lipid pathway on int

37 cessory subunit of the vacuolar H(+)-ATPase (V-ATPase) that may also function within the renin-angiot

38 ction of the endosomal vacuolar H(+)-ATPase (V-ATPase) with cytohesin-2, a GDP/GTP exchange factor (G

39 The vacuolar H(+)-ATPase (V-ATPase), a multisubunit proton pump, has come into foc

40 n is activation of the vacuolar H(+)-ATPase (V-ATPase), a proton pump that acidifies lysosomes.

41 rectly interacted with vacuolar H(+)-ATPase (V-ATPase), and ZnT2 deletion impaired vesicle biogenesis

42 eassembly of the yeast vacuolar H(+)-ATPase (V-ATPase).

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

44 nd have implicated the vacuolar H(+)-ATPase (V-ATPase).

45 enetic disruption of the Vacuolar H+ ATPase (V-ATPase), the key proton pump for endo-lysosomal acidif

46 ted with a multi-subunit vacuolar H+-ATPase (V-ATPase).

47 ver, it affects vacuolar-type proton ATPase (V-ATPase) activity, thereby compromising acidification o

48 cated in vacuolar H(+)-translocating ATPase (V-ATPase) assembly and activity.

49 Vacuolar proton-translocating ATPase (V-ATPase) is a central regulator of cellular pH homeosta

50 the vacuolar-type H(+)-translocating ATPase (V-ATPase), whose V1domain subunitsBandCbind actin.

51 inhibition of the H(+) vacuolar-type ATPase (V-ATPase) caused drastic cell swelling and depolarizatio

52 y of inhibitors of the vacuolar-type ATPase (V-ATPase), a heteromultimeric proton pump.

53 chnique, we have found that Vacuolar ATPase (V-ATPase) and the V-ATPase regulator Rabconnectin-3 are

54 dosomal trafficking through vacuolar ATPase (V-ATPase) inhibition enhanced caspase-8 activation in ap

55 The vacuolar ATPase (V-ATPase) is a 1MDa transmembrane proton pump that opera

56 The vacuolar ATPase (V-ATPase) is a multisubunit complex that carries out ATP

57 In cancer cells, vacuolar ATPase (V-ATPase), a multi-subunit enzyme, is expressed on the p

58 In cancer cells, vacuolar ATPase (V-ATPase), a multi-subunit enzyme, is expressed on the p

59 in vacuolar sorting and the vacuolar ATPase (V-ATPase).

60 Rag GTPases, Ragulator and vacuolar ATPase (V-ATPase).

61 (Vo) of the proton pumping vacuolar ATPase (V-ATPase, V1Vo-ATPase) from Saccharomyces cerevisiae was

62 s of rotary motors, namely vacuolar ATPases (V-ATPase), which are present at many of the multiple cel

63 The vacuolar H(+) ATPases (V-ATPases) are ATP-driven proton pumps that transport pr

64 The vacuolar (H(+))-ATPases (V-ATPases) are a family of ATP-driven proton pumps that

65 The vacuolar (H(+))-ATPases (V-ATPases) are ATP-driven proton pumps composed of a per

66 Vacuolar H(+)-ATPases (V-ATPases) acidify intracellular organelles and help to

67 Vacuolar H(+)-ATPases (V-ATPases) drive organelle acidification in all eukaryot

68 Vacuolar proton-translocating ATPases (V-ATPases) are highly conserved, ATP-driven proton pumps

69 Vacuolar-type ATPases (V-ATPases) are ATP-powered proton pumps involved in proc

70 Vacuolar ATPases (V-ATPases) are essential proton pumps that acidify the l

71 Because V-ATPase is fully assembled in pfk2Delta, and glycolysis

72 GLD-1, a translational repressor that blocks V-ATPase synthesis.

73 Amino acid-dependent changes in both V-ATPase assembly and activity are independent of PI3K a

74 body directed against the V5 epitope on both V-ATPase-mediated proton translocation across the plasma

75 with bafilomycin and EIPA suggest that both V-ATPases and Na(+)/H(+) exchangers are required for gly

76 Glucose depletion causes V-ATPase disassembly and its inactivation.

77 a model of the a subunit in the S. cerevisae V-ATPase that explains numerous biochemical studies of t

78 chanistic role of subunit F of S. cerevisiae V-ATPase, composed of 118 amino acids, the crystal struc

79 structure of F from Saccharomyces cerevisiae V-ATPase, showing an N-terminal egg shape, connected to

80 are thus needed to functionally characterize V-ATPase and to fully evaluate the therapeutic relevance

81 ATP6AP2 protein in XPDS brain may compromise V-ATPase function, as seen with siRNA knockdown in HEK29

82 th PI(3,5)P2 loss may arise from compromised V-ATPase stability and regulation.

83 is necessary for assembly of Vph1-containing V-ATPase complexes but not Stv1-containing complexes.

84 or efficient localization of Stv1-containing V-ATPases.

85 1, combined with defects in Stv1p-containing V-ATPases caused by the second mutation.

86 ependent assembly of active Stv1p-containing V-ATPases in vacuoles.

87 portant regulatory mechanism for controlling V-ATPase activity in vivo.

88 fy an important new stimulus for controlling V-ATPase assembly.

89 nase/mTOR pathway is involved in controlling V-ATPase assembly during dendritic cell maturation.

90 drug as well as a chemical tool to decipher V-ATPase-related cell death signaling.

91 rturbed the vacuolar structure and decreased V-ATPase activity and proton pumping in isolated vacuola

92 al epithelial cells, we found that decreased V-ATPase expression and activity in the intercalated cel

93 onsistent with its role in glucose-dependent V-ATPase assembly.

94 Deletion of Pfk2p alters glucose-dependent V-ATPase reassembly and vacuolar acidification.

95 the mechanisms underlying glucose-dependent V-ATPase regulation.

96 Independent strains with depleted V-ATPase or adaptin-3 subunits were isometamidium resist

97 Binding of disassembled V-ATPase (V1 domain) to its assembly factor RAVE (subuni

98 Consistent with kinetoplast dispensability, V-ATPase defective cells were oligomycin resistant, sugg

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

100 he T. thermophilus V/A-ATPase and eukaryotic V-ATPase from Saccharomyces cerevisiae allowed identific

101 us is similar in structure to the eukaryotic V-ATPase but has a simpler subunit composition and funct

102 QITPETQEK(35), which is unique in eukaryotic V-ATPases.

103 ly restores PHD catalytic activity following V-ATPase inhibition, revealing important links between t

104 Because Pfk1p and Pfk2p are necessary for V-ATPase proton transport at the vacuole in vivo, a role

105 nced, indicating that Pfk2p is necessary for V-ATPase regulation by glucose.

106 ofructokinase-1 subunits Pfk1p and Pfk2p for V-ATPase function.

107 Because ATP6ap2 is a subunit required for V-ATPase assembly of insulin granules, it has been repor

108 sides its canonical proton-pumping function, V-ATPase's membrane sector, Vo, has been implicated in n

109 Furthermore, V-ATPase dysfunction either results in or aggravates var

110 mino terminal (NT) domain of the yeast Golgi V-ATPase a-isoform Stv1.

111 rom amino acid-starved cells possess greater V-ATPase-dependent proton transport, indicating that ass

112 pH of the acidic region is dependent on H(+) V-ATPase, together with carbonic anhydrase and five furt

113 between WFS1 and the V1A subunit of the H(+) V-ATPase (proton pump) by co-immunoprecipitation in huma

114 ioenergizer, but can be replaced by the H(+) V-ATPase in renal intercalated cells.

115 ed by plasma membrane expression of the H(+) V-ATPase.

116 ly, of the V1 domain of the heteromultimeric V-ATPase complex.

117 es from a position near the membrane in holo V-ATPase to a position at the bottom of V1 near an open

118 A recent cryo-EM study of holo V-ATPase revealed three major conformations correspondin

119 ons to prevent unintended reassembly of holo V-ATPase when activity is not needed.

120 oach is used as a new viewpoint to study how V-ATPase can be modulated for therapeutic purposes.

121 However, V-ATPase-deficient lysosomes remain competent to fuse wi

122 The cytosolic NT domain of the human V-ATPase a2 isoform specifically interacts with PI(4)P i

123 e performed a proteomic analysis to identify V-ATPase associated proteins and construct a V-ATPase in

124 nal tubular acidosis as a result of impaired V-ATPase activity.

125 he cytosol acidified, suggestive of impaired V-ATPase proton transport.

126 Previous studies have implicated V-ATPases in cancer cell invasion.

127 ow that certain stress-responsive changes in V-ATPase activity and assembly require the signaling lip

128 ight involve amino acid-dependent changes in V-ATPase assembly.

129 idification of the cytosol and a decrease in V-ATPase-dependent proton flux across the plasma membran

130 istinct from that associated with defects in V-ATPase core subunits, suggest a more general role for

131 1p-driven transcription, which is induced in V-ATPase mutants to limit transcription of the iron regu

132 tions of diverse protein families, including V-ATPase ion pumps, DNA-binding transcription regulators

133 Moreover, we show that increased V-ATPase activity during cold acclimation requires the p

134 abilizes V1-V(o) assembly and thus increases V-ATPase activity.

135 MP/PKA pathway-dependent mechanism to induce V-ATPase-dependent H(+) secretion.

136 ine or an ADORA2A or ADORA2B agonist induced V-ATPase translocation from vesicles to the plasma membr

137 and ADORA2B purinergic P1 receptors induced V-ATPase apical membrane accumulation in medullary A-ICs

138 eracting proteins, DMXL1 and WDR7, inhibited V-ATPase-mediated intracellular vesicle acidification in

139 s exquisitely selective inhibition of insect V-ATPases.

140 Yeast mutants lacking the intracellular V-ATPase proton pump (vma mutants) have reduced levels o

141 We have investigated V-ATPase assembly in bone marrow-derived, murine dendrit

142 ulatory role of cancer associated a2-isoform V-ATPase on neutrophil migration, suggesting a2V as a po

143 Yeast vma mutants lack V-ATPase activity and allow exploration of connections b

144 Mutants lacking V-ATPase activity are avirulent and fail to acidify endo

145 Our findings link V-ATPase to cell-cycle progression and DNA synthesis in

146 trans-Golgi network/early endosome-localized V-ATPase to vacuolar pH.

147 ysosomal function via promotion of lysosomal V-ATPase assembly.

148 ility of the V1G1 component of the lysosomal V-ATPase.

149 To test this, we measured V-ATPase assembly by cell fractionation in HEK293T cells

150 Correlation between plasma membrane V-ATPase activity and invasiveness was limited, but RNAi

151 ntibody inhibits activity of plasma membrane V-ATPases in transfected cells.

152 These studies suggest that plasma membrane V-ATPases play an important role in invasion of breast c

153 ches to specifically inhibit plasma membrane V-ATPases.

154 present two in vivo assays and use a mutant V-ATPase subunit to establish that it is the H(+)-transl

155 as a screen for functionally important novel V-ATPase-regulating proteins.

156 gene that encodes the catalytic subunit A of V-ATPase in GC.

157 We show that the impaired ability of V-ATPase mutants to properly govern intracellular pH aff

158 ed expression, distribution, and activity of V-ATPase isoforms in invasive prostate adenocarcinoma (P

159 insights and directions for the analysis of V-ATPase cell biology and (patho)physiology.

160 t is thought to regulate the dissociation of V-ATPase.

161 The soluble, cleaved N-terminal domain of V-ATPase a2 isoform is associated with in vitro inductio

162 ht the basis for the clinical exploration of V-ATPase as a potentially generalizable therapy for brea

163 t direct evidence that surface expression of V-ATPase is associated with macrophage polarization in t

164 philic quinazolines modulate the function of V-ATPase in cells.

165 Acute inhibition of V-ATPase activity with concanamycin A triggers Pma1p ubi

166 (p < 0.001), and responded to inhibition of V-ATPase with profound acidification to the 6.3-6.5 rang

167 , cleaved N-terminal domain of a2 isoform of V-ATPase (a2NTD) is associated with in vitro induction o

168 is regulated, in part, by the a2 isoform of V-ATPase (a2V) and the concurrent infiltration of M1 (in

169 This activity of a2 isoform of V-ATPase (a2V) caused us to investigate its role in canc

170 otein (LAMP)-1, LAMP-2 and the a2 isoform of V-ATPase (a2V, an enzyme involved in lysosome acidificat

171 on glucose and assembled wild-type levels of V-ATPase pumps at the membrane.

172 ) growth phenotype characteristic of loss of V-ATPase activity only at high temperature.

173 istent with specificity in signaling loss of V-ATPase activity to Pma1p, another plasma membrane tran

174 Here we show that loss of V-ATPase subunits in the Drosophila fat body causes an a

175 We hypothesize that loss of V-ATPase-mediated organelle acidification signals ubiqui

176 To investigate the mechanism of V-ATPase regulation by reversible disassembly, we recent

177 Existing small-molecule modulators of V-ATPase either are restricted to targeting one membrano

178 to a cysteine residue located in a region of V-ATPase subunit A that is thought to regulate the disso

179 e of these results for in vivo regulation of V-ATPase assembly is discussed.

180 or intracellular targeting and regulation of V-ATPase assembly.

181 d the role of adenosine in the regulation of V-ATPase in ICs.

182 fully evaluate the therapeutic relevance of V-ATPase in human diseases.

183 Thus, the data support a role of V-ATPase c-ring in membrane fusion and neuronal communic

184 The present data establish the role of V-ATPase in modulating a macrophage phenotype towards TA

185 the physiological and pathological roles of V-ATPase.

186 icted to targeting one membranous subunit of V-ATPase or have poorly understood mechanisms of action.

187 lently modify a soluble catalytic subunit of V-ATPase with high potency and exquisite proteomic selec

188 maintaining the coupling of V1-V0domains of V-ATPase through the binding of microfilaments to subuni

189 and is important in regulated disassembly of V-ATPases.

190 of a3 significantly increased expression of V-ATPases at the plasma membrane.

191 Subunit F of V-ATPases is proposed to undergo structural alterations

192 responsible for subcellular localization of V-ATPases, with a3 and a4 targeting V-ATPases to the pla

193 The paucity of V-ATPases in M1 phagosomes was associated with, and like

194 amination of the thermodynamic properties of V-ATPases.

195 A unique mode of regulation of V-ATPases is the reversible disassembly of V1 and VO, wh

196 In this study, we evaluated the role of V-ATPases in the invasiveness of two closely matched hum

197 lysis and assessed its direct involvement on V-ATPase function.

198 In particular, V-ATPase can be regulated by using external fields, such

199 immuno-gold labeling confirmed the presence V-ATPase in the cell membrane of RON astrocyte processes

200 We propose V-ATPase as a promising drugable target in cancer therap

201 and synaptic vesicular proton pump protein (V-ATPase H) levels.

202 he prorenin receptor (PRR) and increases PRR/V-ATPase-driven ATP release, thereby enhancing the produ

203 The ATP-dependent proton pump V-ATPase ensures low intralysosomal pH, which is essenti

204 Acidification by the proton-pumping V-ATPase requires charge compensation by counterion curr

205 5-bisphosphate (PI3,5P2) and greatly reduced V-ATPase proton transport in inositol-deprived wild-type

206 e a new mechanism by which glucose regulates V-ATPase catalytic activity that occurs at steady state

207 in vivo, a role for glycolysis at regulating V-ATPase proton transport is discussed.

208 An important mechanism of regulating V-ATPase activity is reversible assembly of the V1 and V

209 These successfully remove V-ATPase, neutralize, and form huge postlysosomes.

210 rther demonstrate that a previously reported V-ATPase inhibitor, 3-bromopyruvate, also targets the sa

211 ng acidic compartment defects in resistance; V-ATPase acidifies lysosomes and related organelles, whe

212 crystallin in those same astrocytes restored V-ATPase activity and normal endolysosomal acidification

213 Ac45, but not its disease mutants, restored V-ATPase-dependent growth in Voa1 mutant yeast.

214 Our analysis using kidney tissue revealed V-ATPase-associated protein clusters involved in protein

215 assembly of Saccharomyces cerevisiae (ScDF) V-ATPase at 3.1 A resolution.

216 Thus RAVE is the first isoform-specific V-ATPase assembly factor.

217 zed a biotin-conjugated form of the specific V-ATPase inhibitor bafilomycin.

218 ion was completely sensitive to the specific V-ATPase inhibitor concanamycin.

219 and reveals a novel link of tissue-specific V-ATPase assembly with immunoglobulin production and cog

220 Sperm stimulate V-ATPase activity in oocytes by signalling the degradati

221 th vacuolar (Vph1p) and non-vacuolar (Stv1p) V-ATPase activity is necessary to affect in vitro virule

222 ploy particular a subunit isoforms to target V-ATPases to the plasma membrane, where they function in

223 ation of V-ATPases, with a3 and a4 targeting V-ATPases to the plasma membrane of specialized cells.

224 mic nature of lysosomal metabolites and that V-ATPase- and mTOR-dependent mechanisms exist for contro

225 We concluded that V-ATPase activity at steady state and V-ATPase reassembl

226 Previous work has shown that V-ATPase assembly increases during maturation of bone ma

227 It has been proposed that V-ATPases participate in invasion by localizing to the p

228 The V-ATPase is a multisubunit, rotary proton pump whose pre

229 The V-ATPase is necessary for amino acid-induced activation

230 The V-ATPase is the main regulator of intra-organellar acidi

231 The V-ATPase undergoes amino acid-dependent interactions wit

232 enge in designing lead compounds against the V-ATPase is its ubiquitous nature, such that any therape

233 y of the plasma membrane proton pump and the V-ATPase complex.

234 ound that Vacuolar ATPase (V-ATPase) and the V-ATPase regulator Rabconnectin-3 are required for subce

235 ry that acts upstream of Rag-GTPases and the V-ATPase to activate mTORC1.

236 molecular mechanism of signaling between the V-ATPase, cytohesin-2, and Arf GTP-binding proteins.

237 ition, revealing important links between the V-ATPase, iron metabolism and HIFs.

238 mal degradation of HIF1alpha, disrupting the V-ATPase results in intracellular iron depletion, thereb

239 Hence, the V-ATPase membrane domain would allow the exocytotic mach

240 trafficking caused by genetic defects in the V-ATPase complex.

241 We hypothesized that changes in the V-ATPase/Ragulator interaction might involve amino acid-

242 ves Ca(2+) into the lysosome, inhibiting the V-ATPase H(+) pump did not prevent Ca(2+) refilling.

243 Ac45 plays a central role in navigating the V-ATPase to the plasma membrane, and hence it is an impo

244 at are parts of the mechanical stator of the V-ATPase are clearly resolved as unsupported filaments i

245 and membrane-bound a-subunit isoforms of the V-ATPase are implicated in organelle-specific targeting

246 an evolutionarily conserved function of the V-ATPase as a novel cytohesin-signaling receptor.

247 o-inhibition of the V1 and VO regions of the V-ATPase by starving the yeast Saccharomyces cerevisiae,

248 loss-of-function approaches that lack of the V-ATPase cannot be compensated for by increased V-PPase

249 either the assembly or the stability of the V-ATPase complex.

250 ly through regulation of the assembly of the V-ATPase complex.

251 be essential in mechanistic processes of the V-ATPase enzyme.

252 ocking experiments revealed that part of the V-ATPase formed by its a2N(1-17) epitope competes with t

253 ytes was 6.82 +/- 0.06 and inhibition of the V-ATPase H(+) pump by Cl(-) removal or via the selective

254 4T1 model of metastatic breast cancer of the V-ATPase inhibitor archazolid suggested that its ability

255 d cells, suggesting that perturbation of the V-ATPase is a consequence of altered PI3,5P2 homeostasis

256 In comparison, the vacuolar pH of the V-ATPase mutant vph1Delta or vph1Delta fab1Delta double

257 kp1 of RAVE; the E, G, and C subunits of the V-ATPase peripheral V1 sector; and Vph1 of the membrane

258 um resistant, and chemical inhibition of the V-ATPase phenocopied this effect.

259 n of the yeast vacuole in the absence of the V-ATPase rescues vacuole-fusion defects.

260 which it binds to and locks the axle of the V-ATPase rotary motor would need to be re-evaluated.

261 ct of the membrane-embedded c subunit of the V-ATPase, allowing for extracellular expression of the V

262 lide archazolid B, a potent inhibitor of the V-ATPase, as an experimental drug as well as a chemical

263 on, rather than the physical presence of the V-ATPase, that promotes homotypic vacuole fusion in yeas

264 set of proteins involved in assembly of the V-ATPase.

265 leting drug VPA leads to perturbation of the V-ATPase.

266 ower transmission between the domains of the V-ATPase.

267 ia its interaction with the V0 sector of the V-ATPase.

268 een the lipid and the membrane sector of the V-ATPase.

269 gh resolution structure for subunit a of the V-ATPase.

270 6AP1, encoding accessory protein Ac45 of the V-ATPase.

271 e have characterized the binding site on the V-ATPase of pea albumin 1b (PA1b), a small cystine knot

272 The principal result is that the V-ATPase-mediated control of the cell membrane potential

273 This has implications for understanding the V-ATPase mechanism and that of inhibitors with therapeut

274 ZNRF2 also interacts with the V-ATPase and preserves lysosomal acidity.

275 ar to that observed after treatment with the V-ATPase inhibitor bafilomycin.

276 Based on studies with the V-ATPase inhibitor BafilomycinA1, lysosomal acidificatio

277 low organellar pH is primarily driven by the V-ATPases, proton pumps that use cytoplasmic ATP to load

278 Comparison of the three V-ATPase conformations with the structure of nanodisc-bo

279 pfk2Delta, suggesting that Pfk1p binding to V-ATPase may be inhibitory in the mutant.

280 bunit, the other subunit retained binding to V-ATPase.

281 cific targeting or regulation information to V-ATPases.

282 uced vacuolar H(+)-adenosine triphosphatase (V-ATPase) activity, accounts for the reduced acidifying

283 the vacuolar H(+)-adenosine triphosphatase (V-ATPase) increased the luminal concentrations of most m

284 vacuolar-type H(+)-adenosine triphosphatase (V-ATPase) is directly implicated in secretory vesicle ex

285 vacuolar-type H(+)-adenosine triphosphatase (V-ATPase) or neutralize to form postlysosomes.

286 fication, and two previously uncharacterised V-ATPase assembly factors, TMEM199 and CCDC115, stabilis

287 he optic nerve rely to a greater degree upon V-ATPase for HCO3(-)-independent pHi regulation than do

288 the Vph1p isoform is essential for vacuolar V-ATPase activity in C. albicans.

289 tein interactions that regulate these varied V-ATPase functions.

290 ry in RON astrocyte was achieved largely via V-ATPase with sodium-proton exchange (NHE) playing a min

291 he level of Pfk1p co-immunoprecipitated with V-ATPase decreased 58% in pfk2Delta, suggesting that Pfk

292 kinase-1 subunits co-immunoprecipitated with V-ATPase in wild-type cells; upon deletion of one subuni

293 P1 complex (CCT) were found to interact with V-ATPase for the first time in this study.

294 Yeast V-ATPase assembly and activity are glucose-dependent.

295 sks Ac45 as the functional ortholog of yeast V-ATPase assembly factor Voa1 and reveals a novel link o

296 as the long-sought human homologue of yeast V-ATPase assembly factor Voa1.

297 called C17orf32) as a human homolog of yeast V-ATPase assembly factor Vph2p (also known as Vma12p).

298 on and biophysical characterization of yeast V-ATPase c subunit ring (c-ring) using electron microsco

299 The yeast V-ATPase a subunit is present as two isoforms, Stv1p in

300 d reciprocal homology with Vma22p, the yeast V-ATPase assembly factor located in the endoplasmic reti