ライフサイエンスコーパス: V-ATPase

1 V-ATPase activity is controlled by the regulated assembl

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

3 V-ATPase activity is regulated by reversible disassembly

4 V-ATPase assembly defects are thus a form of hereditary

5 V-ATPase assembly increases upon amino acid starvation,

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

7 V-ATPase is a rotary motor, and recent structural analys

8 V-ATPase reassembly and reactivation requires interventi

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

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 h1, and that this interaction both activates V-ATPase activity and protects cells from stress.

15 Vph1-containing vacuolar vesicles activates V-ATPase activity and proton pumping.

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

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

18 al mutants previously implicated in altering V-ATPase assembly state or glucose-induced assembly.

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 cial role in acidifying the urine via apical V-ATPase pumps.

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

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

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

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

27 ophosphatase (V-PPase) and the H(+) -ATPase (V-ATPase), establish the proton gradient that powers mol

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

29 Vacuolar (H(+))-ATPase (V-ATPase) is fundamental in inflammatory cytokine traffi

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

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

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

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

34 Here we report that vacuolar H(+)-ATPase (V-ATPase) inhibition differentially affects regulation o

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

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

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

38 The vacuolar H(+)-ATPase (V-ATPase) is an ATP-dependent proton pump that is essent

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

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

41 The yeast vacuolar H(+)-ATPase (V-ATPase) of budding yeast (Saccharomyces cerevisiae) is

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

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

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

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

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

47 The vacuolar H(+)-ATPase (V-ATPase; V(1)V(o)-ATPase) is an ATP-dependent proton pu

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

49 ular subunit of the vacuolar-type H+ ATPase (V-ATPase), which is responsible for proper lysosomal aci

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

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

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

53 Vacuolar type ATPase (V-ATPase) has recently emerged as a promising novel anti

54 leavage or shedding of vacuolar-type ATPase (V-ATPase) subunits Ac45 and prorenin receptor, respectiv

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

56 that binds and inhibits the vacuolar ATPase (V-ATPase) and by SopF, a bacterial effector that catalyt

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

58 Here we identify vacuolar ATPase (V-ATPase) as an essential regulator of RAS-induced macro

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

60 , a critical subunit of the vacuolar ATPase (V-ATPase) pump.

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

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

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

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

65 The vacuolar-type H(+)-ATPases (V-ATPase) hydrolyze ATP to pump protons across the plasm

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

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

68 embly and activity of vacuolar H(+)-ATPases (V-ATPases) containing the vacuolar a-subunit isoform Vph

69 Vacuolar-type H(+)-ATPases (V-ATPases) contribute to pH regulation and play key role

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

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

72 Proton-translocating vacuolar-type ATPases (V-ATPases) are necessary for numerous processes in eukar

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

74 tivation of V-ATPase without affecting basal V-ATPase activity.

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

76 These observations establish a link between V-ATPase trafficking and nutrient supply by macropinocyt

77 Blocking V-ATPase pharmacologically in beta-cells increased mTORC

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

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

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

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

82 We isolated homogeneous rat brain V-ATPase through its interaction with SidK, a Legionella

83 more susceptible to cell death induction by V-ATPase inhibitors.

84 lyticus T3SS effector VopQ targets host-cell V-ATPase, resulting in blockage of autophagic flux and n

85 In both tumor and healthy cells, V-ATPase inhibition induced a distinct metabolic regulat

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

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

88 Vacuolar H+-ATP complex (V-ATPase) is a multisubunit protein complex required for

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

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

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

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

93 elucidated a mechanism whereby RAS controls V-ATPase association with the plasma membrane to drive R

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

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

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

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

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

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

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

101 Vma2Delta cells have dysfunctional V-ATPases, rendering their vacuoles nonacidic.

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

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

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

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

106 nits form a luminal glycan coat critical for V-ATPase folding, localization, and stability.

107 Moreover, glycolysis is essential for V-ATPase-mediated proton pumping.

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

109 M2 polarization, implying a crucial role for V-ATPase in the resolution of inflammation.

110 icate that AMPK regulation is uncoupled from V-ATPase activity in cancer cells and that this makes th

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

112 Q kills cells in the absence of a functional V-ATPase.

113 Vacuoles with functional V-ATPases appear unnecessary in W303 cells for iron to e

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

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

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

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

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

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

120 or their inability to reconstitute into holo V-ATPase in vitro Here, using the model organism Sacchar

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

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

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

124 cryoelectron microscopy structures of human V-ATPase in three rotational states at up to 2.9- angstr

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

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

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

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

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

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

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

132 isplayed a significantly reduced increase in V-ATPase activity and assembly upon starvation.

133 both the catalytic nature of RAVE's role in V-ATPase assembly and the likelihood of glucose signalin

134 ine by ectonucleotidases plays a key role in V-ATPase-dependent proton secretion, and is part of a fe

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

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

137 that amino acid starvation rapidly increases V-ATPase assembly and activity in mammalian lysosomes, b

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

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

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

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

142 activation of the cGAS-STING pathway induces V-ATPase-dependent LC3B lipidation that may mediate cell

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

144 Disassembly inhibits V-ATPase activity under low-glucose conditions by releas

145 report two cryo-EM structures of the intact V-ATPase from bovine brain with all the subunits includi

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

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

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

149 ) inhibitor dorsomorphin decreased lysosomal V-ATPase activity and also blocked any increase upon sta

150 e starvation-dependent increase in lysosomal V-ATPase activity without altering basal activity.

151 e starvation-dependent increase in lysosomal V-ATPase activity, indicating that H89 and dorsomorphin

152 t AKT2, was required for increased lysosomal V-ATPase activity in response to amino acid starvation i

153 nase (PKA) inhibitor H89 increases lysosomal V-ATPase activity and blocks any further change upon sta

154 controlling the rapid response of lysosomal V-ATPase activity to changes in amino acid availability

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

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

157 ructures reveal unique features of mammalian V-ATPase and suggest a mechanism of V1-Vo torque transmi

158 In mammals, V-ATPase subunit isoforms are differentially targeted to

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

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

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

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

163 ches to specifically inhibit plasma membrane V-ATPases.

164 indicating that H89 and dorsomorphin modify V-ATPase activity through other cellular targets.

165 Moreover, V-ATPase-independent AMPK induction in tumor cells prote

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

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

168 Accumulation of V-ATPase at the plasma membrane is necessary for the cho

169 n microscopy shows a greater accumulation of V-ATPase proton pumps at the apical surface of A-ICs in

170 lished the PI(3,5)P2-dependent activation of V-ATPase without affecting basal V-ATPase activity.

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

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

173 Blockade of V-ATPase by archazolid during IL-4-induced human M2 pola

174 d explain the tumor-specific cytotoxicity of V-ATPase inhibition.

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

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

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

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

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

180 lipid mediator formation was independent of V-ATPase activity.

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

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

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

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

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

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

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

188 ighlighting H(CT)'s role in the mechanism of V-ATPase regulation.

189 This study identifies mechanisms of V-ATPase assembly and biogenesis that rely on the integr

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

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

192 he molecular events underlying regulation of V-ATPase activity by reversible disassembly.

193 binding to DCVs and for CAPS1 regulation of V-ATPase activity via Rbcn3beta/WDR7 interactions.

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

195 ibitory role for Gpr116 in the regulation of V-ATPase trafficking and urinary acidification.

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

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

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

199 the physiological and pathological roles of V-ATPase.

200 regulation contributes to the selectivity of V-ATPase inhibitors for tumor cells.

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

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

203 Oncogenic RAS promotes the translocation of V-ATPase from intracellular membranes to the plasma memb

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

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

206 the archazolids as well as the evaluation of V-ATPases as a novel and powerful class of anticancer ta

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

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

209 ide an invaluable tool for future studies on V-ATPase-mediated membrane fusion and autophagy.

210 While disruption of either V-PPase or V-ATPase had no obvious effect on plant embryo developme

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

212 de macrolides, which present the most potent V-ATPase inhibitors known to date.

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

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

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

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

217 rotons into the lumen via the proton pumping V-ATPase located in their apical membrane, a process tha

218 ear cells is achieved via the proton pumping V-ATPase located in their apical membrane.

219 We show that purified V-ATPase complexes containing Vph1p have higher ATPase a

220 5-bisphosphate (PI3,5P2) and greatly reduced V-ATPase proton transport in inositol-deprived wild-type

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

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

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

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

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

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

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

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

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

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

231 Targeting V-ATPase in M2 influenced neither IL-4-triggered JAK/STA

232 Targeting V-ATPase in vivo delayed resolution of zymosan-induced m

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

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

235 mmary, the results of our work indicate that V-ATPase inhibition has differential effects on AMPK-med

236 Together, our data propose that V-ATPase regulates 15-lipoxygenase-1 expression and cons

237 In this study, we show that V-ATPase activity is required for the induction of SPM-b

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

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

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

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

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

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

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

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

246 In nonmalignant cells, the V-ATPase inhibitor archazolid increased phosphorylation

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

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

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

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

251 ial effector that catalytically modifies the V-ATPase to inhibit LC3B lipidation via ATG16L1.

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

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

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

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

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

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

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

259 4T1 model of metastatic breast cancer of the V-ATPase inhibitor archazolid suggested that its ability

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

261 e while binding directly to subunit c of the V-ATPase membrane-embedded subcomplex V(o).

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

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

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

265 ORC1 activity, suggesting involvement of the V-ATPase proton pump in the phenotype.

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

267 of VopQ bound to the V(o) subcomplex of the V-ATPase.

268 6AP1, encoding accessory protein Ac45 of the V-ATPase.

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

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

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

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

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

274 Genetic defects in four of these V-ATPase assembly factors show overlapping clinical feat

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

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

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

278 We also show that the VMA21 variants lead to V-ATPase misassembly and dysfunction.

279 re and are not located in close proximity to V-ATPase containing vesicles.

280 cific targeting or regulation information to V-ATPases.

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

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

283 or vacuolar-type adenosine triphosphatases (V-ATPases) are ATP-driven proton pumps comprised of a cy

284 or vacuolar-type adenosine triphosphatases (V-ATPases).

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

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

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

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

289 RAVE localization did not correlate with V-ATPase assembly levels reported previously in these mu

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

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

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

293 ed by the reported association of Rbcn3 with V-ATPase, we found that knocking down CAPS1, Rbcn3alpha,

294 last where it serves a job-sharing role with V-ATPase in vacuolar acidification.

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

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

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

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

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

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