ライフサイエンスコーパス: H K ATPase

1 -affinity ouabain binding in a mutant of the H,K ATPase.

2 he presence of Lys791, Glu936, and Glu795 in H,K-ATPase.

3 ) conformational equilibria of the Na,K- and H,K-ATPase.

4 pendent, and energized by an apical membrane H,K-ATPase.

5 due in the conformational equilibrium of the H,K-ATPase.

6 ta-subunits was essential for the functional H,K-ATPase.

7 coplasmic reticulum Ca-ATPase or the gastric H,K-ATPase.

8 potassium, sodium can be transported via the H,K-ATPase.

9 ve regions of the alpha-beta subunits of the H,K-ATPase.

10 n of the K+-dependent ATPase activity of the H,K-ATPase.

11 osaccharides of the beta-subunit from rabbit H,K-ATPase.

12 tinct from the known Na,K-ATPase and gastric H,K-ATPase.

13 e exo-endocytosis of vesicles containing the H/K ATPase.

14 astric acid secretion by down-regulating the H/K-ATPase.

15 mino acids Asn908-Ala933 of rat distal colon H, K-ATPase.

16 no acids of the alpha subunit of the gastric H, K-ATPase.

17 the corresponding residues common to gastric H,K-ATPases.

18 ystallography are conserved in the Na,K- and H,K-ATPases.

19 encoding the alpha and beta subunits of the H+,K+-ATPase.

20 ate role as the beta-subunit for the colonic H+,K+-ATPase.

21 he rate of acid secretion through the apical H+,K+ -ATPase.

22 blished for the alpha subunit of the colonic H+,K+ -ATPase.

23 nteract with the gastric proton pump enzyme, H+/K(+)-ATPase.

24 inhibition of ATP hydrolysis by the gastric H(+),K(+)-ATPase.

25 and palytoxin, which do not inhibit gastric H(+),K(+)-ATPase.

26 confirms the monomeric state of solubilized H(+),K(+)-ATPase.

27 to the electroneutral transport mode of the H(+),K(+)-ATPase.

28 utive in vivo processing and presentation of H(+)/K(+)-ATPase.

29 h low pH can be maintained in the absence of H(+), K(+) ATPase.

30 and endoplasmic-reticulum Ca(2+)-ATPases and H(+),K(+)-ATPases.

31 antiserum against human intrinsic factor and H/K ATPase (a parietal cell marker), counting the percen

32 The gastric proton pump H(+),K(+)-ATPase acidifies the gastric lumen, and thus i

33 RNA and protein expression, Na, K-ATPase and H,K-ATPase activities and protein expression were determ

34 as ouabain-sensitive and ouabain-insensitive H,K-ATPase activities are localized solely to apical mem

35 increased ouabain-sensitive Na,K-ATPase and H,K-ATPase activities by only 30% and 42%, respectively.

36 e and H(+)-ATPase activity without augmented H(+),K(+)-ATPase activity.

37 8080 or luminal K+ removal to inhibit P-type H+,K+-ATPase activity, and 5-10 nM bafilomycin A1 or 1-1

38 exchange and higher H+-ATPase but not higher H+-K+-ATPase activity mediated increased H+ secretion in

39 ty without differences in Na+/H+ exchange or H+-K+-ATPase activity.

40 very early differential ion flux created by H+/K+-ATPase activity.

41 in turn depends on left-right differences in H+/K+-ATPase activity.

42 receptors that are required for and regulate H+K+-ATPase activity should lead to the development of n

43 substantially increased ouabain-insensitive H, K-ATPase activity and HKcalpha protein expression by

44 istant Na,K-ATPase and kinetic parameters of H,K-ATPase activity analyzed.

45 The K+-stimulated H,K-ATPase activity of 0.82 +/- 0.2 micromol/mg/h satura

46 The contribution of H,K-ATPase activity on active Cl flux (J(A)Cl) and passi

47 ular mass is calculated, corresponding to an H(+),K(+)-ATPase alpha,beta-protomer of 147.3 kDa.

48 tion, measured by Western blots with an anti-H(+)/K(+)-ATPase alpha-subunit antibody.

49 pression by Northern blotting using a canine H(+)/K(+)-ATPase alpha-subunit cDNA probe.

50 Ad.Myr-Akt induced H(+)/K(+)-ATPase alpha-subunit gene expression 3-fold, w

51 l growth factor (EGF) for 6-16 h, stimulates H(+)/K(+)-ATPase alpha-subunit gene expression through t

52 Shh induced H(+)/K(+)-ATPase alpha-subunit gene expression, assessed

53 (EGF) stimulates gastric acid secretion and H(+)/K(+)-ATPase alpha-subunit gene expression.

54 EGF-responsive sequence (ERE) of the canine H(+)/K(+)-ATPase alpha-subunit gene promoter, and it ind

55 In the transgenic mice, levels of the H+/K+-ATPase alpha-subunit protein and messenger RNA wer

56 An antibody directed against the H, K-ATPase alpha subunit (HKcalpha) inhibited apical Na

57 ps composed of complementary portions of the H, K-ATPase alpha subunit and the highly homologous Na,K

58 Moreover, the synthesis of the H,K-ATPase alpha subunit is also limited in MDCK cells,

59 This motif resides within the fourth of the H,K-ATPase alpha subunit's ten predicted transmembrane d

60 he corresponding portions of the rat gastric H,K-ATPase alpha subunit, and the constructs were transf

61 he corresponding sequence of the rat gastric H,K-ATPase alpha subunit, the chimeric alpha subunit ass

62 s between the structurally related Na,K- and H,K-ATPase alpha subunits to localize regions that deter

63 The co-expression of the H,K-ATPase alpha- and beta-subunits was essential for th

64 The rabbit H,K-ATPase alpha- and beta-subunits were transiently exp

65 The gastric H,K-ATPase alpha-beta heterodimer was expressed as a fus

66 We conclude that ablation of the H,K-ATPase alpha-subunit causes achlorhydria and hyperga

67 reported that sodium depletion up-regulates H,K-ATPase alpha-subunit mRNA and protein expression, wh

68 TM3-TM4 ectodomain sequence with that of the H,K-ATPase alpha-subunit result in a pump that exhibits

69 101 (HKM0) or 139 (HKM1) amino acids of the H,K-ATPase alpha-subunit, a linker region and a reporter

70 01 (HK-M0) or 139 (HK-M1) amino acids of the H,K-ATPase alpha-subunit, a linker region and the C-term

71 brane segment (TM4) of the Na,K- and gastric H,K-ATPase alpha-subunits appear to play a major role in

72 nic TxA23 mouse recognize a peptide from the H/K-ATPase alpha-chain.

73 The H(+)/K(+)-ATPase alpha2 subunit (HK alpha 2) of distal c

74 K+ deprivation promotes H+-K+-ATPase alpha2 (HKalpha2) gene expression in the me

75 operties of the alpha-subunit of the colonic H+,K+-ATPase (alphaC) were studied in Xenopus laevis ooc

76 th those of the sharply up-regulated colonic H(+),K(+)-ATPase and epithelial Na(+) channel to mediate

77 actively repressed through the activities of H(+)K(+) ATPase and serotonin-dependent signaling, thus

78 lts in long-lasting AIG associated with both H(+)K(+)ATPase and intrinsic factor autoantibody respons

79 cking machinery that are associated with the H+-K+-ATPase and of components of the actin-based cytosk

80 The trafficking of the H+-K+-ATPase and the remodelling of the apical membrane

81 ordinated regulation of both apical membrane H,K-ATPase and basolateral membrane KCC1 protein.

82 ty is an alternate mode of ouabain-sensitive H,K-ATPase and does not solely represent basolateral mem

83 n cation dependence and differs from gastric H,K-ATPase and Na,K-ATPase in sensitivity to inhibitors.

84 the specificity of nucleotides to power the H,K-ATPase and several of its partial reactions, includi

85 of the K+-dependent partial reactions of the H,K-ATPase and show that Glu857 located at the M7 bounda

86 l domain of the alpha-subunit of the gastric H,K-ATPase and the C-terminal domain of the beta-subunit

87 e proximal and distal colon, whereas colonic H,K-ATPase and the epithelial sodium channel showed mass

88 ignal is required for the internalization of H/K-ATPase and for the termination of acid secretion.

89 Because acid secretion is via the H/K-ATPase and the effects of LPS on this enzyme are unk

90 atoms) at its site of action in the gastric H+/K+-ATPase, and the aromaticity of the agonist binding

91 allowing for both recycling of K(+) for the H,K-ATPase, and Cl(-) secretion, necessary for the gener

92 es to the gastric parietal cell proton pump, H/K ATPase, and aberrant expression of the H/K ATPase in

93 Na(+),K(+)-ATPase and H(+),K(+)-ATPase are electrogenic and nonelectrogenic io

94 The Na(+),K(+)-ATPase and the H(+),K(+)-ATPases are closely related members of the P-t

95 The Na,K- and H,K-ATPases are plasma membrane enzymes responsible for

96 the catalytic subunits of Ca2+-, Na+,K+- and H+,K+-ATPases argues that their extracytosolic cation ex

97 -receptor antagonists, (2) identification of H(+)K(+)-ATPase as the parietal cell proton pump and dev

98 ted by omeprazole, implicating parietal cell H,K-ATPase as the dominant regulator of surface pH under

99 d the electron crystallographic structure of H(+),K(+)-ATPase at 6.5 A resolution in the E2P state wi

100 +),K(+)-ATPase with arginine, present in the H(+),K(+)-ATPase at the corresponding position, converte

101 the secretagogue-regulated re-cycling of the H+-K+-ATPase at the apical membrane.

102 tively secrete acid and continuously express H/K-ATPase at their cell surfaces.

103 d that the alpha-subunit of human nongastric H,K-ATPase (Atp1al1) can assemble with the gastric H,K-A

104 titutively presenting the endogenous gastric H(+)/K(+) ATPase autoantigen in its normal physiological

105 lished, and it has not been revealed how the H(+),K(+)-ATPase avoids binding of Na(+) at the site cor

106 d phosphoprotein, focal adhesion kinase, the H(+)/K(+) ATPase beta (flippase), the hematopoietic cell

107 ma under the control of the stomach-specific H(+)/K(+) ATPase beta promoter to test the potential rol

108 of the gastric H+,K+-ATPase (betaG, the only H+, K+-ATPase beta-subunit identified in rat), or the be

109 ars to require coexpression with the gastric H+-K+-ATPase beta subunit for optimal functional activit

110 on of HKalpha2b with and without the gastric H+-K+-ATPase beta subunit in HEK 293 cells indicated tha

111 The promoter of the mouse H+/K+-ATPase beta-subunit gene, which is specifically ex

112 The H, K-ATPase beta subunit, which contains a tyrosine-base

113 aining the Y898R,C908G mutations and gastric H, K-ATPase beta was less than 10% of wild type Na,K-ATP

114 usly been shown to assemble with the gastric H,K-ATPase beta subunit (gH,Kbeta) to form a functionall

115 parated from the last 177 amino acids of the H,K-ATPase beta subunit by cDNA encoding CCK-A receptor

116 Mutation of tyrosine-20 of the H,K-ATPase beta subunit cytoplasmic sequence to an alani

117 the enzyme formed by ATP1AL1 and the gastric H,K-ATPase beta subunit in HEK 293 cells mediates primar

118 Hence, the steady state distribution of the H,K-ATPase beta subunit in polarized cells depends on th

119 for plasma membrane delivery of the gastric H,K-ATPase beta subunit in polarized cells, the protein

120 d between the Na+ pump beta1 isoform and the H,K-ATPase beta subunit indicates that sequences in the

121 is also limited in MDCK cells, although the H,K-ATPase beta subunit is efficiently expressed.

122 g of an apical membrane protein, the gastric H,K-ATPase beta subunit linked to yellow fluorescent pro

123 chimera in which the cytoplasmic tail of the H,K-ATPase beta subunit protein was replaced with the an

124 Hence, co-sorting of the H,K-ATPase beta subunit with the Na,K-ATPase alpha(1) su

125 ssembled preferentially with the rat gastric H,K-ATPase beta subunit.

126 es showed that a significant fraction of the H,K-ATPase beta subunits associate with the endogenous N

127 The major fraction of unassociated monomeric H,K-ATPase beta subunits is detected in the apical membr

128 Pase (Atp1al1) can assemble with the gastric H,K-ATPase beta-subunit (betaHK) into an active ion pump

129 The H,K-ATPase beta-subunit and CD63 colocalize in parietal

130 stribution occurs by enhanced endocytosis of H,K-ATPase beta-subunit complexed with CD63.

131 on, whereas potassium depletion up-regulates H,K-ATPase beta-subunit mRNA and protein expression.

132 on and the C-terminal 177 amino acids of the H,K-ATPase beta-subunit that contain five N-linked glyco

133 hs and again ending in the C-terminus of the H,K-ATPase beta-subunit.

134 tes in the C-terminal 177 amino acids of the H,K-ATPase beta-subunit.

135 We generated transgenic mice expressing H/K-ATPase beta subunit in which this motif's tyrosine r

136 The cytoplasmic tail of the H/K-ATPase beta subunit includes a four residue sequence

137 artial loss of the membrane-proximal markers H,K-ATPase-beta and F-actin, increased and redistributed

138 ta-subunits, the beta-subunit of the gastric H+,K+-ATPase (betaG, the only H+, K+-ATPase beta-subunit

139 did not inhibit the specific activity of the H,K-ATPase, but reversal of the side chain charge by sub

140 ugs that inhibit the acid-secreting gastric (H(+), K(+))-ATPase by acid activation to reactive thioph

141 Inhibition of the gastric H,K-ATPase by the imidazo[1,2-alpha]pyridine, SCH28080,

142 ith an apical Cl-HCO3 exchanger and that the H,K-ATPase can function, under certain conditions, as a

143 cific for a naturally expressed autoantigen (H+/K+ ATPase) can be converted to Foxp3+ T regulatory ce

144 ., the analogous region from the rat gastric H,K-ATPase catalytic subunit or a region from the human

145 The vesicular gastric H,K-ATPase catalyzes an electroneutral H for K exchange

146 The gastric H,K-ATPase catalyzes electroneutral exchange of H(+) for

147 region (~pH 2), however the genome lacks the H(+)/K(+) ATPase characteristic of the mammalian gastric

148 ng isolated tissues suggest that the colonic H, K-ATPase (cHKA), expressed in the colon and kidney, p

149 n of hepcidin and hydrogen potassium ATPase (H,K-ATPase) compared to those on a regular diet.

150 t 177 amino acids of the beta subunit of the H,K-ATPase containing five N-linked glycosylation consen

151 protein and syntaxin 3, were associated with H+/K(+)-ATPase-containing tubulovesicles while the remai

152 d secretion by preventing the recruitment of H,K-ATPase-containing tubulovesicles to the apical membr

153 Whereas the H,K-ATPase contains a plasma membrane targeting motif, t

154 idues in the Na,K-ATPase sequence with their H,K-ATPase counterparts (L319F, N326Y, T340S) and replac

155 n which these residues are replaced by their H,K-ATPase counterparts either singly or in combinations

156 ly localized in chick embryos, an endogenous H+/K+-ATPase-dependent difference in membrane voltage po

157 s demonstrated that the alpha subunit of the H, K-ATPase encodes localization information responsible

158 mediating autoimmune gastritis, we isolated H/K ATPase-enriched preparations of parietal cell micros

159 cid secretion by LPS is due to inhibition of H/K-ATPase enzymatic function or changes in cytoskeletal

160 Taken together, these results indicate that H(+),K(+)-ATPases-especially the HKalpha(2)-containing H

161 d secretion through the omeprazole-sensitive H+,K+ -ATPase even in the absence of the classical stimu

162 Immunofluorescence labeling detected the H-K-ATPase exclusively on the apical pole of gastric par

163 eptides resolved from the [14C]DCCD-modified H,K-ATPase exhibited various K+ sensitivities with pepti

164 gastric acid secretion through induction of H(+)/K(+)-ATPase expression.

165 asolateral membranes or an alternate mode of H,K-ATPase expression.

166 gnized in other members of the Na+-K+-ATPase/H+-K+-ATPase family.

167 ates of NTP hydrolysis and H+ pumping by the H,K-ATPase for CTP are about 10% of those for ATP and un

168 etal cells resulting in the incorporation of H+/K(+)-ATPase from a cytoplasmic membrane pool, the tub

169 , the stimulation-mediated relocation of the H,K-ATPase from the cytoplasmic membrane compartment to

170 in exocytic recruitment of the proton pump (H(+),K(+)-ATPase) from a pool of intracellular membranes

171 os requires gap junctional communication and H,K-ATPase function.

172 We examined the role of Akt in H(+)/K(+)-ATPase gene expression by Northern blotting us

173 d on H+-ATPase (H flux), and 35% depended on H+,K+-ATPase (H,K flux).

174 n (an alpha subunit of the human non-gastric H,K-ATPase) has previously been shown to assemble with t

175 he alpha subunits of the Na+,K+ -ATPases and H+,K+ -ATPases have a protein kinase A (PKA) consensus s

176 In this family, only Na,K- and H,K-ATPases have been shown to have a second subunit, a

177 trated that the alpha-subunit of the colonic H+, K+-ATPase (HKalpha2) requires coexpression with a be

178 cent studies have suggested that the colonic H+,K+-ATPase (HKalpha2) can secrete either Na+ or H+ in

179 sus site of the alpha subunit of the colonic H+,K+ -ATPase [HKalpha2]) to alanine (S955/A) or asparti

180 To study this question, we generated an H(+)/K(+)-ATPase-IFN-gamma transgenic mouse that overexp

181 + recycling for the recently proposed apical H+ -K+ -ATPase in Calu-3 cells.

182 ) and wheat germ agglutinin (anti-beta), the H+, K(+)-ATPase in its native state exists in a dimeric

183 cts by irreversibly blocking ATP4A, a P-type H+/K+ ATPase in gastric parietal cells.

184 rane segments (TM4) of the Na,K- and gastric H, K-ATPases in determining the distinct cation selectiv

185 New models of the gastric H,K ATPase in the E1K and E2P states are presented as th

186 [14C]DCCD was incorporated into the H,K-ATPase in a time course identical to that describing

187 Here we present homology modeling of the H,K-ATPase in the E(2)-P conformation as a means of pred

188 llowing trypsinization of the intact gastric H,K-ATPase in the presence of K+ ions, identified as M1M

189 intracellular compartments that contain the H,K-ATPase in unstimulated gastric parietal cells.

190 , H/K ATPase, and aberrant expression of the H/K ATPase in the neonatal thymus prevents the induction

191 singly, immunization with the AIG target Ag, H/K ATPase, in IFA failed to induce disease in normal an

192 hat functional differences between Na,K- and H,K-ATPase, including differences in ion transport speci

193 In either the absence or presence of the H(+),K(+)-ATPase inhibitor omeprazole (60 mg kg(-1) I.P.

194 In rats treated for up to 5 days with the H(+)-K(+)-ATPase inhibitor omeprazole, VMAT2, histidine

195 The H,K-ATPase inhibitor Sch 28080 (1 to 10 microM) abolishe

196 h 28080 and A80915a (a structurally distinct H,K-ATPase inhibitor) significantly inhibited K(Na) in t

197 is series to reasonably predict the in vitro H+/K(+)-ATPase inhibitory potency in the purified enzyme

198 is associated with reinternalization of the H/K-ATPase into an intracellular storage compartment.

199 tion of acid secretion involves insertion of H/K-ATPase into the parietal cell plasmalemma, while its

200 ion and insertion of the proton pump enzyme, H,K-ATPase, into the apical plasma membrane of parietal

201 RNA interference of the H(+),K(+)-ATPase ion pump results in membrane hyperpolar

202 Thus, alpha,beta H(+),K(+)-ATPase is active at least in detergent and may

203 Gastric H(+),K(+)-ATPase is inhibited by SCH28080, which has no

204 H+/K(+)-ATPase is the proton pump in the gastric parieta

205 Acid transport by the gastric H, K-ATPase is covalently inhibited by several substitut

206 Gastric H,K-ATPase is an electroneutral transmembrane pump that

207 The gastric H,K-ATPase is covalently inhibited by substituted pyridy

208 the data show that neither NHE2 nor colonic H,K-ATPase is essential for initiation of TGF responses.

209 re, that the cation selectivity of Na,K- and H,K-ATPase is generated through a cooperative effort bet

210 The gastric H,K-ATPase is inhibited selectively and K(+)-competitive

211 The gastric H,K-ATPase is related to other cation transport ATPases,

212 The gastric H,K-ATPase is responsible for acid secretion by parietal

213 The beta-subunit of the gastric H,K-ATPase is the most abundant glycoprotein in the tubu

214 The integral membrane protein, the gastric H,K-ATPase, is an alpha-beta heterodimer, with 10 putati

215 Two distinct H,K-ATPase isoforms exist; one of which, the ouabain-ins

216 The H,K-ATPase kinetics were unaffected by the introduction

217 TGF responses in NHE2 and colonic H,K-ATPase knockout mice were not different from those o

218 kt inhibited EGF, but not Shh stimulation of H(+)/K(+)-ATPase-luciferase activity.

219 DOCP treatment increased the rate of H(+),K(+)-ATPase-mediated H(+) secretion in intercalated

220 Proteins implicated in H-K-ATPase membrane trafficking include myosin IIB, F-ac

221 ve suggested that the membrane-bound gastric H,K-ATPase might be a dimeric alpha,beta-heterodimer.

222 each of the proteolytic preparations of the H,K-ATPase modified by [14C]DCCD.

223 a+ channel activity is increased and colonic H+,K+-ATPase mRNA is massively induced.

224 Maternal H+/K+-ATPase mRNA is symmetrically expressed in the 1-ce

225 Furthermore, changes in H/K-ATPase mRNA expression may not be related to changes

226 The H+-K+-ATPase of renal collecting duct mediates K+ conser

227 The H,K-ATPase of the gastric parietal cell is the most crit

228 Gastric acid secretion is mediated by the H/K-ATPase of parietal cells.

229 present in the alpha subunit of the gastric H,K-ATPase, of which 10 are found in the predicted trans

230 during exposure to inhibitors of the apical H(+)/K(+) ATPase (omeprazole and SCH28080), thereby unma

231 d pp75/Rip11 also coenriched with Rab11a and H(+)K(+)-ATPase on parietal cell tubulovesicles, and Rab

232 It has been proposed that apical colonic H,K-ATPase, perhaps in concert with the Na/H exchanger (

233 ATPases-especially the HKalpha(2)-containing H(+),K(+)-ATPases-play an important role in the effects

234 d CD80 and CD86 expression on the surface of H+/K+ ATPase presenting DC in vitro.

235 ve T cells, and appear to do so by acting on H+/K+ ATPase presenting dendritic cells (DC).

236 effect of EGF on both aminopyrine uptake and H(+)/K(+)-ATPase production, measured by Western blots w

237 H(+)/K(+)-ATPase protein was found within vesicular comp

238 es of Pi per hour per milligram of expressed H+,K+-ATPase protein), apparent Km for ammonium (a K+ su

239 rom rat colon which were enriched in colonic H+,K+-ATPase protein.

240 ell receptor specific for a peptide from the H(+)/K(+) ATPase proton pump, a protein expressed by par

241 The H(+),K(+)-ATPase pumps protons or hydronium ions and is

242 ), and apparent Ki for SCH28080 equal to the H+, K+-ATPase purified from hog gastric mucosa.

243 ologic or genetic perturbation of endogenous H+/K+-ATPase randomized the sided pattern of asymmetrica

244 Characterizations of the H/K ATPase-reactive and self-reactive T cell populations

245 It is likely that the H/K ATPase-reactive T cells are actually the effector ce

246 generated two homology models of the gastric H+/K+-ATPase reflecting the E1 and E2 conformations adop

247 Thus, the human nongastric H,K-ATPase represented by the recombinant Atp1al1-betaHK

248 upport the recruitment and redistribution of H,K-ATPase-rich membranes, including those involved in s

249 ion-associated redistribution of VAMP-2 from H,K-ATPase-rich tubulovesicles to co-localize with SNAP-

250 ne and VAMP-2 is associated with cytoplasmic H,K-ATPase-rich tubulovesicles.

251 cells requires trafficking and exocytosis of H/K-ATPase-rich tubulovesicles (TVs) toward apical membr

252 ) M), H+-ATPase (bafilomycin, 10(-7) M), and H+-K+-ATPase (Sch 28080 [10(-5) M] and ouabain [10(-3) M

253 ive, K+-competitive inhibitor of the gastric H+,K+ ATPase, SCH28080.

254 n both of its flanking sequences derive from H,K-ATPase sequence.

255 branes expressing the chimera with the colon H,K-ATPase sequence.

256 d tryptic fragments of detergent-solubilized H, K-ATPase showed that a fragment Leu855 to Arg922 of t

257 H+/K+ ATPase specific iTregs were able to inhibit the in

258 ate proliferation and cytokine production by H+/K+ ATPase specific T cells.

259 the process of peripheral clonal deletion of H(+)/K(+) ATPase-specific CD4 T cells or promote the dev

260 H/K ATPase-specific T cell proliferative responses could

261 Poised in the middle of these, the H,K-ATPase substitutes lysine in place of a serine impli

262 Although H+/K+-ATPase subunit mRNAs are symmetrically localized i

263 LPS increased alpha- and beta-H/K-ATPase subunit mRNA expression (Northern blot) in th

264 or changes in cytoskeletal rearrangements in H/K-ATPase subunits rather than by down-regulation of tr

265 as in all LPS-treated rats, it appeared that H/K-ATPase subunits remained within the tubulovesicles.

266 ased staining in the secretory membranes for H/K-ATPase subunits whereas in all LPS-treated rats, it

267 K+-ATPase or the beta-subunit of the gastric H+,K+-ATPase, suggesting that different beta-subunits ma

268 s activated in the parietal cell converge on H K -ATPase that catalyzes the exchange of luminal K for

269 We detected a ouabain-sensitive (nongastric) H+,K+-ATPase that acidified ASL, but its activity was no

270 of hitherto unknown human ouabain-sensitive H,K-ATPase that represents a novel third group of X,K-AT

271 at determine the trafficking and activity of H K -ATPase, the proton pump of the parietal cell.

272 Hence, in the H(+),K(+)-ATPase, the ability of the M8 arginine to dona

273 Whether mineralocorticoids act through H(+),K(+)-ATPases to maintain K(+) and acid-base homeost

274 contribution of a SCH28080-sensitive apical H(+)-K(+)-ATPase to basal intracellular pH regulation an

275 cking events in the regulated recruitment of H+/K(+)-ATPase to the plasma membrane after parietal cel

276 rid analysis were carried out on the gastric H,K-ATPase to determine interactive regions of the extra

277 reciprocal change in the sensitivity of the H,K-ATPase to K+ and SCH 28080.

278 present studies examine the contribution of H,K-ATPase to this ouabain-insensitive Cl absorption and

279 cific for the gastric parietal cell antigen, H(+)K(+)-ATPase, to induce autoimmune gastritis after tr

280 Rab11-FIP2 translocated with Rab11a and the H(+)K(+)-ATPase upon stimulating parietal cells with his

281 this residue in SCH28080 selectivity of the H,K-ATPase versus Na,K-ATPase.

282 When the gastric H+, K(+)-ATPase was solubilized by n-dodecyl beta-D-malt

283 s prepared and reversal of inhibition of the H+,K+-ATPase was measured as the time-dependent restorat

284 The K+-dependent ATPase activity of the H,K-ATPase was irreversibly inhibited by the carboxyl ac

285 onent of the [14C]DCCD incorporated into the H,K-ATPase was K+-sensitive where K+ reduced the [14C]DC

286 FPIP), a reversible inhibitor of the gastric H+/K+-ATPase, was retained in its predefined conformatio

287 Both subunits of the parietal cell H+/K+-ATPase were present, and both partially colocalize

288 the noncatalytic beta subunit gene of mouse H+/K+-ATPase were used to direct expression of an attenu

289 20, Asp824, Glu936, and unique Lys791 in the H,K-ATPase were mutated, and the effects of mutations on

290 recognized in autoimmune gastritis, gastric H(+)/K(+) ATPase, which is naturally expressed in the st

291 ation of gastric parietal cell (PC)-specific H(+)/K(+)-ATPase, which induces a destructive autoimmune

292 we have identified a portion of the gastric H,K-ATPase, which is sufficient to redirect the normally

293 However, we observed that H,K-ATPase will catalyze NTP/ADP phosphate exchange at s

294 how pure and functionally active pig gastric H(+),K(+)-ATPase with an apparent Stokes radius of 6.3 n

295 iated by the parallel operation of an apical H,K-ATPase with an apical Cl-HCO3 exchanger and that the

296 ene belongs to the family of Na,K-ATPase and H,K-ATPase (X,K-ATPases) genes.