ライフサイエンスコーパス: ENaC

1 ENaC activation by DHHCs was lost when gamma subunit pal

2 ENaC activity was significantly increased by DHHCs 1, 2,

3 ENaC and HDAC7 form a complex, as detected by coimmunopr

4 ENaC belongs to a family of ion channels that sense the

5 ENaC internalization by SPX-101 in primary human bronchi

6 ENaC is a trimer of three homologous subunits (alpha, be

7 ENaC is probably a heterotrimer consisting of three well

8 ENaC is regulated in part through signaling pathways tha

9 ENaC represents a therapeutic target to treat all patien

10 n H441 cells overexpressing wild type and 1M ENaC-alpha channels, but not 3M or 2M ENaC-alpha channel

11 3M and 2M ENaC-alpha, but not 1M ENaC-alpha, displayed significantly reduced binding capa

12 3M and 2M ENaC-alpha, but not 1M ENaC-alpha, displayed significant

13 and 1M ENaC-alpha channels, but not 3M or 2M ENaC-alpha channels.

14 ilar in cells overexpressing either WT or 3M ENaC-alpha subunits.

15 ated to elucidate the pathogenesis of absent ENaC function in the MG and associated ocular surface di

16 The serine protease trypsin I can activate ENaC in vitro but is unlikely to be the physiologically

17 C and that trypsin IV and trypsin I activate ENaC by cleavage at distinct sites.

18 ficity has previously been shown to activate ENaC in CF airways.

19 , whereas DHHCs 1, 2, and 14 still activated ENaC lacking beta subunit palmitoylation sites.

20 tic systems, increased fluid depth activates ENaC and decreased depth inhibits it, suggesting that se

21 ggesting that secretion indirectly activates ENaC to reduce ASL depth.

22 iologically relevant protease that activates ENaC in CF airways.

23 of the lectin-like domain of TNF, activates ENaC by binding to glycosylated residues in the extracel

24 In airways, ENaC is mainly responsible for fluid absorption, while a

25 g increase in beta and gamma (but not alpha) ENaC mRNA and protein expression and ENaC activity.

26 alpha-ENaC protein was reduced, whereas phosphorylation of the

27 d phosphorylation of AMPK and decrease alpha-ENaC expression in cortical collecting duct cells.

28 tal and cell-surface NHE3, NKCC2, NCC, alpha-ENaC and cleaved gamma-ENaC compared to NSD.

29 PK abolished the effect of caffeine on alpha-ENaC.

30 The renal alpha-ENaC expression and ENaC activity of rats decreased afte

31 e ability to silence expression of the alpha-ENaC subunit gene.

32 nts in H441 monolayers and of alphabetagamma-ENaC channel activity in oocytes.

33 However, AnkG did alter ENaC insertion from constitutive recycling pathways.

34 AnkG did not alter ENaC delivery to the membrane from biosynthetic pathways

35 rectly regulates Na(+) transport by altering ENaC activity in the apical membrane.

36 l surface, it is unknown how [Na(+)]i alters ENaC cleavage.

37 The demonstration that amiloride, an ENaC inhibitor, lowers the blood pressure of hypertensiv

38 we demonstrate that utilization of either an ENaC blocker or a COX-2 inhibitor results in a marked re

39 Both our structural model of an ENaC alpha subunit and the resolved structure of an acid

40 channel (ENaC) and reductions in ERK1/2 and ENaC subunit phosphorylation.

41 C7 overexpression reduced ENaC abundance and ENaC current, whereas ENaC abundance and current were in

42 f the renal outer medullary K(+) channel and ENaC, to which angiotensin II may contribute.

43 The renal alpha-ENaC expression and ENaC activity of rats decreased after chronic caffeine a

44 alpha) ENaC mRNA and protein expression and ENaC activity.

45 rin-positive intercalated cells (PP-ICs) and ENaC subunits in principal cells (PCs).

46 retion of a saline load and enhances NCC and ENaC abundance and activation, which may facilitate K(+)

47 ithin the DCT2, we hypothesized that NCC and ENaC interactions might be modulated by aldosterone (Ald

48 do promotes increased interaction of NCC and ENaC, within the DCT2 revealing a novel method of regula

49 of RhoA and increased TGF-beta signaling and ENaC activity.

50 he DCT gradually restored ASDN structure and ENaC and ROMK expression, concurrent with the restoratio

51 +)/2Cl(-) (NKCC1/SLC12A2) co-transporter and ENaC are targets of Nedd4L in the colon.

52 epithelial Na(+) absorption by antagonizing ENaC ubiquitination.

53 educed renal creatinine clearance and apical ENaC localization, and caused severe hyperkalemia in AS(

54 generate a coordinated stimulation of apical ENaC and basolateral Na(+),K(+)-ATPase.

55 gional pulmonary function assessment in beta-ENaC-overexpressing mice, a well-established model of lu

56 d marked heterogeneous lung function in beta-ENaC-Tg mice compared to wild-type littermate controls;

57 The peptide increases survival of beta-ENaC-transgenic mice to greater than 90% with once-daily

58 utic effect was assessed by survival of beta-ENaC-transgenic mice, mucus transport in these mice, and

59 PX-101 increased mucus transport in the beta-ENaC mouse model as well as the sheep model of CF.

60 ent of hormonal stimulus, cross-talk between ENaC and Na,K-ATPase coordinates Na(+) transport across

61 Mutation of Cys that blocked ENaC palmitoylation also reduced channel open probabilit

62 beta subunit palmitoylation was increased by ENaC co-expression with DHHC 7.

63 Instead, pendrin changes ENaC abundance and function at least in part by altering

64 sterone-induced Na(+) absorption by changing ENaC abundance and function through a kidney-specific me

65 ding the alpha-subunit of the sodium channel ENaC in cell lines and primary epithelial cells, in subm

66 d cleaved forms of epithelial Na(+) channel (ENaC) alpha and gamma subunits, which associated with a

67 The renal epithelial Na(+) channel (ENaC) expression and function were measured by in vivo a

68 Epithelial Na(+) channel (ENaC) function is regulated by the intracellular Na(+) c

69 The epithelial Na(+) channel (ENaC) functions as a pathway for Na(+) absorption in the

70 The epithelial Na(+) channel (ENaC) has a key role in the regulation of extracellular

71 s stability of the epithelial Na(+) channel (ENaC) in salt-absorbing epithelia in the kidney, lung, a

72 nephron where the epithelial Na(+) channel (ENaC) is expressed, we hypothesized that PON-2 would sim

73 BSTRACT: All three epithelial Na(+) channel (ENaC) subunits (alpha, beta and gamma) are located in va

74 The epithelial Na+ channel (ENaC) is essential for Na+ homeostasis, and dysregulatio

75 te-limited by the epithelial sodium channel (ENaC) activity in lung, kidney, and the distal colon.

76 Conversely, epithelial sodium channel (ENaC) activity was largely preserved, suggesting that th

77 (MRs) to increase epithelial sodium channel (ENaC) activity.

78 pically expressed epithelial sodium channel (ENaC) and basolaterally localized Na(+)-K(+)-ATPase in t

79 iloride-sensitive epithelial sodium channel (ENaC) and characterized by neonatal life-threatening hyp

80 yperactive kidney epithelial sodium channel (ENaC) and reductions in ERK1/2 and ENaC subunit phosphor

81 nd attenuation of epithelial sodium channel (ENaC) and ROMK expression and apical localization.

82 regulation of the epithelial sodium channel (ENaC) and the Ca(2+)-activated K(+) channel BKCa.

83 ed with increased epithelial sodium channel (ENaC) expression in lung and kidney.

84 The epithelial sodium channel (ENaC) has an important role in regulating extracellular

85 Inhibitors of the epithelial sodium channel (ENaC) have therapeutic potential in CF airways to reduce

86 The epithelial sodium channel (ENaC) is a member of the ENaC/degenerin ion channel fami

87 The epithelial sodium channel (ENaC) is activated upon endoproteolytic cleavage of spec

88 The epithelial sodium channel (ENaC) is composed of three homologous subunits (alpha, b

89 The epithelial sodium channel (ENaC) is the limiting entry point for Na(+) reabsorption

90 The epithelial sodium channel (ENaC) of the kidney is necessary for extracellular volum

91 The renal epithelial sodium channel (ENaC) provides regulated sodium transport in the distal

92 tion mutations in epithelial sodium channel (ENaC) subunits exhibit meibomian gland (MG) dysfunction.

93 alpha- and gamma-epithelial sodium channel (ENaC) subunits from the discovery set were verified usin

94 the expression of epithelial sodium channel (ENaC) subunits in enterocytes (ECs) to maintain osmotic

95 regulation of the epithelial sodium channel (ENaC) sufficient to increase the electrochemical driving

96 ter (NCC) and the epithelial sodium channel (ENaC), are regulated is paramount.

97 ely regulates the epithelial sodium channel (ENaC), Na(+)/Cl(-) cotransporter (NCC), and with no-lysi

98 porter (NCC), the epithelial sodium channel (ENaC), the renal outer medullary potassium channel (ROMK

99 sodium taste, the epithelial sodium channel (ENaC), throughout development dramatically impacted the

100 Regulation of the epithelial sodium channel (ENaC), which regulates fluid homeostasis and blood press

101 iloride-sensitive epithelial sodium channel (ENaC).

102 ue feature of the epithelial sodium channel (ENaC).

103 ma-subunit of the epithelial sodium channel (ENaC).

104 activation of the epithelial sodium channel (ENaC).

105 n, mainly via the epithelial sodium channel, ENaC.

106 ical membrane via epithelial Na(+) channels (ENaC) and is extruded into the interstitium by Na,K-ATPa

107 mediated by both epithelial Na(+) channels (ENaC) and Na-H exchangers (NHE), inhibition of NHE-media

108 regulates human epithelial sodium channels (ENaC) in H441 and expressed in Xenopus oocytes and expos

109 gradient through epithelial sodium channels (ENaC).

110 Epithelial Na(+) channels (ENaCs) are members of the ENaC/degenerin family of ion c

111 nce suggests that epithelial Na(+) channels (ENaCs) in the brain play a significant role in the regul

112 s is mediated by epithelial sodium channels (ENaCs) and causes increased secretion of proinflammatory

113 k3 increased and depletion of Ank3 decreased ENaC-mediated sodium transport in mCCD cells.

114 salveolar Na(+) transport, through decreased ENaC activity and enhanced membrane depolarization, and

115 als that RhoGDIalpha significantly decreases ENaC current density and prevents its up-regulation by R

116 nd membrane expression, both of which define ENaC activity, following addition of TIP peptide.

117 Deg/ENaC channels are characterized by a trimeric subunit co

118 nterestingly, the balboa locus encodes a DEG/ENaC ion channel subunit highly similar in amino acid se

119 the degenerin/epithelial sodium channel (DEG/ENaC) family are broadly expressed in epithelial and neu

120 the degenerin/epithelial Na(+) channel (Deg/ENaC) family of ion channels.

121 the degenerin/epithelial sodium channel (DEG/ENaC) family.

122 ing degenerin/epithelial sodium channel (DEG/ENaC) proteins MEC-4 and MEC-10.

123 alian nicalin may have a similar role in DEG/ENaC biology, therefore influencing pathological conditi

124 Many Deg/ENaC channels contain regulatory domains and sequence mo

125 fic neurophysiological functions of most DEG/ENaC-encoding genes remain poorly understood.

126 Two members of the pickpocket family of DEG/ENaC channel subunits (ppk23 and ppk29) are required to

127 t model for deciphering the functions of DEG/ENaC genes because its genome encodes an exceptionally l

128 encodes an exceptionally large number of DEG/ENaC subunits termed pickpocket (ppk) 1-31 Here we demon

129 Together, our data indicate that DEG/ENaC ion channels play a fundamental role in the postsyn

130 In these neurons, the loss of the DEG/ENaC channel PPK19 function also eliminated the cellular

131 hanotransduction channel formed from the DEG/ENaC proteins MEC-4 and MEC-10.

132 oral approaches, we demonstrate that the DEG/ENaC-encoding gene pickpocket 29 contributes to baseline

133 ceptors led us to hypothesize that these DEG/ENaC subunits form an ion channel complex in vivo.

134 of degenerin/epithelial sodium channels (DEG/ENaCs) is composed of diverse animal-specific, non-volta

135 y-dependent mechanism required the Degenerin/ENaC sodium channel MEC-4, the L-type voltage-gated calc

136 ent genetic recombination strategy to delete ENaC function after terminal field maturation occurred.

137 More specifically, deleting ENaCs during development prevented the normal maturation

138 F508del homozygotes) were used to determined ENaC activity (Ussing chamber recordings), ASL height (c

139 Importantly, diminished ENaC activity correlates with improved airway hydration

140 ediated CAP inhibition results in diminished ENaC-mediated Na(+) absorption in CF airway epithelial c

141 However, K(+) restriction also enhanced ENaC expression in Nedd4L(Pax8/LC1) mice, and treatment

142 ), a histone deacetylase inhibitor, enhanced ENaC acetylation and increased ENaC abundance in the tot

143 The enhanced ENaC current contributed to the more depolarized basal m

144 ch also absorbs salt and fluid and expresses ENaC, is unknown.

145 idic cleft is a key ligand binding locus for ENaC and perhaps other members of the ENaC/degenerin fam

146 findings provide an allosteric mechanism for ENaC activation regulated by the N termini and sheds lig

147 Moreover, both alpha- and gamma-ENaC transcripts were down-regulated.

148 E3, NKCC2, NCC, alpha-ENaC and cleaved gamma-ENaC compared to NSD.

149 ity of extracellular cleavage sites in gamma-ENaC.

150 roteolysis is dependent on Tyr(370) in gamma-ENaC.

151 elical propensity in the N terminus of gamma-ENaC.

152 uitination sharply limit access of the gamma-ENaC extracellular domain to proteases.

153 ly conserved cluster of lysines in the gamma-ENaC N terminus regulates accessibility of extracellular

154 esent a structural model of heterotetrameric ENaC alpha1betaalpha2gamma that is consistent with previ

155 However, ENaCs appear to have only a minor role in the regulation

156 e expressions of all three subunits of human ENaC.

157 njugated (t-CDCA, t-CA, t-DCA) form on human ENaC in its alphabetagamma- and deltabetagamma-configura

158 clamp and flow cytometry studies--identified ENaC as the target of TGF-beta.

159 These changes were due to a change in ENaC directly rather than through alterations to the Na(

160 tential role for this histone deacetylase in ENaC regulation.

161 ics-driven model for the gain-of-function in ENaC by alphaW493R.

162 bases of pathologically linked mutations in ENaC subunits alpha, beta, and gamma are largely unknown

163 siologically relevant activating protease in ENaC-expressing tissues in vivo.

164 ivity was reduced, reflecting a reduction in ENaC surface expression.

165 ther hand, TIP peptide-mediated reduction in ENaC ubiquitination was similar in cells overexpressing

166 y, this study has identified a novel site in ENaC-alpha that is crucial for activation of the open pr

167 uman renal epithelial cells and can increase ENaC-mediated sodium transport in cultured human airway

168 tor, enhanced ENaC acetylation and increased ENaC abundance in the total cell lysate and at the cell

169 Increasing AnkG expression increased ENaC activity while depleting AnkG reduced ENaC-mediated

170 Moreover, TSA increased ENaC current in Fischer rat thyroid and kidney collectin

171 ause constitutive inactivation of individual ENaC subunits is neonatally lethal in mice.

172 ndicates that mTOR preferentially influences ENaC function.

173 d kinase 1 (SGK1), which is known to inhibit ENaC internalization and degradation; however, it is not

174 opious airway gland secretion, also inhibits ENaC-mediated absorption.

175 tension and also provides novel insight into ENaC activation, which is relevant for kidney sodium rea

176 tion (and possibly synergistic MCC) is lost, ENaC inhibition via exogenous agents may provide therape

177 At times when [Na(+)]i is low, ENaC subunits develop mature N-glycans and are processed

178 In the lung, ENaC is responsible for movement of sodium.

179 tection against neutrophil elastase-mediated ENaC activation and Pseudomonas aeruginosa exotoxin A-in

180 er beta subunit palmitoylation in modulating ENaC gating.

181 Moreover, ENaC activity did not affect the initiation, sustention,

182 s (termed DHHCs) regulate the channel, mouse ENaCs were co-expressed in Xenopus oocytes with each of

183 When overexpressed in H441 cells, 3M mutant ENaC-alpha formed functional channels with similar gatin

184 associated with amiloride-resistant but not ENaC fraction.

185 which correlated with increased abundance of ENaC in the plasma membrane and a reduction in ASL volum

186 l activation, does not mediate activation of ENaC by alphaW493R.

187 The activity of ENaC and Na,K-ATPase must be highly coordinated to accom

188 show that LPRs can modulate the activity of ENaC and this approach might be promising as co-adjuvant

189 erstanding of the regulation and activity of ENaC in VP neurons is of great interest.

190 Activity of ENaC is enhanced by proteolytic cleavage of the gamma-su

191 n increase in the expression and activity of ENaC which resulted in the steady state depolarization o

192 ctance regulator can elevate the activity of ENaC, suggesting that Drosophila could be used as a mode

193 centration may provide a useful biomarker of ENaC activation in future clinical studies.

194 Blockade of ENaC, prostaglandin synthesis, or PGE2 receptors all red

195 deficient apical orientation and cleavage of ENaC, despite the salt wasting.

196 the RhoGDIalpha/Rac1 axis in the control of ENaC and the effect of EGF on ENaC in this pathway.

197 her, the efficiency of allosteric control of ENaC proteolysis is dependent on Tyr(370) in gamma-ENaC.

198 erved residue in the extracellular domain of ENaC and likely involved in a disulfide bridge with the

199 cond transmembrane and C-terminal domains of ENaC-alpha, as a critical site for binding of the TIP pe

200 ding of structure, dynamics, and function of ENaC in its disease-causing state.

201 Hyperactivation of ENaC, which creates an osmotic gradient that pulls fluid

202 The inhibition of ENaC may have therapeutic potential in CF airways by red

203 Long-lasting inhibition of ENaC-dependent Isc was also produced by basolateral carb

204 In conclusion, lack of ENaC-mediated sodium transport along the nephron cannot

205 ylated residues in the extracellular loop of ENaC-alpha, as well as to a hitherto uncharacterized int

206 olyte imbalance partly due to malfunction of ENaC regulation.

207 ing acidic phospholipids and modification of ENaC cytoplasmic cysteine residues by palmitoylation, wh

208 ostasis through SGK1-dependent modulation of ENaC activity.

209 Using a constitutively open mutant of ENaC, we demonstrate that the augmentation of Na(+) tran

210 egulates the posttranslational processing of ENaC subunits during channel biogenesis.

211 aC ubiquitination, TSA decreased the rate of ENaC degradation.

212 e that SPX-101 promotes durable reduction of ENaC membrane concentration, leading to significant impr

213 ed Ala replacement mutants in this region of ENaC-alpha and examined its interaction with TIP peptide

214 peptide mimetic of the natural regulation of ENaC activity by short palate, lung, and nasal epithelia

215 g that PON-2 did not alter the regulation of ENaC by these factors.

216 tified CAP1/Prss8 as an in vivo regulator of ENaC in colon.

217 i uptake destroyed the polarized response of ENaC to [Ca(2+)]i.

218 PON-2 did not alter the response of ENaC to extracellular Na(+), mechanical shear stress, or

219 However, the role of ENaC deficiency remains incompletely defined, because co

220 to the pore region at the degenerin site of ENaC.

221 ays that control the ubiquitination state of ENaC lysines.

222 Stimulation of ENaC activity by bile acids is accompanied by a signific

223 onstructs blunted aldosterone stimulation of ENaC transport.

224 Because the quaternary structure of ENaC is yet undetermined, the bases of pathologically li

225 ion primarily through direct upregulation of ENaC, whereas increased BK channel expression has a less

226 take enhances the expression and activity of ENaCs, which augments synaptic drive by depolarizing the

227 ed predominantly by increasing the number of ENaCs at the surface.

228 itoylation of the beta and gamma subunits of ENaCs enhances interactions of their respective cytoplas

229 is known about the effects of bile acids on ENaC function.

230 uced the stimulatory effect of bile acids on ENaC, suggesting that this site is critical for the func

231 To determine the mechanism of AnkG action on ENaC surface number, changes in rates of internalization

232 dministration may have a polarized effect on ENaC, where apical application of ATP and the subsequent

233 ation through direct and indirect effects on ENaC, distal nephron K(+) channels, and WNK signaling.

234 the control of ENaC and the effect of EGF on ENaC in this pathway.

235 a polarized effect of increased [Ca(2+)]i on ENaC and what underlying mechanism is responsible.

236 aluated the effect of dietary salt intake on ENaC regulation and activity in VP neurons.

237 ssed or extracellular soluble proteases once ENaC resides at the cell surface.

238 s co-expressed with ENaC in Xenopus oocytes, ENaC activity was reduced, reflecting a reduction in ENa

239 s regardless of prior treatment with CFTR or ENaC inhibitors.

240 ty conformation of the channel and preserves ENaC-alpha protein expression, by means of blunting the

241 heal PLY, correlating with reduced pulmonary ENaC-alpha subunit expression.

242 owed that the mean amplitude of the putative ENaC currents was significantly greater in VP neurons fr

243 MEC-6 also reduced ENaC activity when co-expressed in Xenopus oocytes.

244 d ENaC activity while depleting AnkG reduced ENaC-mediated Na(+) transport.

245 HDAC7 overexpression reduced ENaC abundance and ENaC current, whereas ENaC abundance

246 general inhibitor of palmitoylation reduced ENaC-mediated Na(+) currents within minutes.

247 acetylation and ubiquitination; TSA reduced ENaC ubiquitination, whereas HDAC7 increased ubiquitinat

248 atch at the alpha1beta interface, we reduced ENaC activation of alphaW493R by more than 2-fold.

249 vealed that mTOR inhibition markedly reduces ENaC activity, but does not alter activity of K+ inwardl

250 By reducing ENaC ubiquitination, TSA decreased the rate of ENaC degr

251 Thus, trypsin IV may regulate ENaC function in epithelial tissues.

252 er, these results indicate that MRs regulate ENaC directly, but modulation of NCC is mediated by seco

253 thesized that PON-2 would similarly regulate ENaC expression.

254 ether, our data suggest that PON-2 regulates ENaC activity by modulating its intracellular traffickin

255 The hypothesis that [Na(+)]i regulates ENaC maturation within the biosynthetic pathways is furt

256 a physiological means of acutely regulating ENaC activity in the lung and other organs.

257 er beta subunit palmitoylation in regulating ENaC.

258 hat specific DHHCs have a role in regulating ENaC.

259 Removing ENaC from the membrane with SPX-101 causes a significant

260 lar twofold increases in amiloride-sensitive ENaC current.

261 < 0.00001, I(2) = 42%), amiloride-sensitive (ENaC) (-2.87 mV, 95% CI: -4.02 to -1.72, P < 0.00001, I(

262 This stabilizes ENaC, and hence, increases its abundance at the cell sur

263 Bile acids stimulate ENaC-mediated currents by increasing the open probabilit

264 he first time, that trypsin IV can stimulate ENaC and that trypsin IV and trypsin I activate ENaC by

265 that trypsin IV and trypsin I can stimulate ENaC heterologously expressed in oocytes.

266 onjugated bile acids significantly stimulate ENaC in the alphabetagamma- and in the deltabetagamma-co

267 Our previous study demonstrated that ENaC mediates a Na(+) leak current that affects the stea

268 We found that ENaC does indeed respond to increased [Ca(2+)]i in a pol

269 Our results indicate that ENaC responds to small changes in sodium concentration w

270 We have recently shown that ENaC activity contributes to the development of salt-ind

271 Overall, our data suggest that ENaC is regulated by [Ca(2+)]i in a polarized fashion an

272 h the five activating DHHCs, suggesting that ENaC forms a complex with multiple DHHCs.

273 The ENaC inhibitor benzamil increased basal MCCV as well as

274 Basal Isc was inhibited 20-70% by the ENaC inhibitor, benzamil.

275 activity, regardless of sodium loss, in the ENaC-mediated salt-losing PHA-1 phenotype.

276 al Na(+) channels (ENaCs) are members of the ENaC/degenerin family of ion channels that evolved to re

277 us for ENaC and perhaps other members of the ENaC/degenerin family.

278 ial sodium channel (ENaC) is a member of the ENaC/degenerin ion channel family, which also includes t

279 pulmonary edema, this binding stabilizes the ENaC-PIP2-MARCKS complex, which is necessary for the ope

280 inflammatory mediators and suggest that the ENaC pathway is a potential target for a strategy to pre

281 edd4L(Pax8/LC1) mice, and treatment with the ENaC inhibitor, benzamil, reversed excessive K(+) wastin

282 SPX-101 binds selectively to ENaC and promotes internalization of the alpha-, beta-,

283 f renal AMPK and inhibition of renal tubular ENaC.

284 Both wild type ENaC and channels lacking beta and gamma palmitoylation

285 roximal and distal components of this unique ENaC regulatory pathway in lung fluid balance.

286 ng cross-talk between apical Na(+) entry via ENaC and its basolateral exit via Na,K-ATPase, which may

287 ntake affects the activity of VP neurons via ENaC activity.

288 The PON-2 inhibitory effect was ENaC-specific, as PON-2 had no effect on functional expr

289 e aldosterone-sensitive distal nephron where ENaC is localized.

290 in the distal aspects of the nephron, where ENaCs couple the absorption of filtered Na(+) to K(+) se

291 ced ENaC abundance and ENaC current, whereas ENaC abundance and current were increased by silencing o

292 This review addresses mechanisms by which ENaC activity is regulated by extracellular factors, inc

293 o determine the molecular mechanism by which ENaC senses high external Na(+) concentrations, resultin

294 performing patch clamp experiments in which ENaC activity was measured during apical or basolateral

295 Moreover, SpO2 correlated with ENaC-associated NPD positively in patients only, but app

296 When PON-2 was co-expressed with ENaC in Xenopus oocytes, ENaC activity was reduced, refl

297 PON-2 also co-immunoprecipitated with ENaC when co-expressed in HEK293 cells.

298 herefore, increased [Na(+)]i interferes with ENaC N-glycan maturation and prevents the channel from e

299 transport in the distal colon together with ENaC.

300 e DHHC2 that also co-immunoprecipitates with ENaCs.