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 in epithelial cells contributes to electro

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

4 ENaC belongs to the degenerin/ENaC protein family and is

5 ENaC functional expression was decreased by DeltaKEEL ER

6 ENaC internalization by SPX-101 in primary human bronchi

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

8 ENaC is probably a heterotrimer consisting of three well

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 ed here to directly quantify possible PIP(2)-ENaC interactions.

12 -ENaC subunits as being important for PIP(2)-ENaC interactions.

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 also show that bilirubin conjugates activate ENaC.

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

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

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

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

21 have reduced membrane permeability, affected ENaC activity more strongly than did their more membrane

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

23 show that protons interfere with allosteric ENaC inhibition by extracellular sodium ions, thereby in

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

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

26 To verify that the GNPs and alpha-ENaC antibodies formed conjugates (GNPs-antiENaC) that m

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

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

29 or kidney tubule-specific beta-ENaC or alpha-ENaC knockout mice did not alter claudin-8 abundance.

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 t was not observed in Xenopus alphabetagamma-ENaC or human ENaC orthologs.

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

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

36 9 overexpression did not significantly alter ENaC functional expression.

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

38 postprandial Sprague Dawley rats to analyze ENaC expression and activity.

39 hesis that NLRP3 inflammasome activation and ENaC upregulation drives exaggerated innate-immune respo

40 f the intricate interactions between DGK and ENaC and is consistent with available literature data.

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

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

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

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

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

46 dneys significantly affected CFTR, NHE3, and ENaC, altering the cyst phenotype from one poised toward

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

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

49 +)/2Cl(-) (NKCC1/SLC12A2) co-transporter and ENaC are targets of Nedd4L in the colon.

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

51 Again, beta-ENaC expression at the apical surface was unaltered by e

52 functional expression without altering beta-ENaC expression at the apical surface.

53 onal expression, again without altering beta-ENaC expression at the apical surface.

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

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

56 local conformation of the N terminus of beta-ENaC, and two sites of gamma-ENaC adjacent to the plasma

57 Overexpression of beta-ENaC, in the absence of CFTR dysfunction, increased NLRP

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

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

60 nit silencing or kidney tubule-specific beta-ENaC or alpha-ENaC knockout mice did not alter claudin-8

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

62 ur data reveal the specific coupling between ENaC gamma-subunit and claudin-8 expression.

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

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

65 nels to include the epithelial Na(+) channel ENaC.

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

67 0) report that the epithelial sodium channel ENaC, which serves as the salty receptor, is co-expresse

68 nduced increase in epithelial Na(+) channel (ENaC) activity in the cortical collecting duct.

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

70 nonical vertebrate epithelial Na(+) channel (ENaC) formed by alpha-, beta-, and gamma-subunits is a s

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

72 ce overexpress the epithelial Na(+) channel (ENaC) in their lungs, driving increased sodium absorptio

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

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

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

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

77 ular loops of the epithelial sodium channel (ENaC) alpha and gamma subunits increases the channel's o

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

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

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

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

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

83 expression in the epithelial sodium channel (ENaC) in membrane platelets can be related with the pres

84 The epithelial sodium channel (ENaC) is present in the apical membrane of sodium-absorb

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

86 The epithelial sodium channel (ENaC) mediates Na(+) transport in several epithelia, inc

87 n or silencing of epithelial sodium channel (ENaC) subunits and claudin-8 affect paracellular permeab

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

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

90 nsulin to augment epithelial sodium channel (ENaC) transport.

91 o-localization of epithelial sodium channel (ENaC) with the plasma membrane was reduced in cysts in p

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

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

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

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

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

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

98 activation of the epithelial sodium channel (ENaC).

99 or (CFTR) and the epithelial sodium channel (ENaC).

100 nnels (ASICs) and epithelial sodium channel (ENaCs), these channel families display very different fu

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

102 dysregulation of epithelial sodium channels (ENaC).

103 the activity of epithelial sodium channels (ENaC).

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

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

106 e-sensitivity in epithelial sodium channels (ENaCs) are not fully understood.

107 t this regulation is distinct from classical ENaC regulation by RAAS.

108 ng and found that KDEL-R depletion decreases ENaC functional expression, again without altering beta-

109 emonstrated to interact with ENaC, decreases ENaC functional expression without altering beta-ENaC ex

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

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

112 Here, we functionally characterize a DEG/ENaC channel from the early-diverging animal Trichoplax

113 ons (TRNs), and is dependent on MEC-4, a DEG/ENaC channel.

114 the degenerin/epithelial sodium channel (DEG/ENaC) family activate in response to extracellular proto

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

116 enerin/epithelial sodium channel family (DEG/ENaC).

117 C6 was potently activated by the general DEG/ENaC channel blocker amiloride, a rare feature only repo

118 ver, this study offers new insights into DEG/ENaC activation by highlighting a novel means of regulat

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

120 For many DEG/ENaC channels, extracellular Ca(2+) ions modulate gating

121 re detected by distinct mechanosensitive DEG/ENaC/ASIC channels, which trigger distinct cellular outp

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

123 ton, Ca(2+), and amiloride regulation of DEG/ENaC channels and insight into the possible core-gating

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

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

126 r proton and Ca(2+) sensitivity in other DEG/ENaC channels, and a mutation of one conserved residue (

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

128 We found that the DEG/ENaC channel ppk301 and sensory neurons expressing ppk30

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

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

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

132 of the epithelial sodium channel/degenerin (ENaC/DEG) superfamily of ion channels and are expressed

133 ENaC belongs to the degenerin/ENaC protein family and is the only member that opens wi

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

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

136 We propose that Xenopus deltabetagamma-ENaC can serve as a model for investigating ENaC transfo

137 , we demonstrate that Xenopus deltabetagamma-ENaC is profoundly activated by extracellular acidificat

138 oal of this study was to test Nox4-dependent ENaC regulation in two models: SS hypertension and STZ-i

139 Importantly, diminished ENaC activity correlates with improved airway hydration

140 and increased open probability by directing ENaC to the Golgi via coat complex II (COP II) during bi

141 During ENaC biogenesis, such cleavage is regulated by the novel

142 inflammation, indicating that dysregulated, ENaC-dependent signalling may drive exaggerated inflamma

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

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

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

146 ctrophysiology of Xenopus oocytes expressing ENaC isoforms assembled from alphabetagamma- or deltabet

147 Furthermore, ENaC in endothelial cells mediates vascular responsivene

148 N termini of beta- (K(d) ~5.2 mum) and gamma-ENaC (K(d) ~13 mum).

149 Sodium retention and gamma-ENaC cleavage were independent of the increased plasma l

150 in the cytosolic portions of beta- and gamma-ENaC subunits as being important for PIP(2)-ENaC interac

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

152 peptides of these regions of beta- and gamma-ENaC.

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

154 otassium diet prevented hyperkaliemia, gamma-ENaC cleavage, and led to persistent increased phosphory

155 n site within the carboxyl terminus of gamma-ENaC (K(d) ~800 mum) was also observed.

156 erminus of beta-ENaC, and two sites of gamma-ENaC adjacent to the plasma membrane, suggesting direct

157 nd cleavage and apical localization of gamma-ENaC increased in nephrotic mice.

158 ed cleavage and apical localization of gamma-ENaC persisted at day 5 in nephrotic mice when hypovolem

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

160 However, ENaC regulation by bile acids and conjugated bilirubin,

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

162 s more widespread, where, for example, human ENaC Na(+) leak channels are potentiated and mouse BASIC

163 e expressions of all three subunits of human ENaC.

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

165 rved in Xenopus alphabetagamma-ENaC or human ENaC orthologs.

166 Importantly, ENaC beta-subunit or alpha-subunit silencing or kidney t

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

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

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

170 whether such ancestral traits are present in ENaC isoforms of the aquatic pipid frog Xenopus laevis U

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

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

173 sted whether the KDEL-R itself has a role in ENaC forward trafficking and found that KDEL-R depletion

174 was enhanced by amino acid substitutions in ENaC that depress open probability and was precluded by

175 r processes and membrane proteins, including ENaC.

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

177 the cystic mice, VX-809 treatment increased ENaC levels at the apical plasma membrane consistent wit

178 esting that acute hyperinsulinemia increases ENaC activity independent of the RAAS signaling cascade.

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

180 Decreased SF-induced ENaC currents were observed following removal of the ECM

181 ol 4,5-bisphosphate (PI(4,5)P(2)) influences ENaC activity and, consequently, airway surface liquid.

182 model of hyperglycemia-induced renal injury ENaC activity in hyperglycemic animals was elevated in S

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

184 -ENaC can serve as a model for investigating ENaC transformation from a proton-activated toward a con

185 kidney tubule-specific knockout mice lacking ENaC subunits to assess the ENaC's effect on claudin-8 e

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

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

188 , bile acids both activate and inhibit mouse ENaC.

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

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

191 associated with amiloride-resistant but not ENaC fraction.

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

193 the FURIN site is critical for activation of ENaC.

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

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

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

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

198 Genetic alteration of ENaC-alpha causes aldosterone dysregulation in patients,

199 the KDEL-R plays a role in the biogenesis of ENaC and in its exit from the ER through its association

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

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

202 ws significant overlap between expression of ENaC-alpha and the viral receptor ACE2 in cell types lin

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

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

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

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

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

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

209 be driven in part by its targeted mimicry of ENaC-alpha, a protein critical for the homeostasis of ai

210 Using homology modeling of ENaC structure and site-directed mutagenesis, we identif

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

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

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

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

215 ntion, strongly influences its regulation of ENaC biogenesis.

216 the KDEL receptor to exert its regulation of ENaC biogenesis.

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

218 sults demonstrate that insulin regulation of ENaC is a potential mechanism to preserve sodium and vol

219 Whether PIP(2) regulation of ENaC is due to a direct phospholipid-protein interaction

220 ults strongly suggest that the regulation of ENaC is primarily exerted through the control of PI(4,5)

221 eting hypotheses regarding the regulation of ENaC.

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

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

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

225 Here we describe the structure of ENaC resolved by cryo-electron microscopy at 3 angstrom.

226 in the biogenesis and forward trafficking of ENaC.

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

228 iated pathway in maladaptive upregulation of ENaC-mediated sodium reabsorption in the distal nephron

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

230 ligase protein which regulates the number of ENaCs at the plasma membrane.

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

232 , consistent with an effect of bile acids on ENaC open probability.

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

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

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

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

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

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

239 ered the location of CFTR but not of NHE3 or ENaC in normal mice.

240 ee of selectivity for sodium over potassium, ENaCs are constitutively active and display a remarkably

241 utionarily conserved activity of presynaptic ENaC channels in both Drosophila and mouse.

242 ERp29 may promote ENaC cleavage and increased open probability by directin

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

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

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

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

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

248 yme of the phosphoinositide pathway, reduces ENaC function.

249 erparts, suggesting that bile acids regulate ENaC extracellularly.

250 Numerous factors regulate ENaC activity, including extracellular ligands, post-tra

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

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

253 Bile acids also regulated ENaC in a cortical collecting duct cell line, mirroring

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

255 These results support that PIP(2) regulates ENaC activity by directly interacting with at least thre

256 tical role of the alpha2 helix in regulating ENaC function.

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 Conditional kidney tubule-specific ENaC gamma-subunit knockout mice displayed decreased cla

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

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

265 We found that after carbohydrate stimulus, ENaC open probability increased in split-open isolated c

266 sed system to express and functionally study ENaC, we found that, depending on the bile acid used, bi

267 man epithelial sodium channel alpha-subunit (ENaC-alpha).

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

269 Previously, we demonstrated that ENaC subunits - alpha, beta, and gamma - assemble in a c

270 Here, we provide evidence that ENaC's ability to mediate SF responsiveness relies on th

271 This study hypothesized that ENaC contributes to the increase in renal sodium reabsor

272 We hypothesized that ENaC evolved from a proton-activated sodium channel pres

273 These results indicate that ENaC responds to compounds abundant in bile and that the

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

275 (GNPs) conjugated to an antibody against the ENaC present on platelets.

276 out mice lacking ENaC subunits to assess the ENaC's effect on claudin-8 expression.

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

278 on-specific deletion of Scnn1a, encoding the ENaC channel alpha subunit.

279 umber of larger, aromatic side chains in the ENaC M2 helix may contribute to the constitutive activit

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

281 Overexpression or silencing of the ENaC gamma-subunit was associated with parallel and spec

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

283 shear force (SF) sensor and a member of the ENaC/degenerin protein family.

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

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

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

287 We also found that H(2) O(2) upregulated ENaC activity, and H(2) O(2) production was reduced in b

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

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

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

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

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

293 open isolated collecting duct tubules, while ENaC protein levels remained unchanged.

294 To date, possible interaction of PIP(2) with ENaC primarily has been tested indirectly through assays

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 we previously demonstrated to interact with ENaC, decreases ENaC functional expression without alter

299 of PIP(2) is necessary for interaction with ENaC.

300 transport in the distal colon together with ENaC.