ライフサイエンスコーパス: Cx43

1 heart and is partly mediated by Connexin43 (Cx43).

2 tion of the gap junction protein connexin43 (Cx43).

3 and Cx45, and heterotypic Cx43/Cx45 and Cx45/Cx43).

4 of the gap junction (GJ) protein connexin43 (Cx43).

5 d binds to gap junction protein connexin 43 (Cx43).

6 ocyte gap junctions composed of connexin 43 (Cx43).

7 ly influence multiple functions of wild-type Cx43.

8 epress transcription of the key labour gene, Cx43.

9 ap junction communication by phosphorylating Cx43.

10 ormoxic cells expressing a moderate level of Cx43.

11 with wild-type connexins, including Cx26 and Cx43.

12 ibility, allowing aberrant interactions with Cx43.

13 increased MAPK-dependent phosphorylation of Cx43.

14 a significant lower level of gap-junctional Cx43.

15 ncomitant increase in cytoplasmic, vesicular Cx43.

16 ich element in the 3' untranslated region of Cx43.

17 s on wild-type Cx26 and coexpressed Cx30 and Cx43.

18 it also enhanced O-GlcNAcylation of Cx40 and Cx43.

19 n increase in gap junction plaques formed by Cx43.

20 lly regulates Cx43 translation to generate a Cx43-20 K isoform, which facilitates the transport of fu

21 of these regulating factors is Connexin 43 (Cx43), a gap junction protein highly expressed by astroc

22 s their high expression level of connexin43 (Cx43), a protein forming gap junction channels and hemic

23 pling correlated with levels of connexin-43 (Cx43), a protein previously linked to late-stage disease

24 Connexin43 (Cx43), a ubiquitous and important connexin, has several

25 We have recently shown that Cx43 abundance was strongly reduced in fibroblasts of hu

26 peptide mimetic of the carboxyl-terminus of Cx43, accelerates fibroblast migration and proliferation

27 s, reporting that ACT1, a mimetic peptide of Cx43, accelerates healing in the treatment group.

28 n events at S373, S365, and S368, well-known Cx43 Akt, protein kinase A, and protein kinase C phospho

29 e most abundant connexin (Cx) in astrocytes, Cx43, also forms hemichannels.

30 ional paradox produced by oligomerization of Cx43 and Cx26 KID mutants could underlie the severe synd

31 ) is co-expressed with other connexins, like Cx43 and Cx30, and as the KID syndrome is inherited as a

32 f the specific type of GJ channel (homotypic Cx43 and Cx45, and heterotypic Cx43/Cx45 and Cx45/Cx43).

33 was not observed with other lens connexins, Cx43 and Cx46.

34 reas in PRB cells the forward trafficking of Cx43 and GJ formation is inhibited even when Cx43 is ove

35 Both Cx43 and integrin alpha5 are directly phosphorylated by

36 We have recently shown that Cx43 and integrin alpha5 interact directly with each oth

37 KT activated by FFSS directly phosphorylates Cx43 and integrin alpha5, and Ser-373 of Cx43 plays a pr

38 annels and disrupted the interaction between Cx43 and integrin alpha5.

39 GJ proteins, connexin 43 (Cx43) and connexin 47 (Cx47), play a crucial role in pro

40 creased protein accumulation of connexin-43 (Cx43) and N-cadherin, whereas at later stages, apoptosis

41 gase identified to interact with connexin43 (Cx43), and its suppressed expression results in accumula

42 beta25-35 peptide promoted both connexin 43 (Cx43)- and Panx1 HC-dependent MC dye uptake and histamin

43 t, three major connexin (Cx) isoforms, Cx40, Cx43, and Cx45, form GJ channels in cell-type-specific c

44 Collectively, these results suggest that Cx43, and not Cx26, can act as a tumor suppressor during

45 In skeletal formation, Panx3 and Cx43 are the most abundantly expressed gap junction prot

46 Here we show that Cx43 assembled into distinct GJ and HC plaques in GFBLs

47 Connexin43 (Cx43) assembly and degradation, the regulation of electr

48 MetS-VLDL induced downregulation of Cx40 and Cx43 at transcriptional, translational and tissue levels

49 illustrated the significance of connexin 43 (Cx43)-based gap junction in maintaining the homeostasis

50 Coimmunoprecipitation showed Cx43 being pulled down more efficiently with mutant Cx26

51 oprecipitation experiments demonstrated that Cx43-beta-tubulin molecular interaction was depleted due

52 cytokine mRNA expression were blocked by the Cx43 blockers Gap26 and carbenoxolone.

53 e networks and in vivo investigations linked Cx43 breakdown to myeloperoxidase-dependent activation o

54 We found that the expression of Cx43, but not Cx26, significantly reduced cellular proli

55 egulatory amino acid residues located in the Cx43 C-terminal tail.

56 ther, although Panx3 can function in 3 ways, Cx43 cannot function through the ER Ca(2+) channel, only

57 nteraction between Nedd4 (WW1-3 domains) and Cx43 (carboxyl terminus (CT)).

58 ddition, the presence of mutant Cx26 shifted Cx43 channel gating and kinetics toward a more Cx26-like

59 We propose that Cx43 channels are important conduits for dissipating lac

60 Lack of Cx43 expression or blockage of Cx43 channels resulted in increased ROS-induced astrocyt

61 e mimetic alphaCT1, a selective inhibitor of Cx43 channels, sensitized human MGMT-deficient and TMZ-r

62 rting a cell protective effect of functional Cx43 channels.

63 A full-length Cx43 cloned into mammalian expression vector pCI-neo was

64 RATIONALE: Delivery of Cx43 (connexin 43) to the intercalated disc is a continu

65 f the redox-sensitive gap junctional protein Cx43 (Connexin 43) was reduced in the peri-infarct area

66 ed discs, and integral gap junction proteins Cx43 (connexin 43), Cx45 (connexin 45), and ZO-1 (zonula

67 RATIONALE: Downregulation of Cx43 (connexin 43), the major cardiac gap junction prote

68 elevated levels of BMP2/4 signaling in G60S Cx43-containing cells resulted at least in part from ele

69 ed state of cerebral endothelium, astroglial Cx43 controls immune recruitment as well as antigen pres

70 l expression of the 2 connexins, (Cx40/[Cx40+Cx43]) correlated with Ri and Rj (rs=0.58, P<0.01 for Ri

71 However, a reduction in Cx43 coupled with an increased Cx45 protein levels withi

72 Strikingly, heteromeric oligomer formed by Cx43/Cx26 (syndromic mutants) shows exacerbated hemichan

73 ommunications between astrocytes-astrocytes (Cx43-Cx43) and between astrocytes-oligodendrocytes (Cx43

74 Compared to wild-type Cx43 (Cx43WT), Cx43( *)NT37 junctions exhibited several

75 el (homotypic Cx43 and Cx45, and heterotypic Cx43/Cx45 and Cx45/Cx43).

76 43) and between astrocytes-oligodendrocytes (Cx43-Cx47).

77 ipogenesis by up-regulation of Pparg2 in the Cx43-deficient Gja1(Jrt)/+ mouse model.

78 the cell surface and restricted MT-mediated Cx43 delivery to the cell membrane.

79 We therefore speculate the increase in Cx43 dephosphorylation may account for the facilitation

80 Additionally, melanomas expressing Cx43 displayed significantly reduced growth within the i

81 Connexin 43 (Cx43) downregulation is associated with normal wound hea

82 cells and this inhibition was attenuated by Cx43(E2) antibody as well.

83 d this inhibitory effect was attenuated with Cx43(E2), a specific hemichannel-blocking antibody.

84 In addition to the expression of full-length Cx43, endogenously produced carboxyl-terminal segments o

85 tion of Akt, because AM-specific knockout of Cx43 enhanced alveolar neutrophil recruitment and secret

86 mation and function in osteoblasts and other Cx43-expressing cells.

87 antoic membrane, primary tumors derived from Cx43-expressing melanomas were significantly smaller tha

88 Areas of HIV tissue with anomalous Cx43 expression and localization also showed calcium ove

89 energic receptor agonist CL316,243 increased Cx43 expression and mitochondrial localization.

90 n Calu-3 cells was associated with decreased Cx43 expression and reduced apoptosis.

91 PP1 raised Cx43 expression by 69% in the scar border (p = 0.048) an

92 Panx3 promotes Cx43 expression by regulating Wnt/beta-catenin signaling

93 all, we propose that HIV infection increases Cx43 expression in heart, resulting in tissue damage tha

94 s demonstrated that hypoxic stress increases Cx43 expression in melanoma cells via hypoxia-inducible

95 Our results show that the reduction of glial Cx43 expression in Sox10::CreER(T2+/-) /Cx43(f/f) mice s

96 Lack of Cx43 expression or blockage of Cx43 channels resulted in

97 Although Cx43 expression showed no correlation with resistivity v

98 in the germ cell lineage, where it represses Cx43 expression through regulation of the transcriptiona

99 Cx43 expression was higher in BAT compared to white adip

100 Hypoxic cells displaying increased Cx43 expression were less susceptible to NK cell-mediate

101 We propose that PRA is a master regulator of Cx43 expression, GJ formation and myocyte connectivity/s

102 coupled to myocytes, and coupling depends on Cx43 expression.

103 infected individuals to examine connexin 43 (Cx43) expression and distribution and HIV-associated inf

104 LPS increased connexin43 (Cx43) expression and enhanced ATP release from enteric g

105 ssion of connexin 43 in Sox10::CreER(T2+/-) /Cx43(f/f) mice or activating glial calcium responses in

106 lial Cx43 expression in Sox10::CreER(T2+/-) /Cx43(f/f) mice significantly reduced neurogenic ion tran

107 ding connexin-43 (Cx43) (hGFAP::CreER(T2+/-)/Cx43(f/f) mice).

108 ce was more variable in Sox10::CreER(T2+/-) /Cx43(f/f) tissues.

109 The gap junction protein connexin43 (Cx43) forms intercellular channels as well as hemichanne

110 dentified that actin provides rest stops for Cx43 forward trafficking and that Cx43 has a 20 kDa inte

111 GJA1-20k isoform is required for full-length Cx43 forward trafficking to intercalated discs.

112 unication by increasing the turnover rate of Cx43 from the plasma membrane.

113 lasts of human gingival wounds, and blocking Cx43 function in cultured human gingival fibroblasts (GF

114 t Cx26 acts as a trans-dominant negative for Cx43 function in myoepithelial cells, highlighting the i

115 ring peptide mimetics to inhibit lateralized Cx43 function prior to challenge protected mdx mice from

116 pe Cx43 showed a transdominant inhibition of Cx43 gap junction channels, without reductions in Cx43 p

117 Activation of Tyk2 led to a decrease in Cx43 gap junction communication by increasing the turnov

118 A deficiency in LRP6 disrupts Cx43 gap junction formation and thereby impairs the cell

119 20k markedly increases endogenous myocardial Cx43 gap junction plaque size at the intercalated discs.

120 mice consistently exhibit overt reduction of Cx43 gap junction plaques without any abnormality in Wnt

121 The defect in Cx43 gap junction resulting from LRP6 reduction is attri

122 c Delta130-136 transgenic mice with impaired Cx43 gap junctions and hemichannels showed significantly

123 70 mutations in the gap junction connexin43 (Cx43) gene, GJA1, are associated with ODDD, most of whic

124 Cx43-GJ-mediated intercellular communication (GJIC) betw

125 ur data identify a novel and active role for Cx43-GJIC in human NK cell activation and antitumor effe

126 After prolonged incubation periods (60 min), Cx43 GJs reformed and intracellular Cx43 were restored t

127 iffuse within the plaque structures, whereas Cx43 GJs remain persistently immobile for more than 2 mi

128 apid and almost complete loss of connexin43 (Cx43) GJs at cell-cell appositions and a concomitant inc

129 stops for Cx43 forward trafficking and that Cx43 has a 20 kDa internally translated small C terminus

130 The transmembrane protein Cx43 has key roles in fibrogenic processes including inf

131 The gap junction protein, connexin43 (Cx43), has critical roles in the inflammatory, edematous

132 ously produced carboxyl-terminal segments of Cx43 have been described and have been suggested to be i

133 generation of carboxyl-terminal segments of Cx43 have remained elusive.

134 ke by astrocytes, whereas Gap19, a selective Cx43 HC blocker, has no effect on dye uptake at this tim

135 histamine release, responses that were only Cx43 HC dependent in Panx1(-/-) mice.

136 Specific blockage of Cx43 HC function by TAT-Gap19, a Cx43 mimetic peptide, s

137 Collectively, our data suggest that reduced Cx43 HC function could promote fast and scarless gingiva

138 Thus, selective suppression of Cx43 HCs may provide a novel target to modulate wound he

139 s not known whether these responses involved Cx43 HCs or GJs.

140 by 7 h treatment, connexin 43 hemichannels (Cx43 HCs) are also opened.

141 onnexons resulted in significantly increased Cx43 hemichannel activity in the presence of Cx26 mutant

142 This work demonstrates that astroglial Cx43 hemichannel activity is associated with D-serine re

143 Pharmacological and genetic inhibition of Cx43 hemichannel activity reduced the amplitude of NMDA

144 imulation was reduced by prior inhibition of Cx43 hemichannel activity.

145 ctivation of PI3K appears to be required for Cx43 hemichannel opening by mechanical stimulation.

146 e interaction between these two proteins and Cx43 hemichannel opening, a crucial step to mediate the

147 Cx43 hemichannels allow passage of small molecules betwe

148 However, whether astroglial Cx43 hemichannels are active in resting conditions and r

149 involving microtubule highways, vesicles of Cx43 hemichannels are efficiently trafficked to adherens

150 These data reveal Cx43 hemichannels as a novel astroglial release pathway

151 The opening of osteocytic Cx43 hemichannels by mechanical stimulation had similar

152 onate (ALN) or zoledronic acid (ZOL), opened Cx43 hemichannels in osteocytes.

153 We showed that the activity of Cx43 hemichannels recorded in cultured astrocytes was [C

154 Cx43 hemichannels serve as a portal for the release of p

155 rafficking machinery, increasing delivery of Cx43 hemichannels to cardiac intercalated discs.

156 h the specific inhibitory role of osteocytic Cx43 hemichannels, and exploiting the activity of this c

157 were mediated by ATP released from osteocyte Cx43 hemichannels.

158 ses in enteric glia of mice were mediated by Cx43 hemichannels.

159 disruption of the gene encoding connexin-43 (Cx43) (hGFAP::CreER(T2+/-)/Cx43(f/f) mice).

160 monolayer culture, showed markedly increased Cx43 immunoreactivity at areas of invasion in orthotopic

161 Cx43 immunoreactivity was confined to enteric glia withi

162 when overexpressed in normoxic tumor cells, Cx43 improves their susceptibility to N cell-mediated ki

163 Inhibition of Cx43 in cultured adipocytes increased the generation of

164 ) KO) and by overexpression and knockdown of Cx43 in cultured adipocytes.

165 These findings reveal a critical role for Cx43 in epidermal homeostasis, and they provide evidence

166 K and further highlight an emerging role for Cx43 in genetic skin diseases.

167 3(-/-); Cx43(-/-) mice, Panx3 is upstream of Cx43 in osteogenesis.

168 Our findings suggest that the role of Cx43 in response to cellular stress is dependent on the

169 We next investigated if overexpression of Cx43 in Sertoli cells could rescue the PFOS-induced cell

170 Indeed, overexpression of Cx43 in Sertoli cells with an established TJ-barrier blo

171 In summary, overexpression of Cx43 in the testis with aspermatogenesis reboots meiosis

172 s, we sought to examine if overexpression of Cx43 in these adjudin-treated rats would reseal the disr

173 drocytic Cx47, which is mainly stabilized by Cx43 in vivo, was down-regulated, and its characteristic

174 e homeostasis that is not compensated for by Cx43 in vivo.

175 We investigated the role of connexin 43 (Cx43) in maintaining the integrity of mitochondria in br

176 ression and channel activity of connexin 43 (Cx43) in melanoma cells and its impact on their suscepti

177 evel of the gap junction protein connexin43 (Cx43) in polarized human airway epithelial cells upon in

178 olvement of CELF1-regulated genes, including Cx43, in controlling contractility and conduction.

179 Unlike wild-type Cx43, in which ZO-1 binding is restricted to the periphe

180 It was found that overexpression of Cx43 indeed resealed the Sertoli cell tight junction-per

181 ependent TMZ resistance and that combining a Cx43 inhibitor with TMZ could enhance therapeutic respon

182 the myenteric plexus of the mouse colon; the Cx43 inhibitors carbenoxolone and 43Gap26 inhibited the

183 ated in the C-terminal domain of connexin43 (Cx43) into glutamic acid (E) or alanine (A) residues.

184 Expression of Cx43 involved an opposite regulation exerted by JNK and

185 In summary, Cx43 is a good target that might be used to manage PFOS-

186 Altogether, our results demonstrate that Cx43 is a new astroglial factor promoting the immune qui

187 Here, we demonstrate that Cx43 is dysregulated in the hearts of HIV-infected indiv

188 sed only in the luminal epithelial cells and Cx43 is expressed only in myoepithelial cells.

189 Cx43 is mainly expressed by astrocytes in the CNS and fo

190 Cx43 and GJ formation is inhibited even when Cx43 is overexpressed.

191 Collectively, our data demonstrate that Cx43 is required for maintaining the mitochondrial integ

192 Nedd4-mediated ubiquitination of Cx43 is required to recruit Eps15 and target Cx43 to the

193 Cx43 is thus a novel target for influencing metabolite h

194 Connexin 43 (Cx43) is the most ubiquitous connexin in various cells,

195 cytes recovered after 7 h, but was absent in Cx43 knock-out astrocytes.

196 oblast-specific protein-1 driven conditional Cx43 knock-out mice (Cx43fsp1KO).

197 Metabolite assays demonstrated that Cx43 knockdown increased cytoplasmic lactate retention i

198 valuated using inducible, adipocyte-specific Cx43 knockout in mice (Gja1 (adipoq) KO) and by overexpr

199 d the phenotypes of Sertoli cell-conditional Cx43 knockout mice share many of the similarities of the

200 severe skeletal abnormalities than those of Cx43-KO mice.

201 These findings suggest that Cx43 lateralization contributes significantly to DMD arr

202 ma cells selectively degrades gap-junctional Cx43, leading to the destabilization of the immune synap

203 el accompanied upregulated RRP6, and reduced Cx43 level was detected in mouse models with DCM, includ

204 c-Src inhibition improved Cx43 levels and conduction velocity and lowered arrhythm

205 Moreover, Cx43 levels inversely correlated with patient survival,

206 Cx43 levels were inversely correlated with TMZ sensitivi

207 mechanisms by which MHV-A59 infection alters Cx43 localization and examined the effects of viral infe

208 Previously, it has been shown that Cx43 localization and expression is altered due to mouse

209 e delivery of GJA1-20k to the heart protects Cx43 localization to the intercalated discs against acut

210 wn to inhibit the expression of connexin-43 (Cx43, major component of GJs) and GJ formation in myomet

211 Our findings suggest that Cx43 may offer a biomarker to predict the survival of pa

212 tumors by NK cells through the modulation of Cx43-mediated intercellular communications.

213 the underlying ulcer pathophysiology through Cx43-mediated pathways.

214 Our data suggest that GJIC is important for Cx43-mediated ROS resistance.

215 Our data underscore that although Cx43-mediated transport is observed in overexpressing ce

216 tions in EKVP subjects lead to disruption of Cx43 membrane localization and aggregation within the Go

217 responses and changes in glial expression of Cx43 messenger RNA and protein.

218 Based on the generation of Panx3(-/-); Cx43(-/-) mice, Panx3 is upstream of Cx43 in osteogenesi

219 nts, which guides growth trajectories of the Cx43 microtubule trafficking machinery, increasing deliv

220 aCT1 is a Cx43 mimetic peptide that in preclinical studies acceler

221 blockage of Cx43 HC function by TAT-Gap19, a Cx43 mimetic peptide, significantly upregulated the expr

222 Remarkably, Cx43 mislocalization was also evident in autopsied left

223 investigated the mechanism of CELF1-mediated Cx43 mRNA degradation and determined whether elevated CE

224 CELF1 mediated Cx43 mRNA degradation by binding the UG-rich element in

225 ts that RRP6 was required for CELF1-mediated Cx43 mRNA degradation.

226 or increased CELF1 expression downregulating Cx43 mRNA level and a pathogenic role for elevated CELF1

227 on of CELF1 in the infarcted heart preserved Cx43 mRNA level and ameliorated the cardiac phenotypes o

228 CELF1 abolished the ability to downregulate Cx43 mRNA, so nuclear localization was required for its

229 ndogenous RRP6, CELF1 failed to downregulate Cx43 mRNA, which suggests that RRP6 was required for CEL

230 ene (Gja1), resulting in a G60S connexin 43 (Cx43) mutant protein that is dominant negative for Cx43

231 MiaPaCa2 cells, which are Cx43 negative in monolayer culture, showed markedly incr

232 Compared to wild-type Cx43 (Cx43WT), Cx43( *)NT37 junctions exhibited several functional alte

233 replaced the Cx43NT with the Cx37NT (chimera Cx43( *)NT37), leaving the remainder of the Cx43 sequenc

234 Furthermore, both Cx43 osteocyte-specific knockout mice and osteocyte-spec

235 formation of multinucleated cells following Cx43 overexpression due to the failure of spermiogenesis

236 ed in a complete inhibition of ERK-dependent Cx43 phosphorylation and attenuated the inhibition of he

237 oth signaling pathways significantly reduced Cx43 phosphorylation and GJ internalization.

238 increased phospho-p44/42 ERK levels and also Cx43 phosphorylation at Ser(279)-Ser(282) sites.

239 of p44/42 ERK upon continuous FFSS leads to Cx43 phosphorylation at Ser(279)-Ser(282), sites known t

240 44/42 ERK signaling and subsequently, direct Cx43 phosphorylation by activated ERK leads to hemichann

241 signaling pathways leading to alteration of Cx43 phosphorylation states.

242 gap junctional intercellular communication, Cx43 phosphorylation, and hemichannel activity among Cx4

243 ture (active v-Src) in LA-25 cells decreased Cx43 phosphorylation, indicating that although activatio

244 rminus of Cx43 was required for stability of Cx43 plaque arrangement.

245 tes Cx43 and integrin alpha5, and Ser-373 of Cx43 plays a predominant role in mediating the interacti

246 In this study, we report insights into how Cx43 promotes TMZ resistance.

247 In isolated wild-type cardiomyocytes, Cx43 protein content decreased on myeloperoxidase/H2O2 i

248 Thus in P4 stimulated PRA cells Cx43 protein forms GJs, whereas in PRB cells the forward

249 erences in the intracellular localization of Cx43 protein in PRA versus PRB expressing myocytes.

250 In addition, overall Cx43 protein levels were markedly increased in mouse and

251 mutant protein that is dominant negative for Cx43 protein production of <50% of wild-type (WT) levels

252 gap junction channels, without reductions in Cx43 protein synthesis.

253 ibutable to the defective traffic of de novo Cx43 proteins from the endoplasmic reticulum to the Golg

254 tus, leading to the lysosomal degradation of Cx43 proteins.

255 The mechanism by which overexpression of Cx43 reboots meiosis and rescues BTB function was also e

256 Consequently, in the absence of astroglial Cx43, recruited immune cells elaborate a specific humora

257 llular-Src (c-Src) inhibition on connexin43 (Cx43) regulation in a mouse model of myocardial infarcti

258 hese findings suggest that overexpression of Cx43 reinitiated spermatogenesis at least through the st

259 line expresses low basal levels of Cx26 and Cx43, rendering them gap junctional intercellular commun

260 e that the gap junction protein connexin 43 (Cx43) renders GBM cells resistant to TMZ through its car

261 Although the Cx43 residues that undergo ubiquitination are still unkn

262 Tyk2 directly phosphorylated Cx43 residues Tyr-247 and Tyr-265, leading to indirect p

263 argeted the gap junction protein connexin43 (Cx43) responsible for maintaining cardiac conduction.

264 p10), and procontractile proteins (Cox-2 and Cx43) resulting in PTL after 7 h.

265 ging movies indicated phosphorylated Ser-368 Cx43 separated into discrete domains within gap junction

266 Cx43( *)NT37), leaving the remainder of the Cx43 sequence, including the CT and CL, unchanged.

267 up to 2.8-fold increased phosphorylation of Cx43 serine residues 255, 262, 279/282, and 368, and app

268 Coexpression of the mutants with wild-type Cx43 showed a transdominant inhibition of Cx43 gap junct

269 Plakoglobin and Cx43 signals were also reduced in most family members wh

270 as expression of the non-degradable form of Cx43 significantly restore its accumulation at the immun

271 was prevented by lentiviral expression of a Cx43-specific short hairpin RNA.

272 Moreover, blocking Cx43 strongly inhibited the NK cell-mediated tumor cell

273 GJA1 encodes connexin 43 (Cx43), the most widely expressed gap junction protein.

274 Immunofluorescence revealed the presence of Cx43, the main cardiac gap junction protein, localized t

275 Expression of connexins Cx26, Cx30, Cx36, or Cx43, the pannexins Px1 or Px2, or the purinergic recept

276 ich facilitates the transport of full length Cx43 to plasma membrane.

277 Cx43 is required to recruit Eps15 and target Cx43 to the endocytic pathway.

278 The P4 mediated regulation of Cx43 trafficking and GJ formation occurs via non-genomic

279 ince inhibition of this pathway restored the Cx43 trafficking defect in PRB cells.

280 - 20 kDa), which is required for full-length Cx43 trafficking, but by an unknown mechanism.

281 rast, unliganded PRA paradoxically activates Cx43 transcription by interacting with FRA2/JUND heterod

282 that P4, via PRA/B, differentially regulates Cx43 translation to generate a Cx43-20 K isoform, which

283 a novel tyrosine kinase that phosphorylates Cx43, tyrosine kinase 2 (Tyk2).

284 Although all of the Cx43 variants could traffic to the cell surface, there w

285 sphorylation, and hemichannel activity among Cx43 variants, as well as subtle differences in myofibro

286 ing heterozygous p.L7V, p.G138R, and p.G143S Cx43 variants.

287 increased the intracellular protein level of Cx43 via STAT3.

288 mouse models of DMD, and human DMD tissues, Cx43 was found to be pathologically mislocalized to late

289 art samples analyzed, there were areas where Cx43 was overexpressed and found along the lateral membr

290 The cytoplasmic C terminus of Cx43 was required for stability of Cx43 plaque arrangeme

291 d be extrapolated to other connexins, TM1 of Cx43 was scanned revealing similar but not identical sen

292 ic effects of adipocyte-specific knockout of Cx43 were assessed during cold stress and following high

293 The functional effects of Cx43 were evaluated using inducible, adipocyte-specific

294 n and the major cardiac gap junction protein Cx43 were markedly diminished in buccal mucosa cells fro

295 60 min), Cx43 GJs reformed and intracellular Cx43 were restored to levels observed before treatment.

296 and contains a high level of gap-junctional Cx43 whereas that formed with hypoxic cells is less stab

297 ted O-GlcNAcylation at serine 18 of Cx40 and Cx43 which may impair stability of gap junctions.

298 nucleotides 442-637) in the coding region of Cx43, which resides upstream from the nucleotide sequenc

299 Targeting Cx43 with ACT1, a peptide mimetic of the carboxyl-termin

300 ng PKC phosphorylation causes degradation of Cx43 without dephosphorylation, which is in accordance w