ライフサイエンスコーパス: Cx43

1 dependent and mediated by HSPC connexin-43 (Cx43).

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

3 activity that was not displayed by wild-type Cx43.

4 lin led to the intracellular accumulation of Cx43.

5 of BAG3 significantly diminished turnover of Cx43.

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

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

8 hat was 50% shorter than membrane-associated Cx43.

9 ng suggests that Abeta can bind favorably to Cx43.

10 ted by phosphorylation and ubiquitination of Cx43.

11 sting that Dsg1 promotes GJ function through Cx43.

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

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

14 This indicates that Cx43, a typically astrocytic connexin, is the main conne

15 and Xenopus oocytes, we show that Cx43-G8V, Cx43-A44V and Cx43-E227D all formed functional gap junct

16 In addition, we show that Cx43-G8V, Cx43-A44V and Cx43-E227D significantly increase membrane

17 The disease was accompanied by connexin-43 (Cx43) aberrantly enhanced in both cardiac and skeletal m

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

19 osomal activity leads to the accumulation of Cx43 aggregates and suppression of BAG3 significantly di

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

21 n mediators involved in mechanotransduction (Cx43, AKT), tissue remodelling (GAGs, elastin, collagen)

22 y tumors in vivo, and joint up-regulation of Cx43 and ADORA1 in breast cancer patients correlated wit

23 We demonstrate that targeting Cx43 and AKT prevents strain-induced ECM damage and prom

24 CTS increased Cx43 and AKT protein and gene expression and the respons

25 At their occupied territories, Cx43 and Cx40 clustered with tight junctions and, to a l

26 +) through channels made from two connexins, Cx43 and Cx50, that are highly expressed in vertebrate l

27 ild-type EHD1 accelerated internalization of Cx43 and exacerbated ischemia-induced lateralization of

28 These interactions regulate Cx43 and gap junction formation and stability.

29 ith altered mRNA transcript levels of MCP-1, Cx43 and TGFbeta.

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

31 to acidified endolysosomes via connexin 43 (Cx43) and gated by cAMP-EPAC-RAP1-PP2A signaling.

32 n of GJA1 (encoding the gap junction protein Cx43) and other genes related to intercellular communica

33 reserved contractile function, reduced total Cx43, and reduced gap junctions, and they died suddenly

34 e cardiac lymphangiogenesis and function via Cx43, and this represents a new therapeutic pathway for

35 ponse could be reversed with either CTS, the Cx43 antisense or AKT inhibitor.

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

37 ions in the gene (GJA1) encoding connexin43 (Cx43) are responsible for several rare genetic disorders

38 an et al. explore how hypophosphorylation of Cx43 at a triplet of serine residues (S325/S328/S330) in

39 d despite decreased localization of ZO-1 and Cx43 at the ventricular intercalated disc and modestly d

40 easing the amount of functional connexin-43 (Cx43) at the membrane through Cx43 silencing, suppressio

41 be correctly targeted to intercalated discs, Cx43 being the major connexin in the working myocytes.

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

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

44 tagonists of connexin channels, connexin 43 (Cx43) blocking peptide Gap26, or Cx43 gene knock-down; (

45 M213L mutation), which generates full-length Cx43, but not GJA1-20k.

46 on, knock-down of BAG3 reduced the levels of Cx43 by dysregulating Cx43 protein stability.

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

48 y demonstrated interaction between TRPV4 and Cx43 channels in astrocytes.

49 Cx43 channels were permeable to IP(3) and Ca(2+).

50 re mediated by interaction between TRPV4 and Cx43 channels, leading to Cx43-mediated release of ATP w

51 etic reduction of Cx43-copy number in mdx/WT-Cx43(+/-) chimeras protected them from both cardiac and

52 Inhibition of neutrophil Cx43 compromises clearance of wound-colonizing P. aerugi

53 This screen identified Cx43 (connexin 43) hemichannel blockade as a robust supp

54 y backcrossing into a cardiomyocyte-specific Cx43 (connexin 43) heterozygous background.

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

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

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

58 complished by gap junctions (GJ) composed of Cx43 (connexin 43).

59 The gap junction protein Connexin 43 (Cx43) contributes to cell fate decisions that determine

60 Genetic reduction of Cx43-copy number in mdx/WT-Cx43(+/-) chimeras protected

61 Cx43 could therefore be a potential therapeutic target t

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

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

64 in intracranial pressure was not affected by Cx43 deficiency.

65 C or culture with isolated mitochondria from Cx43 deficient HSPCs.

66 Hematopoietic Cx43-deficient chimeric mice show reduced mitochondria t

67 Deficiency of Cx43 delayed mesenchymal and osteogenic regeneration whi

68 Cx43-deleted OECs exhibited features consistent with the

69 es in functional properties, the deletion of Cx43 deletion did not alter the density of OECs.

70 attenuated in mice with a lymphatic-specific Cx43 deletion.

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

72 ntercellular communication (GJIC) influences Cx43-dependent skeletal phenotypes, including segment le

73 Cx43 hemichannel activity does not influence Cx43-dependent skeletal phenotypes.

74 s, cardiomyocyte diameter, glycogen score or Cx43 distribution at the time of surgery was not signifi

75 ytes is reduced after myofibroblast-specific Cx43 down-regulation.

76 fers from another gap junction, connexin 43 (Cx43), during skin wound healing.

77 ocytes, we show that Cx43-G8V, Cx43-A44V and Cx43-E227D all formed functional gap junction channels w

78 dition, we show that Cx43-G8V, Cx43-A44V and Cx43-E227D significantly increase membrane current flow

79 lysosome pathway dysregulates degradation of Cx43, either by inhibiting lysosomal activity or suppres

80 We further show that interruption of Cx43 endocytosis in Abeta(25-35)-exposed astrocytes resu

81 ed GJIC in HaCaT cells, but the silencing of Cx43 exerted the opposite effects.

82 Here, we provide insights into how Cx43, expressed medially, influences changes in gene exp

83 The IL-22-induced down-regulation of Cx43 expression and decrease in GJIC can be significantl

84 effect of increased beta-amyloid (Abeta) on Cx43 expression and function leading to neuronal damage,

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

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

87 Restoring Cx43 expression in endometrial cancer cells reduced cell

88 nificantly decreased GJIC and down-regulated Cx43 expression in HaCaT cells.

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

90 Gap27 treatment results in no change Cx43 expression in the heart of AV-Shunt rats.

91 we found that, compared with WT Cx43, mutant Cx43 expression increases ERK activation, phosphorylatio

92 ermore, the IL-22-induced down-regulation of Cx43 expression mediated by the JNK signaling pathway wa

93 Cx43 expression was higher in BAT compared to white adip

94 In dystrophic skeletal muscle, Cx43 expression was not seen in the fibers but in adjace

95 Similarly, Cx43 expression was significantly lower in the lesional

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

97 uivalents depleted of Dsg1 exhibited reduced Cx43 expression, rescued upon re-introduction of wild-ty

98 JNK signaling pathway, which down-regulates Cx43 expression; this process is a possible pathomechani

99 a distal regulatory region involved in Gja1 (Cx43) expression.

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

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

102 cellular mechanisms by which Abeta modulates Cx43 function in astrocytes, the basic understanding of

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

104 for therapeutic intervention associated with Cx43 function.

105 Connexin43 (Cx43) function is influenced by kinases that phosphoryla

106 T2) ;Rasa1(fx/fx) , Foxc2(Cre/+) , Lyve1-Cre;Cx43(fx/fx) , and Prox1-CreER(T2) ;Cx43(fx/fx) ;Cx37(-/-

107 Lyve1-Cre;Cx43(fx/fx) , and Prox1-CreER(T2) ;Cx43(fx/fx) ;Cx37(-/-) mice, we tested our method on lym

108 HeLa cells and Xenopus oocytes, we show that Cx43-G8V, Cx43-A44V and Cx43-E227D all formed functional

109 In addition, we show that Cx43-G8V, Cx43-A44V and Cx43-E227D significantly increas

110 r findings reveal that soluble Si stimulates Cx43 gap junction communication in hDFC and induces gene

111 20k markedly increases endogenous myocardial Cx43 gap junction plaque size at the intercalated discs.

112 tent stem cell derived-cardiomyocytes reveal Cx43 gap junction remodeling by reduced ZO-1 complexing.

113 lated independently of Cx43, is critical for Cx43 gap junction trafficking, maintenance of Cx43 prote

114 Abeta(25-35) causes rapid internalization of Cx43 gap junctions.

115 cellular processes by which Abeta can alter Cx43 gap junctions.

116 osteogenic differentiation and connexin 43 (CX43) gap junction communication in cultured pluripotent

117 Connexin-43 (Cx43) gap junctions provide intercellular coupling, whic

118 ide inhibitor specific to Cx43, we show that Cx43-gap junctional intercellular communication (GJIC) i

119 onnexin 43 (Cx43) blocking peptide Gap26, or Cx43 gene knock-down; (2) antagonists of TRPV4 channels;

120 The gap junction protein connexin43 (Cx43, gene name GJA1) facilitates rapid propagation of a

121 OSX, RUNX2, BMP2, ALP, OCN, BSP and CX43 genes were expressed in hDFC cultured for 1, 7, 14

122 We also demonstrate that Cx43-GJIC influences the expression of the Smp/beta-cate

123 These data provide evidence that Cx43-GJIC is responsible for regulating cell fate decisi

124 mical experiments indicated that cytoplasmic Cx43 had a half-life that was 50% shorter than membrane-

125 ions of enhancers linked to fgf20a, mdka and cx43 had no effect or partially reduced gene expression.

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

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

128 he cardiac gap junction protein connexin-43 (Cx43) has been suggested as playing a role in the develo

129 astroglial gap junction protein connexin 43 (Cx43) has increasingly been associated to neurotoxicity

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

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

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

133 lly, our findings suggest that inhibition of Cx43 hemichannel activity does not influence Cx43-depend

134 ling in the heart and prevention of aberrant Cx43 hemichannel activity in the skeletal muscle macroph

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

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

137 emodeling, with a corresponding reduction of Cx43 hemichannel activity.

138 rast to WT, MK4 astrocytes displayed reduced Cx43 hemichannel activity.

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

140 ence and rescue strategies, we identify that Cx43 hemichannel function, but not intercellular communi

141 y administration of Gap19 peptide mimetic, a Cx43 hemichannel-specific inhibitor.

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

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

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

145 n MYL4 and Cx43 with altered localization of Cx43 hemichannels to the lateral membrane in MYL4 mutant

146 Activation of Cx43 hemichannels was necessary for nuclear localization

147 Pharmacological blockade of Cx43 hemichannels with TAT-Gap19 also significantly decr

148 fies autocrine purinergic signaling, through Cx43 hemichannels, as a critical pathway in leader cell

149 y reported an important role of Connexin 43 (Cx43) hemichannels in the pathogenesis of lethal sepsis

150 his study shows that opening of connexin 43 (Cx43) hemichannels leading to the release of ATP is the

151 a contact-dependent manner via connexin-43 (Cx43) hemichannels, which are mediators of active ATP re

152 hin the tissues and depended on connexin-43 (Cx43) hemichannels, which opened preferentially in cells

153 substituted for serines at these residues in Cx43, Himelman et al. observed reduced gap junction remo

154 fin regeneration, including fgf20a, mdka and cx43, identifying distinct domains of directed expressio

155 ap junction remodeling and lateralization of Cx43 immunosignals, protection against isoproterenol-ind

156 We here showed an altered distribution of Cx43 in a mouse model of LMNA cardiomyopathy.

157 derlying mechanisms by which Abeta modulates Cx43 in astrocytes remain elusive.

158 Inhibition of Cx43 in cultured adipocytes increased the generation of

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

160 , postnatal endothelial-specific deletion of Cx43 in Cx37(-/-) mice results in rapid regression of va

161 an auxiliary subunit for the trafficking of Cx43 in heterologous expression systems.

162 fer, which was rescued upon re-expression of Cx43 in HSPC or culture with isolated mitochondria from

163 n addition, we show that EHDs associate with Cx43 in human and murine failing hearts.

164 acerbated ischemia-induced lateralization of Cx43 in isolated adult cardiomyocytes.

165 ation of alpha-tubulin lead to remodeling of Cx43 in LMNA cardiomyopathy, which alters the correct co

166 3(-/-); Cx43(-/-) mice, Panx3 is upstream of Cx43 in osteogenesis.

167 ntaining protein 1) as a novel interactor of Cx43 in the heart.

168 on sites in Cx43 reduces the levels of total Cx43 in the myocardium and increases Cx43 phosphorylatio

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

170 ndothelial-specific deletion of connexin 43 (Cx43) in connexin 37 null (Cx37(-/-) ) mice results in r

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

172 ely abolished the expression of connexin 43 (Cx43) in OECs in both juvenile and adult mice.

173 in connexins and specifically in 43 isoform (Cx43) in the heart have been associated with a high inci

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

175 cellular migration; conversely, depletion of Cx43 increased cell migration in immortalized normal EEC

176 on between heterocellular pairs, and reduces Cx43 intensity in contact regions.

177 Direct Cx43 interaction with ZO-1 plays a critical role in gap

178 Our findings also uncovered that Cx43 interacts with the hypoxia-inducible protein N-Myc

179 sion of Cx43 trafficking, or hypoxia-induced Cx43 internalization attenuates heterocellular contact d

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

181 Therefore, Cx43 is a potential target for prevention of aberrant ca

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

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

184 This equilibration does not occur when Cx43 is not present.

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

186 rescued by Gap27, suggesting that increased Cx43 is responsible for the observed Cx43 phenotypes.

187 Cx43 is thus a novel target for influencing metabolite h

188 nducer of kinase activity, but its effect on Cx43 is unknown.

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

190 ndogenous entity translated independently of Cx43, is critical for Cx43 gap junction trafficking, mai

191 rts have found that an internally translated Cx43 isoform, GJA1-20k, is an auxiliary subunit for the

192 In astrocyte-specific Cx43 knock-out mice the magnitude of heart rate response

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

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

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

196 pletion, while lysosomal inhibition restored Cx43 levels.

197 Moreover, we show that the cx43(lh10) allele, which has increased Cx43 protein leve

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

199 Alterations in Cx43 localization and reductions in gap junction couplin

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

201 cardiac edema and correlated with changes in Cx43 localization.

202 ngle internal translation initiation site in Cx43 (M213L mutation), which generates full-length Cx43,

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

204 c Cx43 remodeling and suggest that targeting Cx43 may be a therapeutic strategy for preventing heart

205 Thus, Cx43-mediated astrocyte metabolic networks serve as an e

206 between TRPV4 and Cx43 channels, leading to Cx43-mediated release of ATP which propagates/amplifies

207 We here show that Cx43 mediates gap-junctional coupling between collective

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

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

210 art failure; furthermore, support the use of Cx43 mimetic peptide Gap27 as an effective therapeutic t

211 We propose to determine salutary effect of Cx43 mimetic peptide Gap27 in the progression of heart f

212 Four weeks after AV-Shunt surgery, the Cx43 mimetic peptide Gap27 or scrambled peptide, were ad

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

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

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

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

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

218 myocardium, we found that, compared with WT Cx43, mutant Cx43 expression increases ERK activation, p

219 The three Cx43 mutations all showed the same gain of function acti

220 nal expression systems to characterize three Cx43 mutations linked to palmoplantar keratoderma and co

221 ole in skin-limited diseases caused by human Cx43 mutations.

222 the skeletal muscle macrophages neighboring Cx43 non-expressing fibers.

223 Notably, the expression levels of OCN and CX43 on Day 21 were significantly increased only in the

224 turnover and phosphorylation of connexin 43 (Cx43), one of the major proteins of gap junctions, can a

225 d pharmacological agents that inhibit either Cx43 or AKT, differentially influenced collagen, GAG and

226 gical recordings in cell cultures expressing Cx43 or Cx45, the principal isoforms expressed in cardia

227 HeLa cells expressing Cx43 or Cx50 were loaded with Fluo-8, and IP(3) or Ca(2+

228 Additionally, Cx43 overexpression effectively rescued the IL-22-induce

229 Cx43 overexpression markedly inhibited the proliferation

230 novel regulators of endocytic trafficking of Cx43, participating in the pathological remodeling of ga

231 creased Cx43 is responsible for the observed Cx43 phenotypes.

232 ns, expression of BAG3 affected the state of Cx43 phosphorylation and its degradation.

233 addition to altering gap junction stability, Cx43 phosphorylation directly and dynamically regulates

234 n levels with Ad5 infection rapidly inducing Cx43 phosphorylation events consistent with altered gap

235 f total Cx43 in the myocardium and increases Cx43 phosphorylation on sites phosphorylated by extracel

236 am-regulated gene 1 protein (NDRG1) and that Cx43 phosphorylation status controls this interaction an

237 patients (n = 7) revealed decreased Dsg1 and Cx43 plasma membrane localization compared with control

238 Our results strongly suggest that Cx43 play a pivotal role in the progression of cardiac d

239 Specifically, these Cx43-positive strings originated at the finest capillari

240 he primary arteries and did not overlap with Cx43-positive strings.

241 down of EHD1 impaired the internalization of Cx43, preserving gap junction-intercellular coupling in

242 n kinase 1 (CK1)-mediated phosphorylation of Cx43 promotes gap junction assembly.

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

244 that Si (50 mug/ml) significantly increased CX43 protein expression and gap junction communication i

245 We find reduced Cx43 protein levels due to decreased GJA1 mRNA transcrip

246 ap junction function occurs prior to reduced Cx43 protein levels with Ad5 infection rapidly inducing

247 t the cx43(lh10) allele, which has increased Cx43 protein levels, exhibits increased regenerate lengt

248 reduced the levels of Cx43 by dysregulating Cx43 protein stability.

249 x43 gap junction trafficking, maintenance of Cx43 protein, and normal electrical function of the mamm

250 of Cx43 serine-triplet triggers pathological Cx43 redistribution to the lateral sides of cardiomyocyt

251 mutation of the CK1 phosphorylation sites in Cx43 reduces the levels of total Cx43 in the myocardium

252 Thus, we suggest that Cx43 reduction in symptomatic DMD carrier mice leads to

253 creased upon Dsg1 loss, we hypothesized that Cx43 reduction was due to enhanced protein degradation.

254 tion protein connexin-43 (Cx43), yet whether Cx43 regulates collective invasion remains unclear.

255 ntributes to the understanding of pathologic Cx43 remodeling and encourages further research into dev

256 esults demonstrate a mechanism of dystrophic Cx43 remodeling and suggest that targeting Cx43 may be a

257 325/S328/S330 phosphorylation, and prevented Cx43 remodeling in mdx hearts.

258 ttle is known on the molecular mechanisms of Cx43 remodeling in pathological context.

259 atic DMD carrier mice leads to prevention of Cx43 remodeling in the heart and prevention of aberrant

260 xS3E, but not mdxS3A, mice were resistant to Cx43 remodeling, with a corresponding reduction of Cx43

261 itogen-activated protein kinase (MAPK) sites Cx43(S255/262/279/282A) (MK4) on a permanent middle cere

262 Cx43(S368A), the casein kinase 1 (CK1) sites Cx43(S325A/328Y/330A), and the mitogen-activated protein

263 Supporting this, PKC-dependent Cx43 S368 phosphorylation, which signals Cx43 turnover,

264 mutations at the protein kinase C (PKC) site Cx43(S368A), the casein kinase 1 (CK1) sites Cx43(S325A/

265 We hypothesized that hypophosphorylation of Cx43 serine-triplet triggers pathological Cx43 redistrib

266 , we generated knockin mdx mice in which the Cx43 serine-triplet was replaced with either phospho-mim

267 identified a reduction of phosphorylation of Cx43 serines S325/S328/S330 in human and mouse DMD heart

268 al mechanotransduction processes mediated by Cx43 signalling.

269 sion increased cell-cell dye transfer, which Cx43 silencing inhibited, suggesting that Dsg1 promotes

270 l connexin-43 (Cx43) at the membrane through Cx43 silencing, suppression of Cx43 trafficking, or hypo

271 forward trafficking of the newly synthesized Cx43 that already reached the Golgi was not affected in

272 and subcellular localization of connexin-43 (Cx43), the major ventricular gap junction protein, in DM

273 Connexin43 (Cx43), the predominate connexin in the myocardium and ep

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

275 he Cx32CT domain residue Tyr(243) Unlike for Cx43, the tyrosine phosphorylation of the Cx32CT increas

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

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

278 - 20 kDa), which is required for full-length Cx43 trafficking, but by an unknown mechanism.

279 brane through Cx43 silencing, suppression of Cx43 trafficking, or hypoxia-induced Cx43 internalizatio

280 l function for BAG3 that involves control of Cx43 turnover under normal and stress conditions and pot

281 ent Cx43 S368 phosphorylation, which signals Cx43 turnover, increased after Dsg1 depletion, while lys

282 veal a role for Dsg1 in regulating epidermal Cx43 turnover.

283 Without GJA1-20k, poorly trafficked Cx43 was degraded.

284 We found that Cx43 was expressed in punctate fashion on astroglia, sur

285 Intracellular Cx43 was found to be partly retained in the endoplasmic

286 Given this immunological role of Cx43, we hypothesized that gap junctions would be target

287 sing the Gap27 peptide inhibitor specific to Cx43, we show that Cx43-gap junctional intercellular com

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

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

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

291 atrial cells demonstrated increased phospho-Cx43, which was further accentuated by retinoic acid tre

292 macrophages revealed functional activity of Cx43, which was inhibited by administration of Gap19 pep

293 a(25-35) increased the intracellular pool of Cx43 with a parallel decrease in gap junction assembly a

294 ies revealed an interaction between MYL4 and Cx43 with altered localization of Cx43 hemichannels to t

295 Interaction of Cx43 with EHD1 was mediated by Eps15 and promoted by pho

296 ed the impact of wild-type (WT) and knock-in Cx43 with serine to alanine mutations at the protein kin

297 ction coupling by pharmaceutically targeting Cx43 with verapamil.

298 annels with the same efficiency as wild-type Cx43, with normal voltage gating and a unitary conductan

299 xpress the gap junction protein connexin-43 (Cx43), yet whether Cx43 regulates collective invasion re

300 We find loss of Cx43/ZO-1 complexing during Ad5 infection by co-immunopr