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Cx43 inhibited the growth of U251 cells, promoted morphological changes and migration, and inhibited apoptosis via a mitochondria-associated pathway.
MIF is involved in the pathogenesis of AF, probably by down-regulating the protein and gene expression of Cx43 via ERK1/2 kinase activation
These studies highlight the importance of Cx43 expression and function during osteoblast and chondrocyte differentiation.
The observations identify a novel strategy of prostate cancer cell diapedesis, which depends on the activation of intercellular Cx43/ERK1 (show MAPK3 Proteins)/ERK2 (show MAPK1 Proteins)/Cx43 signaling axis at the interfaces between Cx43-high prostate cancer and endothelial cells.
we present an overview of the key phosphatases known to interact with Cx43 or modulators of Cx43, as well as some possible therapeutic targets to regulate phosphatase activity in the heart.
many of the known non-canonical roles of Cx43 can be attributed to the recently identified six endogenous Cx43 truncated isoforms which are produced by internal translation. In general, alternative translation is a new leading edge for proteome expansion and therapeutic drug development.
Spatio-temporal regulation of connexin43 phosphorylation and gap junction dynamics.
the complex regulatory and signalling networks controlled by the Cx43 CT, including the extensive protein interactome that underlies both gap junction channel-dependent and -independent functions.
Cx43 role in the regulation of the metastatic potential and migration of prostate cancer cells
Results showed that connexin 43 enhanced oxaliplatin cytotoxicity through gap junctional communication function and high concentration of oxaliplatin inhibited connexin 43 expression to counteract its cytotoxicity
The mosaic of Cx43/Cx45 (show GJC1 Proteins)-puncta along cerebral cortex Bergmann glial processes raises the possibility of differential regulation of coupling between these processes via separate but adjacent Cx43-containing and Cx45 (show GJC1 Proteins)-containing gap junctions channels having different permeability and other biophysical properties or may contribute to coupling between Bergmann glia and Purkinje cells.
These data demonstrate non-myocytes in the scar are electrically coupled to myocytes, and coupling depends on Cx43 expression.
The ELF-EMFs did not affect C2C12 myoblast viability or proliferation rate. Conversely, at ELF-EMF intensity in the mT range, the myogenic process was accelerated, through increased expression of MyoD (show MYOD1 Proteins), myogenin (show MYOG Proteins), and connexin 43
These findings suggest that the proteolytic cleavage of the CTD under pathological conditions, such as under the activation of metalloproteinases during tissue injury or inflammation, may account for the deleterious effects of Cx43 in cartilage and bone disorders such as osteoarthritis.
Neonatal hypothyroidism affects germ cell survival and proliferation in prepubertal P mice via impaired testicular glucose homeostasis and decreased expression of connexin 43.
Cdk5 (show CDK5 Proteins) directly phosphorylates Cx43, which regulates the membrane localization and degradation of Cx43 in neurons.
In vivo muCT analysis of cortical bone at age 1 and 3 months confirmed increased thickness in Sost (show SOST Proteins)-/-mice, but revealed no cortical abnormalities in single Gja1+/-or Sost (show SOST Proteins)+/-mice
the presence of the C-terminal domain of Cx43 in osteocytes and other cell types is important to maintain normal structure and mechanical integrity of bone.
The astroglial targeted connexin43 gene knocking-out in APPswe/PS1dE9 mice allowed to diminish gliotransmitter release and to alleviate neuronal damages, reducing oxidative stress and neuritic dystrophies in hippocampal neurons associated to plaques.
Data show that Connexin43 (Cx43) was identified as the gene causing the short-of-fin (sof) phenotype, in which the fin ray segments are shorter but the vertebrae are normal.
serpinh1b is molecularly and functionally downstream of cx43. The gene serpinh1b codes for a protein called Hsp47, a molecular chaperone (show HSP90AA1 Proteins) responsible for proper folding of procollagen molecules.
Hapln1a (show HAPLN1 Proteins)-ECM (show MMRN1 Proteins) stabilizes the secreted growth factor (show WNT2 Proteins) Semaphorin3d (Sema3d (show SEMA3D Proteins)), which has been independently shown to mediate Cx43 dependent phenotypes during regeneration.
Hapln1a (show HAPLN1 Proteins) has a critical role in connexin43-dependent growth and patterning in the regenerating fin skeleton
Sema3d (show SEMA3D Proteins) functions in a common molecular pathway with Cx43 cell proliferation and joint formation
Data show that the cultured fibroblasts from patients with ossification of the posterior longitudinal ligament (OPLL (show COL6A1 Proteins)) exhibited osteogenic characteristics, in which Cx43 played an important role.
Studies indicate that Cardiomyogenesis is determined by stimuli from the cellular microenvironment, where connexin43 may play an important role.
Data demonstrate a cross-talk between IGF-1R (show IGF1R Proteins) and AT-1R in AT-II and IGF-1 (show IGF1 Proteins)-induced Cx43 expression in SV SMCs involving Erk 1 (show MAPK3 Proteins)/2 and downstream activation of the AP-1 (show JUN Proteins) transcription factor.
Gap junctional intercellular communication in human bladder smooth muscle cells and suburothelial myofibroblastsdepend of Cx43 rather than on Cx45 (show GJC1 Proteins).
Critical role of connexin43 in zebrafish late primitive and definitive hematopoiesis.
This study found that down-regulation of Cx43 expression in the junction zone might play an important role in pathogenesis of adenomyosis, and that estradiol modulates gap junctions during adenomyosis.
Cx43 mRNA and protein expression increased after endothelial cell exposure to ketone bodies; this was accompanied by upregulation of gap junctional intercellular coupling and cell migration.
RhoA (show RHOA Proteins) appears to be an important molecular switch that controls Cx43 hemichannel openings and hemichannel-mediated ATP-dependent paracrine intercellular communication under (patho)physiological conditions of stress
Papillary urothelial carcinomas showed moderate cytoplasmic and membrane labelling, while invasive carcinoma showed loss of connexin 43 expression.
Human TGF-beta1 (show TGFB1 Proteins) induces an accumulation of connexin43 in a lysosomal compartment in bovine endothelial cells
Increased degradation of Cx43 and reduction of intracellular communication through gap junctions in high glucose may be of physiological importance by contributing to endothelial cell dysfunction.
intermediate invasive status of bovine trophoblast is supported by the fact that trophoblast giant cells coexpress connexins (Cx)26 (show GJB2 Proteins), Cx32 (show GJB1 Proteins), and Cx43
CBN (show CALB1 Proteins) blocks junctional communication and modulates Cx43 expression in BAEC. These results suggest a feedback mechanism for control of connexin expression based on junctional patency.
Results describe the effect of suppression of connexin 43 and E-cadherin (show CDH1 Proteins) on the development, mRNA and protein expression of bovine blastocysts cultured in vitro or in vivo.
These findings indicated that Cx43/miR (show MYLIP Proteins)-206 is involved in the pathogenesis of early stage steroid-induced avascular necrosis of the femoral head.
Gap junction enhancer AAP10 could attenuate the pro-arrhythmic effect of lysophosphatidic acid, probably by downregulating myocardial nonphosphorylated Cx43 expression.
Ischemic postconditioning protected the heart from I/R injury by attenuating I/R induced decrease of mitochondria Cx43 expression.
In addition to Cx43 dephosphorylation, downregulation of Cx43 plays an essential role in reduced cell coupling in the failing rabbit heart
The localization and distribution of gap junction (GJ) intercellular channels and connexin 43 (Cx43) in cells surrounding spiral ganglion cell bodies in man and guinea pig, were analyzed.
CX43 is therefore essential for the maintenance of spontaneous slow wave activity and subsequent contractile activity in the guinea pig prostate gland.
Data show that connexin 43 (Cx43) is localized in the ooplasmic membrane through zona pellucidae and its level changes over time during culture in porcine oocytes.
The effects of flutamide on connexin 43 expression in porcine placenta and uterus throughout pregnancy are reported.
we demonstrated that modulation of Cx43 expression in the prostate could serve as a sensitive marker of hormonal disruption during different developmental stages.
The in vitro cultivation of cumulus cells was associated with cell proliferation and that Cx43 and Cdk4 (show CDK4 Proteins) gene expression was upregulated after in vitro cultivation, resulting in significantly higher protein levels.
Gonadotropins regulate Cx43 protein expression, degradation and localization in porcine cumulus oocyte complex.
Gene transfer-mediated overexpression of Cx43 increases the absolute amount of phosphorylated and intercalated disk-localized Cx43, improves conduction velocity (CV), and reduces ventricular tachycardia inducibility.
These data suggest that neonatal exposure to flutamide induces long-term effects on the spermatogenic capacity of the pig testis through alterations of Cx43-mediated intercellular communication.
Cx43 expression and distribution are disrupted by ischemia, recovered by the well reperfused regions and further disrupted by no-reflow.
Atrial connexin 43 was reduced in atrial fibrillation. Connexin 43 gene therapy prevented persistent atrial fibrillation.
During ventricular fibrillation, myocardial Cx43 expression was down-regulated, which could be attenuated by administration of ZP123.
This gene is a member of the connexin gene family. The encoded protein is a component of gap junctions, which are composed of arrays of intercellular channels that provide a route for the diffusion of low molecular weight materials from cell to cell. The encoded protein is the major protein of gap junctions in the heart that are thought to have a crucial role in the synchronized contraction of the heart and in embryonic development. A related intronless pseudogene has been mapped to chromosome 5. Mutations in this gene have been associated with oculodentodigital dysplasia and heart malformations.
connexin 43 , connexin-43 , gap junction 43 kDa heart protein , gap junction alpha-1 protein , gap junction membrane channel protein alpha 1 , alpha 1 connexin , etID309742.9 , gap junction protein, alpha 1 , shf , short fin protein , sof , cx43 , gap junction protein, alpha 1, 43 kD (connexin 43) , vascular smooth muscle connexin-43 , alpha 1 gap junction protein , gap junction protein, alpha 1, 43kDa (connexin 43) , Connexin-43 , gap junction protein alpha 1