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Data show that Cx43 was inhibited predominantly via IL-1beta (show IL1B Proteins)-activated ERK1/2 and p38 MAP kinase (show MAPK14 Proteins) cascades.
BMP2 (show BMP2 Proteins) decreases gap junction intercellular communication of luteinized human granulosa cells by downregulating Cx43 expression through an ALK2 (show ACRV1 Proteins)/ALK3 (show BMPR1A Proteins)-mediated SMAD (show SMAD1 Proteins)-dependent signaling pathway.
NO controls the calcium signal propagation through Cx37-containing gap junctions. The tyrosine phosphatase SHP-2 is the essential mediator and NO target.
Taking into account that connexin-43 (Cx43) (together with Cx30 (show GJB6 Proteins)) is heavily expressed in astrocytes and that drebrin (show DBN1 Proteins) supports cell-cell contacts, the understanding of details of how brain cells live and die reveals molecular pathology involved in neurodegeneration, Alzheimer's disease (AD), other cognitive disorders, and aging
at gap junctions drebrin (show DBN1 Proteins) interacts with connexin 43, stabilizes this protein at membranes, and links it to the actin cytoskeleton. In vivo drebrin (show DBN1 Proteins) is widespread in diverse non-neuronal tissues of epithelial, endothelial, and smooth muscle origin, but not ubiquitous.
These results suggested that the AKT (show AKT1 Proteins) pathway was the dominant pathway involved in Cx43-mediated chronic cadmium toxicity.
Gap junctional intercellular communication mediated by the Cx43 channels plays a central role throughout the differentiation of bone marrow stromal cells into osteoblasts, from the early stages to the process of mineralization.
Study identify a role for Cx43 formed gap junction channels in the regulation of T lymphocyte proliferation and pro-inflammatory cytokines release during hypertension.
The article findings propose a novel, lactate-handling role for Cx43 (GJA1 gene) which may be particularly critical in acidotic regions of tumours.
We conclude that the targeted action of JM2 (show FOXP3 Proteins) on Cx43 channels may improve the tolerance of implanted tissue-engineered constructs against the innate inflammatory response.
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.
Thus we propose that Cx43 might enhance the activation of Nrf2 (show NFE2L2 Proteins)/ARE pathway by means of inhibiting c-Src (show SRC Proteins) activity to hinder the nuclear export of Nrf2 (show NFE2L2 Proteins), and then reduce expression of FN, ICAM-1 (show ICAM1 Proteins) and TGF-b1, ultimately attenuating renal fibrosis in diabetes.
Upon the induction of autophagy by dexamethasone (Dex), connexin 43 (Cx43) was internalized into autophagosome/autolysosomes and degraded by autophagy.
Disruption of the Cx43/miR21 pathway leads to osteocyte apoptosis and increased osteoclastogenesis with aging.
findings suggest that GJA1 may be one of the downstream targets of BMPR1A signaling in osteoclasts that mediates osteoclast-osteoblast communication during bone remodeling.
Down-regulation of Cx43 follows increased CELF1 (show CELF1 Proteins) expression in the dilated cardiomyopathy heart.
we performed cotransfections of AP-1 (show JUN Proteins) expression plasmids with different mouse Gja1 promoter/luciferase reporter constructs within TM3 (show TPM1 Proteins) Leydig and TM4 (show TPM4 Proteins) Sertoli cells.We showed that a functional cooperation between cJun (show JUN Proteins) and cFos activates Gja1 expression and requires an AP-1 (show JUN Proteins) DNA regulatory element located between -132 and -26 bp
weightlessness simulated by using a random position machine promoted the retention of Cx43 in the Golgi apparatus
show that knockout of the gap junction subunit connexin 43 in astrocytes throughout the brain causes excessive sleepiness and fragmented wakefulness during the nocturnal active phase.
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.
, gap junction 43 kDa heart protein
, gap junction alpha-1 protein
, gap junction membrane channel protein alpha 1
, connexin 32
, gap junction beta-1 protein
, gap junction membrane channel protein beta 1
, alpha 1 connexin
, gap junction protein, alpha 1
, short fin protein
, 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)
, gap junction protein alpha 1
, alpha 3 connexin
, gap junction alpha-3 protein
, gap junction membrane channel protein alpha 3