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Study highlights the role of polyamines in the regulation of connexin 43 (Cx43) gap junctions. The study found that polyamines augment cell-to-cell communication and prevent uncoupling of Cx43 gap junctions induced by acidification and high [Ca2 (zeige CA2 ELISA Kits)+]i.
Cx43 expression which may positively regulate cell migration is ER-dependent in ER-positive breast cancer cells.
This study observed a progressive increase in Cx43 expression in the SOD1(G93A) mouse model of ALS during the disease course. Notably, this increase in Cx43 was also detected in the motor cortex and spinal cord of ALS patients.
We suggest that lymph node metastatic adenoid cystic carcinoma cells (AdCC) acquire cancer stem cell features involving the up-regulation of nicotinamide N-Methyltransferase (zeige NNMT ELISA Kits) and the loss of gap junction protein alpha-1, leading to epithelial-mesenchymal transition and consequent AdCC metastasis
Data show that Cx43 was inhibited predominantly via IL-1beta (zeige IL1B ELISA Kits)-activated ERK1/2 (zeige MAPK1/3 ELISA Kits) and p38 MAP kinase (zeige MAPK14 ELISA Kits) cascades.
BMP2 (zeige BMP2 ELISA Kits) decreases gap junction intercellular communication of luteinized human granulosa cells by downregulating Cx43 expression through an ALK2 (zeige ACRV1 ELISA Kits)/ALK3 (zeige BMPR1A ELISA Kits)-mediated SMAD (zeige SMAD1 ELISA Kits)-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 (zeige GJB6 ELISA Kits)) is heavily expressed in astrocytes and that drebrin (zeige DBN1 ELISA Kits) 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 (zeige DBN1 ELISA Kits) interacts with connexin 43, stabilizes this protein at membranes, and links it to the actin cytoskeleton. In vivo drebrin (zeige DBN1 ELISA Kits) is widespread in diverse non-neuronal tissues of epithelial, endothelial, and smooth muscle origin, but not ubiquitous.
These results suggested that the AKT (zeige AKT1 ELISA Kits) pathway was the dominant pathway involved in Cx43-mediated chronic cadmium toxicity.
Cdk5 (zeige CDK5 ELISA Kits) 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 (zeige SOST ELISA Kits)-/-mice, but revealed no cortical abnormalities in single Gja1+/-or Sost (zeige SOST ELISA Kits)+/-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.
Thus we propose that Cx43 might enhance the activation of Nrf2 (zeige NFE2L2 ELISA Kits)/ARE pathway by means of inhibiting c-Src (zeige SRC ELISA Kits) activity to hinder the nuclear export of Nrf2 (zeige NFE2L2 ELISA Kits), and then reduce expression of FN, ICAM-1 (zeige ICAM1 ELISA Kits) 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 (zeige CELF1 ELISA Kits) expression in the dilated cardiomyopathy heart.
we performed cotransfections of AP-1 (zeige JUN ELISA Kits) expression plasmids with different mouse Gja1 promoter/luciferase reporter constructs within TM3 (zeige TPM1 ELISA Kits) Leydig and TM4 (zeige TPM4 ELISA Kits) Sertoli cells.We showed that a functional cooperation between cJun (zeige JUN ELISA Kits) and cFos activates Gja1 expression and requires an AP-1 (zeige JUN ELISA Kits) DNA regulatory element located between -132 and -26 bp
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 (zeige HSP90AA1 ELISA Kits) responsible for proper folding of procollagen molecules.
Hapln1a (zeige HAPLN1 ELISA Kits)-ECM (zeige MMRN1 ELISA Kits) stabilizes the secreted growth factor (zeige WNT2 ELISA Kits) Semaphorin3d (Sema3d (zeige SEMA3D ELISA Kits)), which has been independently shown to mediate Cx43 dependent phenotypes during regeneration.
Hapln1a (zeige HAPLN1 ELISA Kits) has a critical role in connexin43-dependent growth and patterning in the regenerating fin skeleton
Sema3d (zeige SEMA3D ELISA Kits) 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 (zeige COL6A1 ELISA Kits)) 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 (zeige IGF1R ELISA Kits) and AT-1R in AT-II and IGF-1 (zeige IGF1 ELISA Kits)-induced Cx43 expression in SV SMCs involving Erk 1 (zeige MAPK3 ELISA Kits)/2 and downstream activation of the AP-1 (zeige JUN ELISA Kits) transcription factor.
Gap junctional intercellular communication in human bladder smooth muscle cells and suburothelial myofibroblastsdepend of Cx43 rather than on Cx45 (zeige GJC1 ELISA Kits).
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 (zeige RHOA ELISA Kits) 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 (zeige TGFB1 ELISA Kits) 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 (zeige GJB2 ELISA Kits), Cx32 (zeige GJB1 ELISA Kits), and Cx43
CBN (zeige CALB1 ELISA Kits) 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 (zeige CDH1 ELISA Kits) on the development, mRNA and protein expression of bovine blastocysts cultured in vitro or in vivo.
These findings indicated that Cx43/miR (zeige MYLIP ELISA Kits)-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 (zeige CDK4 ELISA Kits) 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