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Human Polyclonal GJB1 Primary Antibody pour IHC (p), WB - ABIN965915
Corcos, Lafrenière, Begy, Loch-Caruso, Willard, Glover: Refined localization of human connexin32 gene locus, GJB1, to Xq13.1. dans Genomics 1992
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Rat (Rattus) Monoclonal GJB1 Primary Antibody pour FACS, IF - ABIN5578830
Goodenough, Paul, Jesaitis: Topological distribution of two connexin32 antigenic sites in intact and split rodent hepatocyte gap junctions. dans The Journal of cell biology 1988
Cow (Bovine) Polyclonal GJB1 Primary Antibody pour IHC, WB - ABIN2774855
Dagli, Yamasaki, Krutovskikh, Omori: Delayed liver regeneration and increased susceptibility to chemical hepatocarcinogenesis in transgenic mice expressing a dominant-negative mutant of connexin32 only in the liver. dans Carcinogenesis 2004
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Cx32 mediated reactive oxygen species/endoplasmic reticulum stress/apoptosis signal pathway activation played an important part in Ischemia-reperfusion-induced acute kidney injury.
This study demonstrated that loss of Cx32 promote inflammation and increase vulnerability of myelinated fibers, as shown in Cx32KO mice following EAE induction.
Blocking of connexin32 or connexin43 hemichannels decreased serum levels of pro-inflammatory cytokines, and reduced acetaminophen-induced liver injury.
The results of this study indicated that the Leu89Pro substitution in the second transmembrane domain of CX32 disrupts the trafficking of the protein, inhibiting the assembly of CX32 gap junctions, which in turn may result in peripheral neuropathy.
We show that the cell-surface and secreted isoforms of CSF-1 have opposing effects on macrophage activation and disease progression in a mouse model of connexin32-deficientconnexin32-deficient mice
Results identify CSF-1-activated macrophages as crucial mediators of detrimental Schwann cell dedifferentiation in Cx32-deficient mice
Blockade of endothelial Cx32 increased tissue factor expression induced by TNF-alpha stimulation and cell-cell interaction via ICAM1. Direct Cx32-mediated interaction modulates TF expression in ECs during vascular inflammation.
These findings support a role for Cx32 in non-myelinating and regenerating populations of Schwann cells in normal axonal maintenance in re-myelination, and regeneration of peripheral nerve following injury
Connexin32 interacts with connexin26 and the mitochondrial protein, sideroflexin-1, at the plasma membrane forming a novel signaling nexus.
These results demonstrate that the incidence of hepatocellular carcinoma increases only in male Cx32KO mice, presumably due to enhanced tumor promotion and progression signals associated with Cx32 deficiency.
Cx32 is differentially phosphorylated and exists in a complex with SAP97 and CaM.
Cx32 therapy improves gap junctional conductance results in larger infarct size, and no antiarrhythmic efficacy.
Connexin 36 is expressed in beta and connexins 26 and 32 in acinar cells at the end of the secondary transition of mouse pancreatic development and increase during fetal and perinatal life.
Data show that absence of connexin30 in knockout mice changes the expression patterns of connexin26 and connexin32 in glial cells and leptomeninges.
Cx32 can functionally replace Cx26 in the mouse cochlea resulting in almost normal hearing
Induction of Cxs 29 and 32 in the injury border suggests that altered Cxs may contribute to the propagation of injury-related and/or regeneration signals after acute brain injury.
The data of this study revealed Deletion of oligodendrocyte Cx32 and astrocyte Cx43 causes white matter vacuolation, astrocyte loss and early mortality.
oligodendrocyte-astrocyte gap junction coupling in Cx32 or Cx47 knockout mice. In corpus callosum, oligodendrocytes appeared to be directly coupled to other oligodendrocytes. O:O coupling was more affected in mice lacking Cx32 than in mice lacking Cx47.
Asn(175) of Cx32 is a critical residue for heterotypic docking and functional gap junction channel formation between the Cx32 and Cx26 hemichannels.
These findings suggest that altered Cx32 expression, a loss of intercellular Cx32 and a gain of intracytoplasmic Cx32 in the form of punctate "dot", plays an important role in the formation of gastric adenocarcinomas.
Cx32 expression may induce cisplatin resistance by modulating drug efflux transporter expression and activating the EGFRprotein kinase B signalling pathway in ovarian cancer cells.
EphB1 and EphA1 phosphorylate the Cx32CT domain residue Tyr(243) Unlike for Cx43, the tyrosine phosphorylation of the Cx32CT increased gap junction intercellular communication.
This study showed that an An 8-generation family with X-linked Charcot-Marie-Tooth: Confirmation Of the pathogenicity Of a 3' untranslated region mutation in GJB1.
Findings support the hypothesis that paracrine signalling alteration due to Cx32 hemichannel dysfunction underlies CMTX1 pathogenesis.
These "periferal nervous system-only" mutations form gap junction plaques and produce levels of junctional coupling similar to those for wild-type Cx32. In contrast, mutants with central nervous system manifestations either form no morphological gap junction plaques or, if they do, produce little or no detectable junctional coupling.
Results show that the GJB1 (connexin 32; Cx32) mutants R75P, R75Q and R75W display variable structural conformation and dynamic behavior compared to the native protein.
Point mutation of GJB1 gene, encoding connexin 32, is associated with X-linked Charcot-Marie-Tooth disease.
Cx32 regulates the sensitivity of hepatocellular carcinoma cells to doxorubicin via the Src/FAK signaling pathway
Study verifies that Cx32 exerts an inhibitory effect on extrinsic apoptosis in cervical cancer (CaCx) cells, and suggests that Cx32 may regulate the progression and micro-environment of CaCx cells.
Cx32 is essential for cell-cell interactions that facilitate driving hESCs through hepatic-lineage maturation.
Study provides a novel mechanism for Cx32's anti-apoptotic effect and provides a reasonable explanation for the pro-tumor effect of Cx32 in human cervical cancer cells.
Genetic analysis revealed a total of 43 mutations including 6 novel mutations. Ten mutations were found from two or more unrelated families. p.V95M was most frequently observed. The frequency of CMTX1 was 9.6% of total Korean CMT family and was 14.8% when calculated within genetically identified cases
PBX1 is one of the determinants in the Cx32 promoter targeting site, preventing further damage of gap junction protein in H. pylori-associated gastric carcinogenesis.
Study describes a novel mutation deleting entire P2 promoter of GJB1 gene in a single large family with X-linked Charcot-Marie-Tooth disease. Inheritance and phenotype of affected individuals had classical features of X linked peripheral neuropathy. This study affirms the role of P2 promoter being vital for Schwann cell function.
our results suggest that Cx32 inhibits Hepatocellular carcinoma (HCC) invasion and metastasis through Snail-mediated EMT, Cx32 and this signaling pathway molecules may offer potential targets for HCC cancer therapy
The study indicated that CNS impairment was not rare in Chinese CMT1X patients. Mutations in the EC2 domain of the GJB1 gene were hotspot in Chinese CMT1X patients.
Abnormal Cx32 expression/localization in cervical cancer appears to be both a mechanism and biomarker of chemotherapeutic resistance.
Study reports mutation frequency of GJB1 in 210 Hungarian Charcot-Marie-Tooth neuropathy (CMT) patients and phenotype comparison between male and female CMT X type 1 patients. 13 missense substitutions were found in GJB1; pathogenic alterations were found mainly in males. Statistical analysis of CMT X type 1 patients revealed a significant difference between genders regarding the age of onset, CMT and examination scores.
In conclusion, mutation screening should be first performed in intermediate Charcot-Marie-Tooth patients, especially those with additional features. The novel GJB1 variants c.5A>G, c.8G>A, c.242T>C and c.269T>C are considered pathogenic, and c.317T>C and c.434T>G are classified as probably pathogenic.
Certain Golgi-retained Cx32 mutants may interfere with exogenously delivered Cx32. Screening for mutant-wild type Cx32 interactions should be considered prior to planning gene addition therapy for CMT1X.
intermediate invasive status of bovine trophoblast is supported by the fact that trophoblast giant cells coexpress connexins (Cx)26, Cx32, and Cx43
This gene encodes a member of the gap junction protein family. The gap junction proteins are membrane-spanning proteins that assemble to form gap junction channels that facilitate the transfer of ions and small molecules between cells. According to sequence similarities at the nucleotide and amino acid levels, the gap junction proteins are divided into two categories, alpha and beta. Mutations in this gene cause X-linked Charcot-Marie-Tooth disease, an inherited peripheral neuropathy. Alternatively spliced transcript variants encoding the same protein have been found for this gene.
, connexin 32
, gap junction protein, beta 1, 32kDa
, gap junction beta-1 protein
, gap junction membrane channel protein beta 1
, GAP junction 28 kDa liver protein
, gap junction protein, beta 1, 32 kD
, gap junction protein beta 1