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Blocking of connexin32 or connexin43 (show GJA1 ELISA Kits) 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 (show CSF1 ELISA Kits) have opposing effects on macrophage activation and disease progression in a mouse model of connexin32-deficientconnexin32-deficient mice
Results identify CSF-1 (show CSF1 ELISA Kits)-activated macrophages as crucial mediators of detrimental Schwann cell dedifferentiation in Cx32-deficient mice
Blockade of endothelial Cx32 increased tissue factor (show F3 ELISA Kits) expression induced by TNF-alpha (show TNF ELISA Kits) stimulation and cell-cell interaction via ICAM1 (show ICAM1 ELISA Kits). 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 (show GJB2 ELISA Kits) and the mitochondrial protein (show COX6B2 ELISA Kits), sideroflexin-1 (show SFXN1 ELISA Kits), 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.
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.
Clear clinical/electrophysiological sex differences (intra- and inter family) were shown in patients with hereditary motor-sensory neuropathy 1X with the small es, Cyrillic.259C>G (small er, Cyrillic.P87A) mutation in the GJB1 gene.
In summary, Cx32 is involved in cisplatin resistance, and cytoplasmic Cx32 plays an important role in chemoresistance.
Mutations in noncoding DNA of GJB1 are a major cause of CMTX1 and highlight the importance of mutations in noncoding DNA in human disease.
NMR study of N-terminal mutants of Connexin 26 (show GJB2 ELISA Kits) and Connexin 32
Knockdown of Cx32 by shRNA in HepG2 cells induced EMT (show ITK ELISA Kits), while overexpression of Cx32 converted EMT (show ITK ELISA Kits) to mesenchymal-epithelial transition (MET) in the HepG2/DOX cells. These results suggest that Cx32 is an important regulator of DOX-induced EMT (show ITK ELISA Kits) in hepatocellular carcinoma . Cx32 could be considered as a novel target to reverse DOX resistance in hepatocellular carcinoma
The three novel missense mutations within the GJB1 gene broaden the mutational diversity of X-linked Charcot-Marie-Tooth Disease type I (CMT1X).
A novel point mutation in GJB1 was detected, expanding the spectrum of GJB1 mutations known to be associated with CMTX.
Complete loss of connexin32 function is sufficient to produce central nervous system dysfunction with clinical manifestations.
intermediate invasive status of bovine trophoblast is supported by the fact that trophoblast giant cells coexpress connexins (Cx)26 (show GJB2 ELISA Kits), Cx32, and Cx43 (show GJA1 ELISA Kits)
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