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GJB2 encodes a member of the gap junction protein family. Additionally we are shipping GJB2 Kits (26) and GJB2 Proteins (4) and many more products for this protein.
Showing 10 out of 91 products:
Cow (Bovine) Polyclonal GJB2 Primary Antibody for WB - ABIN2774858
Ulfig: Expression of connexin 26 in the ganglionic eminence of preterm infants after bleedings. in Neuroscience research 2004
Human Polyclonal GJB2 Primary Antibody for WB - ABIN374836
Djalilian, McGaughey, Patel, Seo, Yang, Cheng, Tomic, Sinha, Ishida-Yamamoto, Segre: Connexin 26 regulates epidermal barrier and wound remodeling and promotes psoriasiform response. in The Journal of clinical investigation 2006
Using reconstituted hemichannels in a liposome-based transport-specific fractionation assay, we confirmed that homomeric Cx26 and Cx32 (show GJB1 Antibodies) and heteromeric Cx26/Cx32 (show GJB1 Antibodies) are permeable to GSH and other endogenous reductants.
Reduced Cx26 expression in the mature mouse cochlea may increase susceptibility to noise-induced hearing loss .
mir (show MLXIP Antibodies)-27a was identified as an apoptotic molecule that participates in Cx26 knockout-induced apoptosis in the cochlear sensory epithelium of mice by downregulating sgk1 (show SGK1 Antibodies) expression
Cx26 knockout predisposes the mammary gland to primary mammary tumors in a DMBA-induced mouse model of breast cancer.
Cx26-mediated intercellular communication is required for cochlear development and that deficiency of Cx26 can impair miRNA-mediated intercellular genetic communication in the cochlea, which may lead to cochlear developmental disorders
presence of Cx30 (show GJB6 Antibodies) in the cochlea does not compensate for Cx26 loss, and the absence of both connexins from vestibular sensory epithelia is no more injurious than the absence of one of them
Reciprocal positive regulation between Cx26 and PI3K/Akt (show AKT1 Antibodies) pathway confers acquired gefitinib resistance in non-small-cell lung carcinoma cells by promoting epithelial mesenchymal transition via a gap-junctional communication-independent manner.
The inserting reconstituted gap junction Cx26 liposomes into the oocytes allowed the demonstration of intracellular/extracellular Ca(2 (show CA2 Antibodies)+)-regulated hemi-channel activities.
Study used an inducible gene knockout technique to delete Cx26 expression in the cochlea after birth, results suggest that Cx26 deficiency may impair active cochlear amplification leading to late-onset hearing loss
These results suggest that low levels of Cx26 expression throughout pregnancy and lactation, and not the physiological surge in Cx26, is sufficient for normal gland development and function.
These results suggest that successful treatment of Cx26 deafness requires early intervention before the cochlea fully matures.
There was a high prevalence of IVS1+1G>A mutation in this sample of deaf families in Syria.
homozygous GJB2 c.109G[A mutation may be a cause of sudden death involving both ears.
study suggests that the GJB2 235delC polymorphism, but not the 30-35delG variant, contributes to congenital deafness susceptibility in the Chinese population examined
We report here a non consanguineous assortatively mating hearing impaired family with one of the hearing impaired partners, their hearing impaired sibling and hearing impaired offspring showing compound heterozygosity in the GJB2 gene, involving a dominant mutation p.R184Q and two recessive mutations p.Q124X and c.IVS 1+1G>A in a unique triallelic combination.
There are more than 39 deafness genes reported to cause non-syndromic hereditary hearing loss (HHL) in Iran, of which the most prevalent causative genes include GJB2, SLC26A4, MYO15A, and MYO7A. In addition, we highlight some of the more common genetic causes of syndromic HHL in Iran. [review]
Two GJB2 mutations, c.del35G with an allele frequency of 4.7 % and R32C (3.7 %) were detected in Mauritanian children with non-syndromic hearing loss.
Our results showed that the GJB2 gene is a major contributor to non syndromic hearing loss in Morocco
Compound heterozygous variants c.94C > T (p.R32C) and c.235delC (p.L79Cfs*3) in the GJB2 gene were identified in the two patients of an autosomal recessive non-syndromic hearing loss family, and the heterozygous GJB2 c.94C > T and c.235delC variants were identified in his unaffected father and mother, respectively.
mutations detected in 35 of 156 deaf patients
GJB2 gene mutations are highly prevalent in pre-lingual hearing loss patients from China. 83.64% of the 330 patients carried variations in the GJB2 gene. Seventeen different genotypes were identified. A total of 31.2% of the patients carried 2 confirmed pathogenic mutations. The frequency of c.235delC was higher than that reported previously in the Jiangsu province.
intermediate invasive status of bovine trophoblast is supported by the fact that trophoblast giant cells coexpress connexins (Cx)26, Cx32 (show GJB1 Antibodies), and Cx43 (show GJA1 Antibodies)
This gene encodes a member of the gap junction protein family. The gap junctions were first characterized by electron microscopy as regionally specialized structures on plasma membranes of contacting adherent cells. These structures were shown to consist of cell-to-cell channels that facilitate the transfer of ions and small molecules between cells. The gap junction proteins, also known as connexins, purified from fractions of enriched gap junctions from different tissues differ. 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 are responsible for as much as 50% of pre-lingual, recessive deafness.
gap junction protein, beta 2, 26kDa
, connexin 26
, connexin 29
, gap junction membrane channel protein beta 6
, gap junction protein, beta 2, 26kDa (connexin 26)
, gap junction beta-2 protein
, gap junction membrane channel protein beta 2
, gap junction channel protein connexin 26
, gap junction protein beta 2
, connexin 26 protein