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GJB2 encodes a member of the gap junction protein family. Additionally we are shipping GJB2 Kits (36) and GJB2 Proteins (4) and many more products for this protein.
Showing 10 out of 90 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.
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.
Over-expression of BDNF (show BDNF Antibodies) beginning around 1 month of age resulted in a significant rescue of spiral ganglion degeneration in connexin 26 knockout mice.
Using two models of CX26-associated deafness, we demonstrate that disruption of the CX26-dependent gap junction plaque is the earliest observable change during embryonic development of connexin-associated deafness.
We have found a 148G-A transition in the GJB2 gene, resulting in an asp50-to-asn (D50N) substitution in a girl with congenital deafness. This finding allowed us to diagnose small a, Cyrillic KID syndrome.
The detection rate of the single GJB2 mutation among the 160 SNHL subjects in the present study (6.25%) was higher than 2.58% in normal hearing controls in Korean. The DFNB1 was clearly excluded as a molecular etiology in four (40%) subjects
We found a novel mutation in the GJB2 gene and two trimutations with SNHL not previously reported.
ER-alpha (show ESR1 Antibodies) status of endometrioid adenocarcinomas could restrict eventual proapoptotic or anti-apoptotic impact of aberrantly expressed Cx43 (show GJA1 Antibodies) and Cx26 in these tumors.
GJB2 mutation is associated with hereditary deafness in Yakutiya.
GJB2 and SLC26A4 (show SLC26A4 Antibodies) mutations are associated with good post-implant outcomes.
exon sequencing of GJB2, SLC26A4 (show SLC26A4 Antibodies), and mtDNA12SrRNA reveals that non-syndromic deafness in Xiamen, China appears to have a genetic etiology
Data suggest that ombined hearing screening and genetic screening of gap junction protein beta 2 (GJB2), mtDNA 12srRNA and solute carrier (show SERTAD2 Antibodies) family 26, member 4 protein SLC26A4 (show SLC26A4 Antibodies) mutations can improve the rate of detection.
Cx26 structure is nearly identical with and without bound Ca2 (show CA2 Antibodies)+. Ca2 (show CA2 Antibodies)+ regulates Cx26 via ionic conduction block via an electrostatic barrier rather than steric occlusion of the channel pore.
Connexin26 mutation is responsible for palmoplantar keratoderma and deafness.
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