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anti-Mouse (Murine) GJB2 Antikörper:
anti-Rat (Rattus) GJB2 Antikörper:
anti-Human GJB2 Antikörper:
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Mouse (Murine) Polyclonal GJB2 Primary Antibody für ELISA, WB - ABIN252905
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 (zeige GJB1 Antikörper) and heteromeric Cx26/Cx32 (zeige GJB1 Antikörper) are permeable to GSH and other endogenous reductants.
Excessive accumulation of connexin 26 protein in intracellular domains promotes squamous cell carcinoma progression.
the reduction in microtubules in pillar cells might be responsible for the failure of the tunnel of Corti to open, and the malformed phalangeal processes might negatively affect the supporting framework of the organ of Corti, which would be a new mechanism of Gjb2-related hearing loss.
Cochlea in Cx26(+/-)/Cx30 (zeige GJB6 Antikörper)(+/-) mice displayed normal development and had no apparent hair cell degeneration. Double heterozygous deletion of Cx26 and Cx30 (zeige GJB6 Antikörper) in the epithelial cells did not reduce endocochlear potential and had normal hearing, suggesting that Cx26(+/-)/Cx30 (zeige GJB6 Antikörper)(+/-) may mainly impair gap junctional functions in the cochlear lateral wall and lead to EP reduction and hearing loss.
Our study demonstrated that the homozygousp.V37I variant in GJB2 gene knock-in mouse modeled the hearing phenotype of the human patients and can serve as a useful animal model for further studies
we observed that deletion of CX26 in excitatory neurons around birth significantly reduces the frequency and size of network oscillations and subsequently the frequency of mEPSCs of neocortical excitatory neurons.
Cx26 contributes to epidermal homeostasis by regulating keratinocyte differentiation; mice harboring a disease-linked Cx26 mutant display epidermal abnormalities yet retain most wound healing properties.
the development of a novel strategy to differentiate induced pluripotent stem cells into functional CX26-gap junction plaque-forming cells.
The hearing loss and the reduction of active amplification in the Cx26 targeted-deletion mice are progressive and different at high and low frequency regions, first occurring in the high frequency region and then progressively extending to the middle and low frequency regions with mouse age increased.
In connexin knock-outs, Cx26 and Cx30 (zeige GJB6 Antikörper), inner hair cells remained stuck at a prehearing stage of development.
Reduced Cx26 expression in the mature mouse cochlea may increase susceptibility to noise-induced hearing loss .
It was shown that thiol levels increased and disulphide levels decreased in patients with autosomal recessive non-syndromic hearing loss and GJB2 gene mutations.
The mutation frequencies of GJB2, SLC26A4 (zeige SLC26A4 Antikörper), GJB3 (zeige GJB3 Antikörper), and mitochondrial genes were 3.04%, 3.51%, 0.16%, and 0.88%, respectively among the Hakka population of Southern China
In conclusion, a novel missense mutation in GJB2 (DFNA3), affecting the second extracellular domain of the protein, was identified in a family with autosomal dominant non-syndromic hearing loss.
our present results indicate an association between GJB2 polymorphisms (rs2274084) and NPC (zeige NPC1 Antikörper) susceptibility. The TT genotype of GJB2 may be a risk factor for NPC (zeige NPC1 Antikörper).
Mutation in GJB2 gene is associated with deafness.
The p.Lys22Asn GJB2 mutation causes a dominant form of hearing loss associated with variable expression of palmoplantar keratoderma, representing a model of full penetrance, with an age-dependent effect on the phenotype
These data suggest that chronic exposure to glucose-evoked TGFbeta1 (zeige TGFB1 Antikörper) induce an increase in CX26 and CX43 (zeige GJA1 Antikörper) expression, consistent with changes observed in tubular epithelia from patients with diabetic nephropathy.
Bi-allelic variations in the GJB2 gene cause up to 50% of cases of newborn hearing loss.
GJB2 mutation is associated with hearing loss.
Family study implicating mutations in GJB2 and USH2A (zeige USH2A Antikörper) in Usher's syndrome with congenital hearing loss
intermediate invasive status of bovine trophoblast is supported by the fact that trophoblast giant cells coexpress connexins (Cx)26, Cx32 (zeige GJB1 Antikörper), and Cx43 (zeige GJA1 Antikörper)
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