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anti-Mouse (Murine) GJB2 Antibodies:
anti-Rat (Rattus) GJB2 Antibodies:
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Mouse (Murine) Polyclonal GJB2 Primary Antibody for 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 (show GJB1 Antibodies) and heteromeric Cx26/Cx32 (show GJB1 Antibodies) are permeable to GSH and other endogenous reductants.
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 (show GJB6 Antibodies), 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 .
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.
our work strongly suggests a pathogenic role for GJB3 (show GJB3 Antibodies) p.V37I in various HL phenotypes and provides a quantitative assessment of the risk associated with carriage of this variant and development of HL
mutations in the GJB2 gene specially c.35delG are important causes of ARNSHL in the center and west of Iran
For the first time, a p.R75Q mutation shows intra-familial phenotypic variability. Profoundly deaf twins and their deaf maternal grandmother exhibit the p.R75Q mutation with palmoplantar keratoderma while their deaf mother shows absence of skin disorders. The twins also had a a recessive 35delG, which leads to a truncated premature protein inhibiting any action of the dominant p.R75Q mutation.
DFNB1 locus does not appear to be a major contributor to nonsyndromic sensorineural hearing loss (NSSHL) in Sao Tome and Principe. However, the presence of both pathogenic and likely pathogenic mutations in GJB2 suggests that GJB2-related NSSHL might still occur in this population.
Given that a previous paper suggested TMPRSS3 (show TMPRSS4 Antibodies) and GJB2 genes as responsible for a digenic form of hearing loss, our data support and reinforce this hypothesis.
a series of molecular dynamics simulations has been performed to investigate the effect of applied static and alternating electric fields on the stability and conformation of human connexin26 hemichannel.
We performed simultaneous hearing screening and genetic screening targeting four common deafness mutations (p.V37I and c.235delC of GJB2, c.919-2A>G of SLC26A4 (show SLC26A4 Antibodies), and the mitochondrial m.1555A>G) in 5173 newborns at a tertiary hospital between 2009 and 2015,We delineated the longitudinal auditory features of the highly prevalent GJB2 p.V37I mutation on a general population basis
The proportion of carriers for GJB2 gene mutations in patients with hearing loss from southern Zhejiang has reached 21.5%.
Genotype may affect deafness severity, but environmental and other genetic factors may also modulate the severity and evolution of GJB2-GJB6 (show GJB6 Antibodies) deafness
results suggest that GJB2 and CIB2 (show CIB2 Antibodies) are common cause of hearing loss in different Pakistani ethnicities
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