Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Weitere Synonyme anzeigen
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.
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 .
mir (zeige MLXIP Antikörper)-27a was identified as an apoptotic molecule that participates in Cx26 knockout-induced apoptosis in the cochlear sensory epithelium of mice by downregulating sgk1 (zeige SGK1 Antikörper) 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
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
Compared with previous studies, we found that the c.109G>A mutation allele of GJB2 was relatively lower in the profound Chinese nonsyndromic sensorineural hearing loss population in comparison to the moderate-to-profound ones, and the c.1174A>T mutation allele of SLC26A4 (zeige SLC26A4 Antikörper) was relatively higher.
the identification of a previously identified c.100C>T mutation, and a novel homozygous mutation, c.1283C>A in TMC1 (zeige TMC1 Antikörper), in this study supports TMC1 (zeige TMC1 Antikörper) gene as one of the second-tier hearing loss genes, after GJB2 in India. Testing for TMC1 (zeige TMC1 Antikörper) may be considered in all GJB2-negative nonsyndromic hearing loss cases
our work strongly suggests a pathogenic role for GJB3 (zeige GJB3 Antikörper) 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.
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