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抗Mouse (Murine) GJB2 抗体:
抗Rat (Rattus) GJB2 抗体:
抗Human GJB2 抗体:
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 (显示 GJB1 抗体) and heteromeric Cx26/Cx32 (显示 GJB1 抗体) are permeable to GSH and other endogenous reductants.
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 (显示 GJB6 抗体), 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 (显示 MLXIP 抗体)-27a was identified as an apoptotic molecule that participates in Cx26 knockout-induced apoptosis in the cochlear sensory epithelium of mice by downregulating sgk1 (显示 SGK1 抗体) 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 (显示 GJB6 抗体) 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 (显示 AKT1 抗体) 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 (显示 CA2 抗体)+)-regulated hemi-channel activities.
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 (显示 SLC26A4 抗体), 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 (显示 GJB6 抗体) deafness
results suggest that GJB2 and CIB2 are common cause of hearing loss in different Pakistani ethnicities
GJB2 and ERO1LB (显示 ERO1LB 抗体) are implicated in pancreatic cancer progression and can be used to predict patient survival
Significant proportion of children with unilateral sensori-neural hearing loss may have positive genetic testing while the vast majority of these children present with heterozygous mutations of connexin 26 (GJB2)
WFS1 (显示 WFS1 抗体) and GJB2 mutations were identified in eight of 74 cases of Low-Frequency Sensorineural Hearing Loss. Four cases had heterozygous WFS1 (显示 WFS1 抗体) mutations; one had a heterozygous WFS1 (显示 WFS1 抗体) mutation and a heterozygous GJB2 mutation; and three cases had biallelic GJB2 mutations. Three cases with WFS1 (显示 WFS1 抗体) mutations were sporadic; two of them were confirmed to be caused by a de novo mutation based on the genetic analysis of their parents.
results demonstrate that 19.2% patients with nonsyndromic deafness were caused by mutations in three common deafness genes (GJB2, SLC26A4 (显示 SLC26A4 抗体) and 12S rRNA) in our northern China patient group
GJB2-related deafness leads to significantly better cochlear implantation outcomes when compared with acquired deafness caused by environmental etiologies. However, GJB2 mutation is not associated with a significantly better prognosis when compared with those whose deafness results from either nonsyndromic hearing loss of unknown origin or other types of genetic mutations in the absence of other neurologic deficits.
expression of Cx26 (also known as GJB2) in HeLa cells specifically enhances cell motility in scrape wounding and sparse culture models.
intermediate invasive status of bovine trophoblast is supported by the fact that trophoblast giant cells coexpress connexins (Cx)26, Cx32 (显示 GJB1 抗体), and Cx43 (显示 GJA1 抗体)
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