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Gap junction protein, beta 2, 26kDa

Cx26, connexin 26, GJB2, KID, HID
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. [provided by RefSeq, Oct 2008] (from NCBI)
Top mentioned proteins: GAP, CAN, HAD, GJB6, PGD2
Papers using Cx26 antibodies
Cyclic stretch enhances gap junctional communication between osteoblastic cells
van Steensel Maurice A M et al., In The Journal of Investigative Dermatology, 1997
... GJB2 WT gene was cloned into the vectors peGFP-N1 (BD Biosciences, Breda, The Netherlands) and ...
Papers on Cx26
Chorioretinal scars and visual deprivation are common in children with cochlear implants after congenital cytomegalovirus infection.
Karltorp et al., Norrköping, Sweden. In Acta Paediatr, 27 Mar 2015
AIM: The aim of this study was to compare visual function and ocular characteristics in children with cochlear implants, due to severe hearing impairment caused by the congenital cytomegalovirus (CMV) infection, with control children fitted with cochlear implants due to connexin 26 mutations (Cx26), a genetic cause of hearing impairment.
Whole-exome sequencing reveals diverse modes of inheritance in sporadic mild to moderate sensorineural hearing loss in a pediatric population.
Choi et al., Seoul, South Korea. In Genet Med, 26 Mar 2015
UNASSIGNED: Purpose:This study was designed to delineate genetic contributions, if any, to sporadic forms of mild to moderate sensorineural hearing loss (SNHL) not related to GJB2 mutations (DFNB1) in a pediatric population.Methods:We recruited 11 non-DFNB1 simplex cases of mild to moderate SNHL in children.
Gap junction connexins in female reproductive organs: implications for women's reproductive health.
Kidder et al., London, Canada. In Hum Reprod Update, 09 Mar 2015
Blocking of CX26 channels in the uterine epithelium disrupted implantation whereas loss or reduction of CX43 expression in the uterine stroma impaired decidualization and vascularization in mouse and human.
Government-funded universal newborn hearing screening and genetic analyses of deafness predisposing genes in Taiwan.
Huang et al., Taipei, Taiwan. In Int J Pediatr Otorhinolaryngol, 07 Mar 2015
OBJECTIVE: To investigate the association of eight connexin genes (GJB2, GJB4, GJA1P1, GJB6, GJB3, GJA1, GJB1, and GJC3) and the SLC26A4 gene with congenital hearing impairment among infants in a universal newborn hearing screening program.
Strategy for the customized mass screening of genetic sensorineural hearing loss in koreans.
Choi et al., Seoul, South Korea. In Korean J Audiol, Sep 2014
The other causative genes were MRNR1, WFS1, COCH, TECTA, MYO6, COL11A2, EYA4, GJB3, OTOF, STRC, MYO3A, and GJB2.
Temporal patterning of neuroblasts controls Notch-mediated cell survival through regulation of Hid or Reaper.
Desplan et al., East New York, United States. In Cell, Sep 2014
Within a single lineage, intermediate precursors initially do not divide and generate only one neuron; subsequently, precursors divide, but their Notch(ON) progeny systematically die through Reaper activity, whereas later, their Notch(OFF) progeny die through Hid activity.
Connexin and pannexin (hemi)channels in the liver.
Vinken et al., Brussels, Belgium. In Front Physiol, Feb 2014
Hepatocytes harbor connexin32 and connexin26, while non-parenchymal liver cells typically express connexin43.
A large-scale screen for coding variants predisposing to psoriasis.
Zhang et al., Hefei, China. In Nat Genet, 2014
We discovered two independent missense SNVs in IL23R and GJB2 of low frequency and five common missense SNVs in LCE3D, ERAP1, CARD14 and ZNF816A associated with psoriasis at genome-wide significance.
Aberrant Cx26 hemichannels and keratitis-ichthyosis-deafness syndrome: insights into syndromic hearing loss.
Verselis et al., United States. In Front Cell Neurosci, 2013
Mutation of the GJB2 gene, which encodes the connexin 26 (Cx26) gap junction (GJ) protein, is the most common cause of hereditary, sensorineural hearing loss.
[Hearing loss associated with GJB2 gene mutation].
Huang et al., In Lin Chuang Er Bi Yan Hou Ke Za Zhi, 2013
The mutation of GJB2 (gap junction protein, beta 2) gene accounts for 80% of NSHL and more than 50% of children NSHL, playing the most important role in deafness genes.
Porokeratotic eccrine nevus may be caused by somatic connexin26 mutations.
van Steensel et al., Maastricht, Netherlands. In J Invest Dermatol, 2012
porokeratotic eccrine nevus may be caused by mosaic GJB2 mutations.
Model for Hearing Loss Identification in Belarus.
Danilenko et al., In Otolaryngol Head Neck Surg, 2012
Results: Among children with SNHL, 45% are homozygous and 15% are heterozygous for 35delG GJB2.
[Analysis of GJB2 gene and mitochondrial DNA A1555G mutations in 16 families with non-syndromic hearing loss].
Li et al., Suzhou, China. In Zhonghua Yi Xue Yi Chuan Xue Za Zhi, 2012
Of the 17 patients with sensorineural hearing loss, 3 were homozygous mutation for GJB2 235 delC.
Genetic Assay for Newborn Auditory Screening.
Lin et al., In Otolaryngol Head Neck Surg, 2012
The 2 most commonly identified genetic mutations identified were the SLC26A4 gene, known to encode the pendrin protein, followed by the GJB2 gene, responsible for gap-junction protein Connexin 26.
Cochlear implantation and congenital deafness: perceptive and lexical results in 2 genetically pediatric identified population.
Garabédian et al., Paris, France. In Otol Neurotol, 2012
After cochlear implantation, perceptive and linguistic evolutions for populations of GJB2 mutation and Waardenburg syndrome were of good quality, but lexical evaluation showed residual language difficulties in both groups.
Aberrant connexin 43 and 26 expression in cervical dysplasia.
Zhang et al., Philadelphia, United States. In Anal Quant Cytol Histol, 2012
In High-grade squamous intraepithelial lesions, Cx26 was expressed in the full thickness of the epithelium, at a high level in 80% of cases and a low level in the rest.
The p.V37I exclusive genotype of GJB2: a genetic risk-indicator of postnatal permanent childhood hearing impairment.
Wu et al., Shanghai, China. In Plos One, 2011
p.V37I exclusive genotype of GJB2 may cause subclinical hearing impairment at birth and increases risk for postnatal permanent childhood hearing impairment
Association analyses identify six new psoriasis susceptibility loci in the Chinese population.
Zhang et al., Hefei, China. In Nat Genet, 2010
We identified six new susceptibility loci associated with psoriasis in the Chinese study containing the candidate genes ERAP1, PTTG1, CSMD1, GJB2, SERPINB8 and ZNF816A (combined P < 5 × 10⁻⁸) and replicated one locus, 5q33.1 (TNIP1-ANXA6), previously reported (combined P = 3.8 × 10⁻²¹) in the European studies.
Structure of the connexin 26 gap junction channel at 3.5 A resolution.
Tsukihara et al., Suita, Japan. In Nature, 2009
X ray structure of connexin 26 gap junction channel at 3.5 A resolution.
Temporal transcription factors and their targets schedule the end of neural proliferation in Drosophila.
Gould et al., London, United Kingdom. In Cell, 2008
Second, they regulate the time at which neuroblasts undergo Prospero-dependent cell-cycle exit or Reaper/Hid/Grim-dependent apoptosis.
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