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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 02 Aug 2015.

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
Supplier
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
Comprehensive analysis via exome sequencing uncovers genetic etiology in autosomal recessive nonsyndromic deafness in a large multiethnic cohort.
New
Tekin et al., Miami, United States. In Genet Med, 30 Aug 2015
METHODS: After excluding mutations in the most common gene, GJB2, we performed WES in 160 multiplex families with ARNSD from Turkey, Iran, Mexico, Ecuador, and Puerto Rico to screen for mutations in all known ARNSD genes.
Mice with conditional deletion of Cx26 exhibit no vestibular phenotype despite secondary loss of Cx30 in the vestibular end organs.
New
Raphael et al., Ann Arbor, United States. In Hear Res, 29 Aug 2015
One member of the connexin family, Connexin 26 (Cx26), is prevalent in gap junctions in sensory epithelia of the inner ear.
Hid arbitrates collective cell death in the Drosophila wing.
New
Abrams et al., Dallas, United States. In Mech Dev, 27 Aug 2015
Here we present evidence that collective cell death does not require cell-cell contact and show that transcription of the IAP antagonist, head involution defective (Abdelwahid, Yokokura et al.), is acutely induced in wing epithelial cells prior to this process.
A novel mutation in the TMC1 gene causes non-syndromic hearing loss in a Moroccan family.
New
Barakat et al., Casablanca, Morocco. In Gene, 27 Aug 2015
After excluding GJB2 mutation and other common mutations associated with hearing loss in Morocco, whole-exome sequencing was performed to study the genetic causes of one sibling with ARSHNL in a consanguineous Moroccan family.
Insights into the role of connexins in mammary gland morphogenesis and function.
Review
New
Laird et al., London, Canada. In Reproduction, Jun 2015
These studies have revealed an important stage-specific role for Cx26 (GJA1) and Cx43 (GJB2), while Cx30 (GJB6) and Cx32 (Gjb1) can be eliminated without compromising the gland.
Gap junction connexins in female reproductive organs: implications for women's reproductive health.
Review
New
Kidder et al., London, Canada. In Hum Reprod Update, May 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.
Reciprocal positive regulation between Cx26 and PI3K/Akt pathway confers acquired gefitinib resistance in NSCLC cells via GJIC-independent induction of EMT.
New
Qin et al., Nanning, China. In Cell Death Dis, Dec 2014
In this study, we first found that connexin 26 (Cx26) is the predominant Cx isoform expressed in various NSCLC cell lines.
Cellular and Deafness Mechanisms Underlying Connexin Mutation-Induced Hearing Loss - A Common Hereditary Deafness.
Review
New
Zhao et al., Lexington, United States. In Front Cell Neurosci, Dec 2014
In particular, connexin 26 (Cx26, GJB2) mutations are responsible for ~50% of non-syndromic hearing loss, which is the highest incidence of genetic disease.
Genetics of hearing loss in Africans: use of next generation sequencing is the best way forward.
Review
New
Wonkam et al., Cape Town, South Africa. In Pan Afr Med J, Dec 2014
The most prevalent mutations associated with autosomal recessive nonsyndromic hearing loss (ARNSHL) are found within connexin genes such as GJB2, mostly in people of European and Asian origin.
Temporal patterning of neuroblasts controls Notch-mediated cell survival through regulation of Hid or Reaper.
New
Impact
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.
A large-scale screen for coding variants predisposing to psoriasis.
Impact
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.
Review
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.
Porokeratotic eccrine nevus may be caused by somatic connexin26 mutations.
GeneRIF
van Steensel et al., Maastricht, Netherlands. In J Invest Dermatol, 2012
porokeratotic eccrine nevus may be caused by mosaic GJB2 mutations.
[Analysis of GJB2 gene and mitochondrial DNA A1555G mutations in 16 families with non-syndromic hearing loss].
GeneRIF
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.
Cochlear implantation and congenital deafness: perceptive and lexical results in 2 genetically pediatric identified population.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
Impact
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.
Impact
GeneRIF
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.
Impact
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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