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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 24 Oct 2014.

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
Fecal Microbiota Transplantation: A New Old Kid on the Block for the Management of Gut Microbiota-related Disease.
Gasbarrini et al., Roma, Italy. In J Clin Gastroenterol, 30 Nov 2014
Gut microbiota is deeply involved in the regulation of both health and disease within our body.
Electroporation Transiently Decreases GJB2 (Connexin 26) Expression in B16/BL6 Melanoma Cell Line.
Dagli et al., São Paulo, Brazil. In J Membr Biol, 09 Nov 2014
This in vitro work aimed to study the interference of electroporation on the expression profile of GJB2 (Cx26 gene) and Connexin 26 in melanoma cell line B16/BL6.
[Screening of common deafness gene mutations in 17 000 Chinese newborns from Chengdu based on microarray analysis].
Zhang et al., Chengdu, China. In Zhonghua Yi Xue Yi Chuan Xue Za Zhi, 31 Oct 2014
Nine hot mutations including GJB2 (35delG, 176del16, 235delC and 299delAT), GJB3 (538C> T), SLC26A4(IVS 7-2A> G, 2168A> G), and mitochondrial DNA 12S rRNA(1555A> G, 1494C> T) were detected by PCR amplification and microarray hybridization.
[Analysis and prenatal diagnosis of deafness-related gene mutations in patients with nonsyndromic hearing loss].
Tang et al., Wenzhou, China. In Zhonghua Yi Xue Yi Chuan Xue Za Zhi, 31 Oct 2014
Potential mutations of GJB2 (35delG, 176del16, 235delC, 299delAT), SLC26A4 (2168A> G, IVS7-2A> G), GJB3 (538C> T) and mtDNA (1494C> T, 12S rRNA 1555A> G) were detected by direct sequencing.
Genetics of non-syndromic hearing loss in the Middle East.
Kahrizi et al., Tehrān, Iran. In Int J Pediatr Otorhinolaryngol, 04 Oct 2014
Non-syndromic deafness is highly heterogeneous and mutations in the GJB2 are responsible for almost 30-50% in northwest to as low as 0-5% in south and southeast of the Middle East, it remain as major gene in ARNSHL in Middle East.
Strategy for the customized mass screening of genetic sensorineural hearing loss in koreans.
Choi et al., Seoul, South Korea. In Korean J Audiol, 30 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, 28 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.
GJB2-associated hearing loss: systematic review of worldwide prevalence, genotype, and auditory phenotype.
Chang et al., San Francisco, United States. In Laryngoscope, Feb 2014
OBJECTIVES/HYPOTHESIS: To perform a systematic review of GJB2-associated hearing loss to describe genotype distributions and auditory phenotype.
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, Jan 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.
The Study of SLC26A4 Gene Causing Autosomal Recessive Hearing Loss by Linkage Analysis in a Cohort of Iranian Populations.
Hashemzade Chaleshtori et al., Ahvāz, Iran. In Int J Mol Cell Med, Dec 2013
According to the studies, mutations in GJB2 are estimated to be involved in 50- 80% of autosomal recessive non-syndromic hearing loss cases, but contribution of other loci in this disorder is yet ambiguous.
[Hearing loss associated with GJB2 gene mutation].
Huang et al., In Lin Chuang Er Bi Yan Hou Ke Za Zhi, Oct 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.
[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.
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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