Results 61 to 70 of about 854 (148)
PLoS ONE, 2013 Connexins (Cx), which constitute gap junction intercellular channels in vertebrates, have been shown to suppress transformed cell growth and tumorigenesis, but the mechanism(s) still remain largely speculative.
Anjana Chandrasekhar +5 more
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Neurobiology of Disease, 2010 Dominant mutations in GJB2, the gene encoding the human gap junction protein connexin26 (Cx26), cause hearing loss. We investigated whether dominant Cx26 mutants interact directly with Cx30.
Sabrina W. Yum +2 more
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Frontiers in Molecular Neuroscience, 2022 BackgroundGap junction (GJ) proteins, connexin26 and 30, are highly prevalent in the human cochlea (HC), where they are involved in transcellular signaling, metabolic supply, and fluid homeostasis.
Wei Liu, Helge Rask-Andersen
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The M34A mutant of Connexin26 reveals active conductance states in pore-suspending membranes
, 2009 Connexin26 (Cx26) is a member of the connexin family, the building blocks for gap junction intercellular channels. These dodecameric assemblies are involved in gap junction-mediated cell-cell communication allowing the passage of ions and small molecules
Kreir, Mohamed +8 more
core +1 more source
Hypothesis of K+-Recycling Defect Is Not a Primary Deafness Mechanism for Cx26 (GJB2) Deficiency
Frontiers in Molecular Neuroscience, 2017 K+-recycling defect is a long-standing hypothesis for deafness mechanism of Connexin26 (Cx26, GJB2) mutations, which cause the most common hereditary deafness and are responsible for >50% of nonsyndromic hearing loss.
Hong-Bo Zhao
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Gap junction mediated intercellular metabolite transfer in the cochlea is compromised in connexin30 null mice. [PDF]
PLoS ONE, 2008 Connexin26 (Cx26) and connexin30 (Cx30) are two major protein subunits that co-assemble to form gap junctions (GJs) in the cochlea. Mutations in either one of them are the major cause of non-syndromic prelingual deafness in humans. Because the mechanisms
Qing Chang +4 more
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Studies of intercellular Ca2+ signaling and gap-junction coupling in the developing cochlea of mouse models affected by congenital hearing loss [PDF]
, 2013 Connexin 26 (Cx26) and connexin 30 (Cx30) form gap junction channels that allow the intercellular diffusion of the Ca2+ mobilizing second messenger IP3.
Rodriguez Hernandez, Laura
core
Inner ear cell therapy targeting hereditary deafness by activation of stem cell homing factors
Frontiers in Pharmacology, 2015 Congenital deafness affects about 1 in 1000 children and more than half of them have a genetic background such as Connexin26 (CX26) gene mutation. Inner ear cell therapy for sensorineural hearing loss has been expected to be an effective therapy for ...
Kazusaku eKamiya
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Deficiency of transcription factor Brn4 disrupts cochlear gap junction plaques in a model of DFN3 non-syndromic deafness. [PDF]
PLoS ONE, 2014 Brn4, which encodes a POU transcription factor, is the gene responsible for DFN3, an X chromosome-linked, non-syndromic type of hearing loss. Brn4-deficient mice have a low endocochlear potential (EP), hearing loss, and ultrastructural alterations in ...
Yoshinobu Kidokoro +6 more
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Neoplasia: An International Journal for Oncology Research, 2005 BACKGROUND, AIMS: Genomewide expression profiling has identified a number of genes expressed at higher levels in colorectal cancer (CRC) than in normal tissues. Our objectives in this study were: 1) to test whether genes were also distinct on the protein
Thomas Knösel +7 more
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