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Sargiannidou, Ahn, Enriquez, Peinado, Reynolds, Abrams, Scherer, Kleopa: Human oligodendrocytes express Cx31.3: function and interactions with Cx32 mutants. in Neurobiology of disease 2008
Induction of Cxs 29 and 32 in the injury border suggests that altered Cx expression may contribute to the propagation of injury-related and/or regeneration signals after acute brain injury.
Cx29 is a second connexin expressed in Schwann cells of sciatic nerve.
Comparative mapping of Y1 and Y5 receptor subtypes within cell bodies and nerve fibers in the brain. Together with physiological and electrophysiological studies, provides better understanding of NPY neural circuitries.
Cx29 is localized to the inner membrane of small myelin sheaths
Our data first provide a comprehensive and detailed pattern of Cx29 gene expression in the mouse and rat cochlea.
Thus, in contrast to connexin32 and connexin47, which are also expressed in myelinating cells, Cx29 does not contribute to the function of myelin in adult mice.
Findings demonstrated the requirement of Cx29 for normal cochlear functions and suggest that Cx29 is a new candidate gene for studying the auditory neuropathy.
Cx29 protein expression was absent from neural crest cells but appeared as neural crest cells generated precursors (embryonic day 12) both in vivo and in vitro. This identifies Cx29 as a novel marker for cells of the defined Schwann cell lineage.
Homomeric interactions of Cx29 and Cx32 require other domains: the N-terminus, transmembrane domains, and extracellular loops. Substituting the intracellular loop and/or tail of Cx32 with those of Cx29 prevents Cx32 from forming functional gap junctions.
Cx23 seems to share functional properties with pannexin (hemi) channels rather than gap junction channels of other connexins.
Based on these findings, we suggest that p.W77S mutant has a dominant negative effect on the formation and function of the gap junction. These results give a novel molecular elucidation for the mutation of GJC3 in the development of hearing loss.
Although p.R15G and p.L23H mutants do not decrease the trafficking of CX proteins, mutations in GJC3 genes result in a loss of hemichannel function of CX30.2/CX31.3 protein, possibly causing hearing loss.
The connexin30.2/CX31.3 shares functional properties with pannexin (hemi) channels rather than gap junction channels of other Connexins.
Mutations in the Cx29 gene do not play a role in the causation of non syndromic hearing impairment in Indian population.
We suggest that the c.[43C-->G(+)230G-->C] compound heterozygous variant of Cx29 may be a risk factor for the development of hearing loss in Taiwanese.
Data show that the p.E269D missense mutation resulted in accumulation of the Cx29 mutant protein in the endoplasmic reticulum rather than in the cytoplasmic membrane.
Cx31.3 is localized to the gray matter along small myelinated fibers and is co-expressed with Cx32 in oligodendrocytes.
This gene encodes a gap junction protein. The encoded protein, also known as a connexin, plays a role in formation of gap junctions, which provide direct connections between neighboring cells. Mutations in this gene have been reported to be associated with nonsyndromic hearing loss.
gap junction protein, gamma 3, 30.2kDa
, connexin 29
, gap junction epsilon-1 protein
, gap junction gamma-3 protein
, gap junction membrane channel protein epsilon 1