Dysfunction of gap junctions (GJs) caused by mutations in connexin26 (Cx26) and Cx30
accounts for nearly half of all cases of hereditary nonsyndromic deafness cases. Although it …

Normal development, function and repair of the sensory epithelia in the inner ear are all
dependent on gap junctional intercellular communication. Mutations in the connexin genes …

Gap junctional intercellular communication (GJIC) plays a major role in cochlear function.
Recent evidence suggests that connexin 26 (Cx26) and Cx30 are the major constituent …

The importance of connexins (Cxs) in cochlear functions has been demonstrated by the
finding that mutations in Cx genes cause a large proportion of sensorineural hearing loss …

Mutations in the Gjb2 gene, which encodes a gap junction protein connexin26 (Cx26), are
the most prevalent form of hereditary deafness in humans and represent about half of non …

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 …

Several different recessive mutations in the connexin26 (Cx26; β2) gene have been
associated with non‐syndromic hereditary deafness. This suggests gap junctions are …

Mutations in genes coding for connexin26 (Cx26) and/or Cx30 are linked to approximately
half of all cases of human autosomal nonsyndromic prelingual deafness. Cx26 and Cx30 …

Gap junctions play a critical role in hearing and mutations in connexin genes cause a high
incidence of human deafness. Pathogenesis mainly occurs in the cochlea, where gap …

Mutations in the gene coding for connexin26 (Cx26) is the most common cause of human
nonsyndromic hereditary deafness. To investigate deafness mechanisms underlying Cx26 …