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Connexin32 mutations cause loss of function in Schwann cells and oligodendrocytes leading to PNS and CNS myelination defects.

Hereditary spastic paraplegia is a novel phenotype for GJA12/GJC2 mutations.

Human oligodendrocytes express Cx31.3: function and interactions with Cx32 mutants.

Cx29 and Cx32, two connexins expressed by myelinating glia, do not interact and are functionally distinct.

Molecular mechanisms of inherited demyelinating neuropathies.

Gap junctions couple astrocytes and oligodendrocytes.

Two distinct heterotypic channels mediate gap junction coupling between astrocyte and oligodendrocyte connexins.

Nectin-like proteins mediate axon-Schwann cell interactions along the internode and are essential for myelination.

Human connexin26 and connexin30 form functional heteromeric and heterotypic channels.

A central role for Necl4/SynCAM4 in Schwann cell-axon interaction and myelination.

Loss-of-function Connexin47 mutations cause Pelizaeus-Merzbacher-like disease.

CMT1X phenotypes represent loss of GJB1 gene function.

Pannexin1 is expressed by neurons and glia but does not form functional gap junctions.

Genetic and physiological evidence that oligodendrocyte gap junctions contribute to spatial buffering of potassium released during neuronal activity.

Inherited neuropathies: new genes don’t fit old models.

Finding the causes of inherited neuropathies.

The effects of a dominant connexin32 mutant in myelinating Schwann cells.

Neuromyotonia and limbic encephalitis sera target mature Shaker-type K+ channels: subunit specificity correlates with clinical manifestations.

Molecular Genetics of X-linked Charcot-Marie-Tooth Disease.

A common ankyrin-G-based mechanism retains KCNQ and NaV channels at electrically active domains of the axon.

T118M PMP22 mutation causes partial loss of function and HNPP-like neuropathy.

Prenylation-defective human connexin32 mutants are normally localized and function equivalently to wild type connexin32 in myelinating Schwann cells.

Transgenic expression of human Connexin32 in myelinating Schwann cells prevents demyelination in connexin32-null mice.

Altered ion channels in an animal model of Charcot-Marie-Tooth disease type IA.

Acute demyelination disrupts the molecular organization of PNS nodes.

Expression analysis of the N-myc downstream-regulated gene 1 (NDRG1) indicates that myelinating Schwann cells are the primary disease target in Hereditary Motor and Sensory Neuropathy-Lom.

Expression analysis of the N-myc downstream-regulated gene 1 (NDRG1) indicates that myelinating Schwann cells are the primary disease target in Hereditary Motor and Sensory Neuropathy-Lom.

Unique distributions of the gap junction proteins connexin29, connexin32, and connexin47 in oligodendrocytes.

KCNQ2 is a nodal K+ channel.

The CNS phenotype of X-linked Charcot-Marie-Tooth disease: more than a peripheral problem.

Connexins are critical for normal myelination in the central nervous system.

Kv3.1b is a novel component of CNS nodes.

Disease mechanisms in inherited neuropathies.

Diverse trafficking abnormalities for connexin32 mutants causing CMTX.