Showing papers by "Betty Soliven published in 2003"
TL;DR: A tripartite intercellular protein complex, comprised of these two proteins, appears critical for axo-glial contacts at juxtaparanodes, suggesting that similar molecules are crucial for different types of axo–glial interactions.
Abstract: Myelination results in a highly segregated distribution of axonal membrane proteins at nodes of Ranvier. Here, we show the role in this process of TAG-1, a glycosyl-phosphatidyl-inositol–anchored cell adhesion molecule. In the absence of TAG-1, axonal Caspr2 did not accumulate at juxtaparanodes, and the normal enrichment of shaker-type K+ channels in these regions was severely disrupted, in the central and peripheral nervous systems. In contrast, the localization of protein 4.1B, an axoplasmic partner of Caspr2, was only moderately altered. TAG-1, which is expressed in both neurons and glia, was able to associate in cis with Caspr2 and in trans with itself. Thus, a tripartite intercellular protein complex, comprised of these two proteins, appears critical for axo–glial contacts at juxtaparanodes. This complex is analogous to that described previously at paranodes, suggesting that similar molecules are crucial for different types of axo–glial interactions.
232 citations
TL;DR: It is found that treatment with platelet-derived growth factor and basic fibroblast growth factor but not ciliary neurotrophic factor resulted in increased I(K) density and upregulation and agents that were effective inhibitors of PDGF-induced I( K) upregulation also attenuated OP proliferation, supporting the concept that I(k) is an important link betweenPDGF-activated signaling cascades and cell cycle progression.
Abstract: An increase in the expression of the delayed rectifier current (I K) has been shown to correlate with mitogenesis in many cell types. However, pathways involved in the upregulation of I K by growth...
35 citations
TL;DR: An autopsy 15 years after the onset of symptoms revealed hypertrophic radiculopathy and peripheral neuropathy due to CIDP with no evidence of neurofibromatosis, illustrating how the hypertrophic neuropathy accompanying C IDP can be mistaken for neurof fibroma.
Abstract: This report illustrates a case of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) masquerading as neurofibromatosis due to multifocal enlargements of spinal nerve roots. The patient initially complained of intermittent numbness of the hands and leg weakness at age 62. Nerve conduction velocities were reported to be abnormally slow, suggesting a diagnosis of demyelinating neuropathy. A complaint of progressive lower back pain 4 years later prompted a lumbar CT myelogram, which demonstrated bilateral nerve root enlargements. A biopsy of an enlarged lumbar root obtained during decompressive laminectomy was interpreted as consistent with a plexiform neurofibroma. He suffered recurrent paraparesis, at times with a sensory level indicating spinal cord compression, which responded to corticosteroid therapy. An autopsy 15 years after the onset of symptoms revealed hypertrophic radiculopathy and peripheral neuropathy due to CIDP with no evidence of neurofibromatosis. This case illustrates how the hypertrophic neuropathy accompanying CIDP can be mistaken for neurofibromatosis.
28 citations