Developmental regulation of the voltage gated sodium channel in PC12G cells
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Developmental regulation of the voltage gated sodium channel in PC12G cells

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Published by National Library of Canada in Ottawa .
Written in English


Book details:

Edition Notes

Thesis (M.Sc.)--University of Toronto, 1990.

SeriesCanadian theses = Thèses canadiennes
The Physical Object
FormatMicroform
Pagination2 microfiches.
ID Numbers
Open LibraryOL14890444M
ISBN 100315583991
OCLC/WorldCa30970861

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Voltage-gated Na (Na v) channels are key regulators of neuronal mammalian genome encodes multiple Na v s, but reported channel kinetics greatly exceeds gene number. Recent studies have identified a range of post-transcriptional modifications that, combined, are sufficient to generate diversity in channel kinetics and expression by: 1. Cardiac voltage-gated Na + channels (Na v) initiate the action potential (AP), are essential for conduction of the electrical impulses, and contribute to control the AP duration (Li et al. ).Na v is the α subunit of the principal Na + channel found in the heart. The pivotal role of Na v in normal cardiac function has been exemplified by the finding of numerous naturally occurring Cited by: Voltage-gated Na + channels (VGSCs) are heteromeric membrane protein complexes containing pore-forming α subunits in association with non-pore-forming β subunits (Figure 1) (Catterall, ). The β subunits regulate channel gating and are also cell adhesion molecules (CAMs) (Brackenbury and Isom, ).Cited by: The role of Na + fluxes through voltage-gated sodium channels in the regulation of sperm cell function remains poorly understood. Previously, we reported that several genes encoding voltage-gated Na + channels were expressed in human testis and mature spermatozoa. In this study, we analyzed the presence and function of the TTX-resistant VGSC α subunit Nav in human capacitated sperm by:

  Abstract. Voltage-gated sodium channels (Na V) are functionally expressed in highly metastatic cancer cells derived from nonexcitable epithelial tissues (breast, prostate, lung, and cervix).MDA-MB breast cancer cells express functional sodium channel complexes, consisting of Na V and associated auxiliary β-subunits, that are responsible for a sustained inward sodium . Voltage-gated sodium channels are transmembrane proteins responsible for the initiation and propagation of action potentials. One subtype, Na v (brain type III) is tetrodotoxin sensitive and fast inactivated. Na v has been shown to be expressed at low levels in the adult rat, but to be upregulated after sciatic nerve axotomy in the dorsal root by:   Voltage-gated sodium (NaV) channels initiate electrical signalling in excitable cells and are the molecular targets for drugs and disease mutations, but the structural basis for their voltage. Pore-forming Na v α proteins in cancer cells. The first descriptions of voltage-dependent sodium currents, and therefore of the functional expression of Na V α proteins at the plasma membrane of cancer cells, and the hypotheses that they could participate in the oncogenic process came in the late 's. In these pioneer works voltage-gated sodium currents were initially recorded in Cited by:

  Structure of voltage-gated sodium channels. (a) Schematic representation of the sodium-channel subunits. The α subunit of the Na v channel is illustrated together with the β1 and β2 subunits; the extracellular domains of the β subunits are shown as immunoglobulin-like folds, which interact with the loops in the α subunits as shown. Roman numerals indicate the Cited by: The voltage-gated sodium channel Na(V) is preferentially expressed in peripheral somatic and visceral sensory neurons, olfactory sensory neurons and sympathetic ganglion neurons. Voltage-gated sodium channels are thus likely to associate in a ternary complex containing neurofascin/NrCAM, and ankyrin-G. Mice with no ankyrin- G expression in the cerebellum exhibit loss of ability of Purkinje neurons to fire action potentials, as well as loss of restriction of neurofascin/NrCAM to axon initial segments Cited by: Regulation of voltage-gated sodium channel expression in cancer: Hormones, growth factors and Available via license: CC BY Content may be subject to copyright.