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Signature Channels of Excitability no More: L-Type Channels in Immune Cells

Although the concept of Ca(2+) as a universal messenger is well established, it was assumed that the regulatory mechanisms of Ca(2+)-signaling were divided along the line of electric excitability. Recent advances in molecular biology and genomics have, however, provided evidence that non-excitable c...

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Detalles Bibliográficos
Autores principales: Davenport, Bennett, Li, Yuan, Heizer, Justin W., Schmitz, Carsten, Perraud, Anne-Laure
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4512153/
https://www.ncbi.nlm.nih.gov/pubmed/26257741
http://dx.doi.org/10.3389/fimmu.2015.00375
Descripción
Sumario:Although the concept of Ca(2+) as a universal messenger is well established, it was assumed that the regulatory mechanisms of Ca(2+)-signaling were divided along the line of electric excitability. Recent advances in molecular biology and genomics have, however, provided evidence that non-excitable cells such as immunocytes also express a wide and diverse pool of ion channels that does not differ as significantly from that of excitable cells as originally assumed. Ion channels and transporters are involved in virtually all aspects of immune response regulation, from cell differentiation and development to activation, and effector functions such as migration, antibody-secretion, phagosomal maturation, or vesicular delivery of bactericidal agents. This comprises TRP channel family members, voltage- and Ca(2+)-gated K(+)- and Na(+)-channels, as well as unexpectedly, components of the Ca(V)1-subfamily of voltage-gated L-type Ca(2+)-channels, originally thought to be signature molecules of excitability. This article provides an overview of recent observations made in the field of Ca(V)1 L-type channel function in the immune context, as well as presents results we obtained studying these channels in B-lymphocytes.