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Polycystins and cellular Ca(2+) signaling

The cystic phenotype in autosomal dominant polycystic kidney disease is characterized by a profound dysfunction of many cellular signaling patterns, ultimately leading to an increase in both cell proliferation and apoptotic cell death. Disturbance of normal cellular Ca(2+) signaling seems to be a pr...

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Detalles Bibliográficos
Autores principales: Mekahli, D., Parys, Jan B., Bultynck, G., Missiaen, L., De Smedt, H.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Basel 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3708286/
https://www.ncbi.nlm.nih.gov/pubmed/23076254
http://dx.doi.org/10.1007/s00018-012-1188-x
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author Mekahli, D.
Parys, Jan B.
Bultynck, G.
Missiaen, L.
De Smedt, H.
author_facet Mekahli, D.
Parys, Jan B.
Bultynck, G.
Missiaen, L.
De Smedt, H.
author_sort Mekahli, D.
collection PubMed
description The cystic phenotype in autosomal dominant polycystic kidney disease is characterized by a profound dysfunction of many cellular signaling patterns, ultimately leading to an increase in both cell proliferation and apoptotic cell death. Disturbance of normal cellular Ca(2+) signaling seems to be a primary event and is clearly involved in many pathways that may lead to both types of cellular responses. In this review, we summarize the current knowledge about the molecular and functional interactions between polycystins and multiple components of the cellular Ca(2+)-signaling machinery. In addition, we discuss the relevant downstream responses of the changed Ca(2+) signaling that ultimately lead to increased proliferation and increased apoptosis as observed in many cystic cell types.
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spelling pubmed-37082862013-07-12 Polycystins and cellular Ca(2+) signaling Mekahli, D. Parys, Jan B. Bultynck, G. Missiaen, L. De Smedt, H. Cell Mol Life Sci Review The cystic phenotype in autosomal dominant polycystic kidney disease is characterized by a profound dysfunction of many cellular signaling patterns, ultimately leading to an increase in both cell proliferation and apoptotic cell death. Disturbance of normal cellular Ca(2+) signaling seems to be a primary event and is clearly involved in many pathways that may lead to both types of cellular responses. In this review, we summarize the current knowledge about the molecular and functional interactions between polycystins and multiple components of the cellular Ca(2+)-signaling machinery. In addition, we discuss the relevant downstream responses of the changed Ca(2+) signaling that ultimately lead to increased proliferation and increased apoptosis as observed in many cystic cell types. Springer Basel 2012-10-18 2013 /pmc/articles/PMC3708286/ /pubmed/23076254 http://dx.doi.org/10.1007/s00018-012-1188-x Text en © The Author(s) 2012 https://creativecommons.org/licenses/by/4.0/ This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.
spellingShingle Review
Mekahli, D.
Parys, Jan B.
Bultynck, G.
Missiaen, L.
De Smedt, H.
Polycystins and cellular Ca(2+) signaling
title Polycystins and cellular Ca(2+) signaling
title_full Polycystins and cellular Ca(2+) signaling
title_fullStr Polycystins and cellular Ca(2+) signaling
title_full_unstemmed Polycystins and cellular Ca(2+) signaling
title_short Polycystins and cellular Ca(2+) signaling
title_sort polycystins and cellular ca(2+) signaling
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3708286/
https://www.ncbi.nlm.nih.gov/pubmed/23076254
http://dx.doi.org/10.1007/s00018-012-1188-x
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