Sphingolipids and cell death |
| |
Authors: | Albert Morales Hyunmi Lee Felix M. Goñi Richard Kolesnick José C. Fernandez-Checa |
| |
Affiliation: | (1) Liver Unit and Centro de Investigaciones Biomédicas Esther Koplowitz, IMDiM, Hospital, Clínic i Provincial, Instituto Investigaciones Biomédicas August Pi i Sunyer (IDIBAPS), CIBER-HEPAD and Department of Cell Death and Proliferation, Instituto Investigaciones Biomédicas Barcelona, Consejo Superior de Investigaciones Científicas, 08036 Barcelona, Spain;(2) Laboratory of Signal Transduction, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA;(3) Unidad de Biofisica (Centro Mixto CSIC-UPV/EHU), and Departamento de Bioquimica, Universidad del Pais Vasco, 48080 Bilbao, Spain |
| |
Abstract: | Sphingolipids (SLs) have been considered for many years as predominant building blocks of biological membranes with key structural functions and little relevance in cellular signaling. However, this view has changed dramatically in recent years with the recognition that certain SLs such as ceramide, sphingosine 1-phosphate and gangliosides, participate actively in signal transduction pathways, regulating many different cell functions such as proliferation, differentiation, adhesion and cell death. In particular, ceramide has attracted considerable attention in cell biology and biophysics due to its key role in the modulation of membrane physical properties, signaling and cell death regulation. This latter function is largely exerted by the ability of ceramide to activate the major pathways governing cell death such as the endoplasmic reticulum and mitochondria. Overall, the evidence so far indicates a key function of SLs in disease pathogenesis and hence their regulation may be of potential therapeutic relevance in different pathologies including liver diseases, neurodegeneration and cancer biology and therapy. |
| |
Keywords: | Ceramide Gangliosides Membranes Transbilayer trafficking Mitochondria Endoplasmic reticulum |
本文献已被 PubMed SpringerLink 等数据库收录! |
|