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a Institute of Biochemistry, Biological Research Center of the Hungarian Academy of Sciences, Szeged, Hungary b Department of Biochemistry and Molecular Biology, Saitama University, Saitama, Japan c Cancer Research Centre, Laval University, Quebec, Canada d Department of Biochemistry and Molecular Biology, University of the Basque Country, Bilbao, Spain e School of Biosciences, Cardiff University, Cardiff, United Kingdom
Key Words: membrane sensor • membrane fluidity • membrane-associated heat shock proteins • sphingomyelin pathway • ceramide • Hsp coinducers • membrane microdomains
Address for correspondence: Laszlo Vigh, Ph.D., D.Sc., Institute of Biochemistry, Biology Research Centre, Hungarian Academy of Sciences,Temesvari krt 62, H-6726, Szeged, Hungary. Voice/fax: +36-62-432-048. vigh{at}brc.hu
"Membrane regulation" of stress responses in various systems is widely studied. In poikilotherms, membrane rigidification could be the first reaction to cold perception: reducing membrane fluidity of membranes at physiological temperatures is coupled with enhanced cold inducibility of a number of genes, including desaturases (see J.L. Harwood's article in this Proceedings volume). A similar role of changes in membrane physical state in heat (oxidative stress, etc.) sensing- and signaling gained support recently from prokaryotes to mammalian cells. Stress-induced remodeling of membrane lipids could influence generation, transduction, and deactivation of stress signals, either through global effects on the fluidity of the membrane matrix, or by specific interactions of boundary (or raft) lipids with receptor proteins, lipases, ion channels, etc. Our data point to membranes not only as targets of stress, but also as sensors in activating a stress response.
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