کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10766306 | 1050646 | 2009 | 4 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
From cell protection to death: May Ca2+ signals explain the chameleonic attributes of the mammalian prion protein?
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
It is now accepted that a conformational change of the cellular prion protein (PrPC) generates the prion, the infectious agent responsible for lethal neurodegenerative disorders, named transmissible spongiform encephalopathies, or prion diseases. The mechanisms of prion-associated neurodegeneration are still obscure, as is the cell role of PrPC, although increasing evidence attributes to PrPC important functions in cell survival. Such a behavioral dichotomy thus enables the prion protein to switch from a benign role under normal conditions, to the execution of neurons during disease. By reviewing data from models of prion disease and PrPC-null paradigms, which suggest a relation between the prion protein and Ca2+ homeostasis, here we discuss the possibility that Ca2+ is the factor behind the enigma of the pathophysiology of PrPC. Ca2+ features in almost all processes of cell signaling, and may thus tell us much about a protein that pivots between health and disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 379, Issue 2, 6 February 2009, Pages 171-174
Journal: Biochemical and Biophysical Research Communications - Volume 379, Issue 2, 6 February 2009, Pages 171-174
نویسندگان
M. Catia Sorgato, Alessandro Bertoli,