کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3056217 | 1186558 | 2009 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Molecular participants in mitochondrial cell death channel formation during neuronal ischemia
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Molecular participants in mitochondrial cell death channel formation during neuronal ischemia Molecular participants in mitochondrial cell death channel formation during neuronal ischemia](/preview/png/3056217.png)
چکیده انگلیسی
Mitochondrial ion channels are involved in numerous cellular processes. Membrane pores and transporters regulate the influx and efflux of calcium, sodium, potassium, zinc and determine the membrane compartmentalization of numerous cytosolic metabolites. The permeability of the inner membrane to ions and solutes helps determine the membrane potential of the inner membrane, but the permeability of the outer membrane, controlled in part by VDAC and the BCL-2 family proteins, regulates the release of important signaling molecules that determine the onset of programmed cell death. BCL-2 family proteins have properties of ion channels and perform specialized physiological functions, for example, regulating the strength and pattern of synaptic transmission, in addition to their well known role in cell death. The ion channels of the inner and outer membranes may come together in a complex of proteins during programmed cell death, particularly during neuronal ischemia, where elevated levels of the divalents calcium and zinc activate inner membrane ion channel conductances. The variety of possible molecular participants within the ion channel complex may be matched only by the variety of different types of programmed cell death.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 218, Issue 2, August 2009, Pages 203-212
Journal: Experimental Neurology - Volume 218, Issue 2, August 2009, Pages 203-212
نویسندگان
Elizabeth Ann Jonas,