Detection of the mitochondrial apoptosis-induced channel (MAC) and its regulation by Bcl-2 family proteins.

Kathleen W. Kinnally, Sonia Martinez-Caballero, Laurent M. Dejean

Research output: Contribution to journalArticle

Abstract

Apoptosis is a phenomenon fundamental to higher eukaryotes that is integral to such diverse cellular processes as tissue homeostasis, organogenesis, and response to toxins. The release from mitochondria of apoptotic factors such as cytochrome c is a key step during apoptosis of most cells. Cytochrome c release occurs through the MAC (mitochondrial apoptosis-induced channel), a pore which forms in the mitochondrial outer membrane during early apoptosis and is exquisitely regulated by the Bcl-2 family of proteins. This unit presents basic and advanced tools for detecting MAC and defining its regulation by Bcl-2 family proteins and pharmacological agents. Protocols include the use of time-lapse video-microscopy to monitor the onset of apoptosis in living cells and patch-clamp techniques for mitochondria or proteoliposomes containing mitochondrial proteins, which allow direct detection of MAC. These approaches enable an evaluation of the role of MAC and mitochondria in apoptosis of a variety of cell types by many inducers.

Original languageEnglish (US)
JournalCurrent protocols in toxicology / editorial board, Mahin D. Maines (editor-in-chief) ... [et al.]
VolumeChapter 2
StatePublished - Dec 2006

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Apoptosis
Proteins
Mitochondria
Cytochromes c
Tissue homeostasis
Video Microscopy
Organogenesis
Mitochondrial Proteins
Clamping devices
Mitochondrial Membranes
Patch-Clamp Techniques
Helper-Inducer T-Lymphocytes
Eukaryota
Microscopic examination
Homeostasis
Cells
Pharmacology
Membranes

ASJC Scopus subject areas

  • Medicine(all)

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Detection of the mitochondrial apoptosis-induced channel (MAC) and its regulation by Bcl-2 family proteins. / Kinnally, Kathleen W.; Martinez-Caballero, Sonia; Dejean, Laurent M.

In: Current protocols in toxicology / editorial board, Mahin D. Maines (editor-in-chief) ... [et al.], Vol. Chapter 2, 12.2006.

Research output: Contribution to journalArticle

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