A Ca2+-regulated mitochondrial (permeability transition) pore in Drosophila melanogaster
نویسندگان
چکیده
منابع مشابه
The mitochondrial permeability transition pore.
This chapter reviews recent advances in the identification of the structural elements of the permeability transition pore. The discovery that cyclosporin A (CsA) inhibits the pore proved instrumental. Various approaches indicate that CsA blocks the pore by binding to cyclophilin (CyP)-D. In particular, covalent labelling of CyP-D in situ by a photoactive CsA derivative has shown that pore ligan...
متن کاملMitochondrial permeability transition pore: an enigmatic gatekeeper
Mitochondrial permeability transition pore (MPTP) is a transient structure formed in the inner mitochondrial membrane (IMM) upon oxidative challenge of the organelle. The transition is a Ca 2+ -dependent increase of permeability of IMM leading to loss of transmembrane potential (∆ψm), mitochondrial swelling and, finally, rupture of outer mitochondrial membrane leading to release of factors caus...
متن کاملMitochondrial permeability transition pore and postconditioning.
Postconditioning has recently been described as a powerful cardioprotection that prevents lethal reperfusion injury. Growing evidence suggests that mitochondrial permeability transition may be a key event in postconditioning. This proposition arises from the complementary observations that: (1) conditions for the mitochondrial permeability transition pore (mPTP) opening are built up during earl...
متن کاملRegulation of total mitochondrial Ca2+ in perfused liver is independent of the permeability transition pore.
Triggering of the permeability transition pore (PTP) in isolated mitochondria causes release of matrix Ca2+, ions, and metabolites, and it has been proposed that the PTP mediates mitochondrial Ca2+ release in intact cells. To study the role of the PTP in mitochondrial energy metabolism, the mitochondrial content of Ca2+, Mg2+, ATP, and ADP was determined in hormonally stimulated rat livers perf...
متن کاملDiazoxide opens the mitochondrial permeability transition pore and alters Ca2+ transients in rat ventricular myocytes.
BACKGROUND The mitochondrial K(ATP) channel (mitoK(ATP)) has been implicated as an end effector or trigger of ischemic preconditioning (IP). Although a mitoK(ATP) opener, diazoxide, mimics IP, mechanisms for the cardioprotective action remain unclear. METHODS AND RESULTS We measured Ca2+ transients (CaTs) and mitochondrial inner membrane potential (Deltapsi(m)) with confocal microscopy and th...
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ژورنال
عنوان ژورنال: Biochimica et Biophysica Acta (BBA) - Bioenergetics
سال: 2010
ISSN: 0005-2728
DOI: 10.1016/j.bbabio.2010.04.389