Permeability Transition Pore
Mostrando 1-12 de 36 artigos, teses e dissertações.
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1. Propofol inhibits burn injury-induced hyperpermeability through an apoptotic signal pathway in microvascular endothelial cells
Recent studies have revealed that an intrinsic apoptotic signaling cascade is involved in vascular hyperpermeability and endothelial barrier dysfunction. Propofol (2,6-diisopropylphenol) has also been reported to inhibit apoptotic signaling by regulating mitochondrial permeability transition pore (mPTP) opening and caspase-3 activation. Here, we investigated
Braz J Med Biol Res. Publicado em: 06/03/2015
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2. Structure-biochemical aspects of adenine nucleotide translocase, cardiolipin and ciclophilin D on Ca2+-induced mitochondrial permeability transition / Aspectos bioquímico-estruturais do transportador de nucleotídeos de adenina, cardiolipinas e ciclofilina D na transição de permeabilidade mitocondrial induzida por Ca2+
Oxidation of the Adenine Nucleotide Translocase (ANT) cysteine residue 56 (ANT-cys56) is potentially involved in Ca2+-induced Mitochondrial Permeability Transition (MPT), a process which is prevented by cyclosporine A (CsA), due to its inhibition of Permeability Transition Pore (PTP) opener component, the peptidyl-prolyl cis-trans isomerase cyclophylin D (cy
Publicado em: 2010
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3. A mechanistic view of mitochondrial death decision pores
Mitochondria increase their outer and inner membrane permeability to solutes, protons and metabolites in response to a variety of extrinsic and intrinsic signaling events. The maintenance of cellular and intraorganelle ionic homeostasis, particularly for Ca2+, can determine cell survival or death. Mitochondrial death decision is centered on two processes: in
Brazilian Journal of Medical and Biological Research. Publicado em: 12/04/2007
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4. Envolvimento do carreador ADP/ATP nos processos de permeabilização da membrana mitocondrial interna
In this work we presented sufficient experimental evidences to propose the direct involvement of the ADP/ATP carrier in the permeabilization processes of the inner mitochondrial membrane. Comparing the protection conferred by ADP - a subtrate of the ADP/ATP carrier, dithiothreitol - a disulfide reductant and butylhydroperoxide - a radical scavenger, it was f
Publicado em: 1993
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5. Vaccinia Virus Infection Disarms the Mitochondrion-Mediated Pathway of the Apoptotic Cascade by Modulating the Permeability Transition Pore
Many viruses have evolved strategies that target crucial components within the apoptotic cascade. One of the best studied is the caspase 8 inhibitor, crmA/Spi-2, encoded by members of the poxvirus family. Since many proapoptotic stimuli induce apoptosis through a mitochondrion-dependent, caspase 8-independent pathway, we hypothesized that vaccinia virus woul
American Society for Microbiology.
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6. BMAP-28, an Antibiotic Peptide of Innate Immunity, Induces Cell Death through Opening of the Mitochondrial Permeability Transition Pore
BMAP-28, a bovine antimicrobial peptide of the cathelicidin family, induces membrane permeabilization and death in human tumor cell lines and in activated, but not resting, human lymphocytes. In addition, we found that BMAP-28 causes depolarization of the inner mitochondrial membrane in single cells and in isolated mitochondria. The effect of the peptide was
American Society for Microbiology.
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7. Regulation and pharmacology of the mitochondrial permeability transition pore
The ‘mitochondrial permeability transition', characterized by a sudden induced change of the inner mitochondrial membrane permeability for water as well as for small substances (≤1.5 kDa), has been known for three decades. Research interest in the entity responsible for this phenomenon, the ‘mitochondrial permeability transition pore’ (mPTP), has dra
Oxford University Press.
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8. BNIP3 and Genetic Control of Necrosis-Like Cell Death through the Mitochondrial Permeability Transition Pore
Many apoptotic signaling pathways are directed to mitochondria, where they initiate the release of apoptogenic proteins and open the proposed mitochondrial permeability transition (PT) pore that ultimately results in the activation of the caspase proteases responsible for cell disassembly. BNIP3 (formerly NIP3) is a member of the Bcl-2 family that is express
American Society for Microbiology.
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9. Glycogen synthase kinase-3β mediates convergence of protection signaling to inhibit the mitochondrial permeability transition pore
Environmental stresses converge on the mitochondria that can trigger or inhibit cell death. Excitable, postmitotic cells, in response to sublethal noxious stress, engage mechanisms that afford protection from subsequent insults. We show that reoxygenation after prolonged hypoxia reduces the reactive oxygen species (ROS) threshold for the mitochondrial permea
American Society for Clinical Investigation.
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10. Plant mitochondria actively import DNA via the permeability transition pore complex
Plant mitochondria are remarkable with respect to their content in foreign, alien and plasmid-like DNA, raising the question of the transfer of this information into the organelles. We demonstrate the existence of an active, transmembrane potential-dependent mechanism of DNA uptake into plant mitochondria. The process is restricted to double-strand DNA, but
Oxford University Press.
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11. The Temperature Dependence of Lipid Membrane Permeability, its Quantized Nature, and the Influence of Anesthetics
We investigate the permeability of lipid membranes for fluorescence dyes and ions. We find that permeability reaches a maximum close to the chain melting transition of the membranes. Close to transitions, fluctuations in area and compressibility are high, leading to an increased likelihood of spontaneous lipid pore formation. Fluorescence correlation spectro
The Biophysical Society.
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12. Effect of Transient and Permanent Permeability Transition Pore Opening on NAD(P)H Localization in Intact Cells*
To study the effect of mitochondrial permeability transition pore (PTP) opening on NAD(P)H localization, intact cells were exposed to the Ca2+ ionophore A23187. PTP opening, mitochondrial membrane potential, mitochondrial volume, and NAD(P)H localization were assessed by time-lapse laser confocal microscopy using the calcein-cobalt technique, tetramethy
American Society for Biochemistry and Molecular Biology.