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0 · The Mitochondrial Permeability Transition Pore: Channel
1 · The Mitochondrial Permeability Transition Pore: Channel
2 · Mitochondrial channels: ion fluxes and more
3 · Mitochondrial Ion Channels: Gatekeepers of Life and Death
4 · Mitochondrial Ion Channels of the Inner Membrane and Their
5 · Mitochondrial Ion Channels
6 · Ion Channels and the Electrical Properties of Membranes
7 · Introduction to the Theme on Membrane Channels
8 · Identification of an ATP
9 · 11.3: Diffusion Across a Membrane
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Therefore, the discovery of mitochondrial ion channels influencing ion permeability through the membrane has defined a new dimension of the function of ion channels in different cell types, . In this review, we critically discuss the intracellular regulatory factors that affect channel activity in the inner membrane of mitochondria and, indirectly, contribute to cell death. .The main types of stimuli that are known to cause ion channels to open are a change in the voltage across the membrane (voltage-gated channels), a mechanical stress (mechanically gated channels), or the binding of a ligand .The field of mitochondrial ion channels has recently seen substantial progress, including the molecular identification of some of the channels. An integrative approach using genetics, .
The mitochondrial permeability transition (PT) is a permeability increase of the inner mitochondrial membrane mediated by a channel, the permeability transition pore (PTP).
The pore-forming and ATP-binding subunits of a mitochondrial protein complex that mediates ATP-dependent potassium currents are identified and characterized, revealing .The mitochondrial permeability transition (PT) is a permeability increase of the inner mitochondrial membrane mediated by a channel, the permeability transition pore (PTP). After a brief .
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Emerging evidence indicates that mitochondrial ion channels activated by reactive oxygen species can induce a mitochondrial "critical" state, which can scale to cause electrical and contractile .
This volume of the Annual Review of Biochemistry contains three reviews on membrane channel proteins: the first by Szczot et al., titled The Form and Function of PIEZO2; . Channels can be "gated" open by many mechanisms including ligand binding, change in membrane potential, lipid interactions, and mechanical stress. Opening a channel to .Therefore, the discovery of mitochondrial ion channels influencing ion permeability through the membrane has defined a new dimension of the function of ion channels in different cell types, mainly linked to the important tasks that mitochondrial ion channels perform in cell life and death.
In this review, we critically discuss the intracellular regulatory factors that affect channel activity in the inner membrane of mitochondria and, indirectly, contribute to cell death. These factors include various ligands, kinases, second messengers, and lipids.
The main types of stimuli that are known to cause ion channels to open are a change in the voltage across the membrane (voltage-gated channels), a mechanical stress (mechanically gated channels), or the binding of a ligand (ligand-gated channels).The field of mitochondrial ion channels has recently seen substantial progress, including the molecular identification of some of the channels. An integrative approach using genetics, electrophysiology, pharmacology, and cell biology to clarify the roles of these channels has thus become possible.The mitochondrial permeability transition (PT) is a permeability increase of the inner mitochondrial membrane mediated by a channel, the permeability transition pore (PTP). The pore-forming and ATP-binding subunits of a mitochondrial protein complex that mediates ATP-dependent potassium currents are identified and characterized, revealing the role of this channel in.
The mitochondrial permeability transition (PT) is a permeability increase of the inner mitochondrial membrane mediated by a channel, the permeability transition pore (PTP). After a brief historical introduction, we cover the key regulatory features of the PTP and provide a critical assessment of putative protein components that have been tested .Emerging evidence indicates that mitochondrial ion channels activated by reactive oxygen species can induce a mitochondrial "critical" state, which can scale to cause electrical and contractile dysfunction of the cardiac cell and, ultimately, the whole heart.
This volume of the Annual Review of Biochemistry contains three reviews on membrane channel proteins: the first by Szczot et al., titled The Form and Function of PIEZO2; the second by Ruprecht & Kunji, titled Structural Mechanism of Transport of Mitochondrial Carriers; and the third by Mc . Channels can be "gated" open by many mechanisms including ligand binding, change in membrane potential, lipid interactions, and mechanical stress. Opening a channel to ion flow allows quick passage of information (in this case an electrical signal) into the cell, leading to quick cellular responses.Therefore, the discovery of mitochondrial ion channels influencing ion permeability through the membrane has defined a new dimension of the function of ion channels in different cell types, mainly linked to the important tasks that mitochondrial ion channels perform in cell life and death. In this review, we critically discuss the intracellular regulatory factors that affect channel activity in the inner membrane of mitochondria and, indirectly, contribute to cell death. These factors include various ligands, kinases, second messengers, and lipids.
The main types of stimuli that are known to cause ion channels to open are a change in the voltage across the membrane (voltage-gated channels), a mechanical stress (mechanically gated channels), or the binding of a ligand (ligand-gated channels).The field of mitochondrial ion channels has recently seen substantial progress, including the molecular identification of some of the channels. An integrative approach using genetics, electrophysiology, pharmacology, and cell biology to clarify the roles of these channels has thus become possible.The mitochondrial permeability transition (PT) is a permeability increase of the inner mitochondrial membrane mediated by a channel, the permeability transition pore (PTP).
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The pore-forming and ATP-binding subunits of a mitochondrial protein complex that mediates ATP-dependent potassium currents are identified and characterized, revealing the role of this channel in.
The mitochondrial permeability transition (PT) is a permeability increase of the inner mitochondrial membrane mediated by a channel, the permeability transition pore (PTP). After a brief historical introduction, we cover the key regulatory features of the PTP and provide a critical assessment of putative protein components that have been tested .
Emerging evidence indicates that mitochondrial ion channels activated by reactive oxygen species can induce a mitochondrial "critical" state, which can scale to cause electrical and contractile dysfunction of the cardiac cell and, ultimately, the whole heart. This volume of the Annual Review of Biochemistry contains three reviews on membrane channel proteins: the first by Szczot et al., titled The Form and Function of PIEZO2; the second by Ruprecht & Kunji, titled Structural Mechanism of Transport of Mitochondrial Carriers; and the third by Mc .
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The Mitochondrial Permeability Transition Pore: Channel
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mitopoiesi chanel|Identification of an ATP
