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関連する概念動画

Feedback Inhibition00:46

Feedback Inhibition

44.2K
Biochemical reactions are occurring constantly in cells, converting starting substances to different products, usually with the help of enzymes that speed the reactions. Without enzymes, it would take far too long for most reactions to occur to be useful to the cell!
44.2K
The Electron Transport Chain01:30

The Electron Transport Chain

13.9K
The electron transport chain or oxidative phosphorylation is an exothermic process in which free energy released during electron transfer reactions is coupled to ATP synthesis. This process is a significant source of energy in aerobic cells, and therefore inhibitors of the electron transport chain can be detrimental to the cell's metabolic processes.
Inhibitors of the electron transport chain
Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q...
13.9K
Mitochondrial Protein Sorting01:39

Mitochondrial Protein Sorting

4.4K
Mitochondria are double-membrane organelles of the eukaryotes involved in cellular metabolism, signaling, ATP synthesis, and programmed cell death.  Each of these processes requires specific proteins and enzymes that must be correctly sorted to the right mitochondrial subcompartment for the proper functioning of the organelle.
Most of these mitochondrial proteins are encoded by the nucleus and imported to the mitochondria as unfolded or loosely folded precursors. Mitochondrial precursors...
4.4K
Mitochondrial Precursor Proteins01:39

Mitochondrial Precursor Proteins

2.9K
Mitochondrial precursors are partially unfolded or loosely folded polypeptide chains. Newly synthesized precursors are inhibited from spontaneously folding into their native conformation by the cytosolic chaperones, heat shock proteins 70 (Hsp70), and mitochondrial import stimulation factors (MSFs). Precursors bound to MSFs are guided to the TOM70-TOM37 receptors, while precursors bound to Hsp70  chaperones are targetted to TOM20-TOM22 receptor complexes.
Most of the mitochondrial...
2.9K
Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

8.9K
Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
8.9K
Energy to Drive Translocation01:37

Energy to Drive Translocation

2.0K
Mitochondrial protein import is powered by two distinct energy sources: ATP hydrolysis and electrochemical potential across the inner membrane. Newly synthesized precursors are bound by cytosolic chaperones of the Hsp70 family, which guide them to the import receptors on the mitochondrial surface. Utilizing the energy of ATP hydrolysis, Hsp70 chaperones transfer these precursors to the TOM receptors on the mitochondrial outer membrane.
Generally, polypeptides are unfolded by two distinct...
2.0K

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関連する実験動画

Updated: May 6, 2026

Multi-parameter Measurement of the Permeability Transition Pore Opening in Isolated Mouse Heart Mitochondria
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Multi-parameter Measurement of the Permeability Transition Pore Opening in Isolated Mouse Heart Mitochondria

Published on: September 7, 2012

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ポストコンディショニングは,ミトコンドリアの透過性移行を阻害する.

Laurent Argaud1, Odile Gateau-Roesch, Olivier Raisky

  • 1INSERM E 0226, Université Claude Bernard Lyon I, France.

Circulation
|January 12, 2005
PubMed
まとめ

リパーフュージョン中の短い介入であるポストコンディショニングは,ミトコンドリアの透過性移行孔 (mPTP) を阻害することにより,心臓発作のサイズを大幅に減らす. この保護効果は強力な抗イシュケミア効果をもたらします.

科学分野:

  • 心血管研究 循環器科の研究
  • ミトコンドリア生物学
  • 発血不全性損傷 発血不全性損傷とは

背景:

  • リパーフュージョン中の短期的な缺血は,ポストコンディショニングとして知られており,心臓発作のサイズを制限することができます.
  • ミトコンドリアの浸透性トランジション孔 (mPTP) の開口は,致命的な再注射損傷に関与しています.
  • この研究では,ポストコンディショニングがmPTPの開通に影響するかどうかを調査した.

研究 の 目的:

  • ポストコンディショニングがミトコンドリアの透過性移行孔 (mPTP) の開口を調節するかどうかを判断する.
  • ischemia-reperfusion injuryに対するポストコンディショニングの保護効果を評価する.

主な方法:

  • 胸を開けたウサギは30分間の不血症と4時間の再注血を受けた.
  • ポストコンディショニングは,初期リフロー後,短期のイシュケミアと再注血のサイクルを伴う.
  • ミトコンドリアCa2+誘発のmPTPの開口と心臓発作の大きさを測定した.

主要な成果:

  • ポストコンディショニング,プリコンディショニング,mPTP阻害剤NIM811により,対照群と比較して心臓発作のサイズが著しく減少しました (29%, 18%, 20% vs. 61%).

さらに関連する動画

Simultaneous Measurement of Mitochondrial Calcium and Mitochondrial Membrane Potential in Live Cells by Fluorescent Microscopy
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Simultaneous Measurement of Mitochondrial Calcium and Mitochondrial Membrane Potential in Live Cells by Fluorescent Microscopy

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Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess
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Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess

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関連する実験動画

Last Updated: May 6, 2026

Multi-parameter Measurement of the Permeability Transition Pore Opening in Isolated Mouse Heart Mitochondria
13:42

Multi-parameter Measurement of the Permeability Transition Pore Opening in Isolated Mouse Heart Mitochondria

Published on: September 7, 2012

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Simultaneous Measurement of Mitochondrial Calcium and Mitochondrial Membrane Potential in Live Cells by Fluorescent Microscopy
08:43

Simultaneous Measurement of Mitochondrial Calcium and Mitochondrial Membrane Potential in Live Cells by Fluorescent Microscopy

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Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess
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Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess

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  • mPTPを開くために必要なCa2+負荷は,後条件,前条件,およびNIM811で治療されたグループ (41, 47, 67 μmol/L CaCl2/mg) と対照群 (16 μmol/L CaCl2/mg) で著しく高かった.

    • 結論:

    • ポストコンディショニングは,ミトコンドリアの透過性移行孔 (mPTP) の開口を効果的に阻害します.
    • この阻害は,心臓発作の大きさを減らす,有意な抗血動性保護を与える.