Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

The mitochondrial potassium cycle.

K D Garlid1, P Paucek

  • 1Department of Biochemistry and Molecular Biology, OGI School of Science and Engineering, Oregon Health & Science University, Beaverton 97006-8921, USA. garlid@bmb.ogi.edu

IUBMB Life
|January 19, 2002
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Mechanism of uncoupling protein action.

Biochemical Society transactions·2001
Same author

Alkylsulfonates as probes of uncoupling protein transport mechanism. Ion pair transport demonstrates that direct H(+) translocation by UCP1 is not necessary for uncoupling.

The Journal of biological chemistry·2001
Same author

Identification and properties of a novel intracellular (mitochondrial) ATP-sensitive potassium channel in brain.

The Journal of biological chemistry·2001
Same author

Pharmacologic characterization of BMS-191095, a mitochondrial K(ATP) opener with no peripheral vasodilator or cardiac action potential shortening activity.

The Journal of pharmacology and experimental therapeutics·2001
Same author

Cardioprotection by ischemic preconditioning preserves mitochondrial function and functional coupling between adenine nucleotide translocase and creatine kinase.

Journal of molecular and cellular cardiology·2001
Same author

Bioenergetic consequences of opening the ATP-sensitive K(+) channel of heart mitochondria.

American journal of physiology. Heart and circulatory physiology·2001

The mitochondrial K+ cycle regulates organelle integrity and cellular pathophysiology. Opening the mitochondrial ATP-sensitive K+ channel (mitoK(ATP)) protects the heart from injury by influencing reactive oxygen species production.

Area of Science:

  • Mitochondrial physiology
  • Cellular pathophysiology

Background:

  • The mitochondrial K+ cycle involves K+ and anion transport across the inner membrane, regulating matrix volume and organelle integrity.
  • Dysregulation of this cycle impacts cellular pathophysiology.
  • The mitochondrial ATP-sensitive K+ channel (mitoK(ATP)) is implicated in cellular signaling and protection.

Purpose of the Study:

  • To review the properties of the mitochondrial K+ cycle.
  • To understand the role of mitoK(ATP) in cellular protection and pathophysiology.
  • To elucidate the mechanisms behind mitoK(ATP) mediated effects.

Main Methods:

  • Review of existing literature on mitochondrial K+ cycle and mitoK(ATP).
  • Analysis of studies on ischemic preconditioning and cardiac protection.

Related Experiment Videos

  • Examination of signaling pathways involving reactive oxygen species.

    • Main Results:

    • MitoK(ATP) opening before ischemia protects the heart from ischemia-reperfusion injury.
    • MitoK(ATP) activation triggers increased mitochondrial reactive oxygen species production, crucial for ischemic protection and gene transcription.
    • MitoK(ATP) opening preserves intermembrane space structure, maintaining low outer membrane permeability to adenine nucleotides.

    Conclusions:

    • The mitochondrial K+ cycle is vital for maintaining mitochondrial structural integrity.
    • MitoK(ATP) plays a significant role in cellular signaling pathways for ischemic protection.
    • Understanding mitoK(ATP) properties provides insight into its protective effects in cellular pathophysiology.