Mitochondrial Function
Mitochondrial Function - Related Videos
02:43
Assessing Mitochondrial Function in Cerebral Vascular Endothelial Cells
0 Views •
2025
This video demonstrates the assessment of the mitochondrial functioning of cerebral vascular endothelial (CVE) cells using an extracellular flux assay. CVE cells are plated in an extracellular flux cell culture plate. Extracellular flux sensors are hydrated before loading and calibration into the bioanalyzer. The plate containing cells is then loaded for analysis.
15:43
Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
0 Views •
Cited by 5 •
2013
The effects of activation of protein kinase C (PKC) isozymes on mitochondrial functions associated with respiration and oxidative phosphorylation and on cell viability are described. The approach adapts adenoviral technique to selectively overexpress PKC isozymes in primary cell culture and a variety of assays to determine mitochondrial functions and energy status of the cell.
02:59
Animal Mitochondrial Genetics
0 Views •
2020
Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...
13:15
Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1
0 Views •
Cited by 5 •
2016
Here, we outline how to study mitochondrial localization of a (cell cycle) kinase, and how to determine its sub-mitochondrial location as well as potential mitochondrial substrates/targets. Forced expression of proteins into the mitochondria provides a useful tool for studying the functional consequences of mitochondrial localization of a protein of interest.
08:40
An Optimized Protocol to Analyze Glycolysis and Mitochondrial Respiration in Lymphocytes
0 Views •
Cited by 38 •
2016
The study of metabolism is becoming increasingly relevant to immunological research. Here, we present an optimized method for measuring glycolysis and mitochondrial respiration in mouse splenocytes, and T and B lymphocytes.
FAQs
Electron transfer through the respiratory chain establishes a proton gradient across the mitochondrial membrane. Oxidative phosphorylation then uses this stored electrochemical difference to drive ATP production, linking fuel oxidation to the cell’s usable energy supply. This coupling is essential because disruption at either electron transfer or gradient formation can reduce the efficiency of energy production in aerobic cells.
The tricarboxylic acid cycle processes fuel-derived molecules, while the respiratory chain transfers electrons generated during that metabolism. These activities are functionally connected: fuel breakdown supplies reducing power for electron transfer, and electron transfer creates the proton gradient required for oxidative phosphorylation. Considering the pathways together explains how mitochondrial metabolism supports cellular energy production rather than treating them as isolated processes.
Mitochondria contribute to calcium regulation and reactive oxygen species signaling in addition to energy production. These activities connect mitochondrial metabolism with broader cellular communication and control. Their importance is therefore not limited to ATP supply: altered signaling can influence cell behavior and survival, helping explain why mitochondrial dysfunction may affect tissues even when the primary problem is not energy production alone.
A functional analysis can follow the pathway from fuel-derived molecule breakdown through electron transfer, proton-gradient formation, and ATP production by oxidative phosphorylation. It can then consider calcium regulation, reactive oxygen species signaling, and programmed cell death. This sequence distinguishes defects in energy conversion from changes in mitochondrial signaling, providing a structured way to interpret altered cellular performance.
Tissues depend on mitochondria not only for energy production but also for metabolic regulation, calcium handling, reactive oxygen species signaling, and programmed cell death. Because these roles influence both cellular activity and survival, impaired mitochondrial function can alter tissue behavior. This broad relevance places mitochondria at the center of biological studies spanning metabolic, neurodegenerative, cardiovascular, and inherited disorders.
Disease research examines how impaired energy production or altered mitochondrial signaling changes cellular and tissue function. The overview specifically connects these disturbances with metabolic, neurodegenerative, cardiovascular, and inherited disorders. Mitochondrial function therefore provides a shared biological framework for comparing conditions that may differ clinically but involve disrupted metabolism, energy handling, or survival-related signaling.