Mitochondrial Protein VDAC2 Links PI3K to Endosome Maturation [Jun. 13, 2023]

Scientists have unveiled that VDAC2, a mitochondrial pore protein, as a PI3K-binding protein and show that endosomes positive for Ras PI3K complexes are tethered to mitochondria through PI3K-VDAC2 interaction. These researchers have further elucidated that this mitochondrion-endosome association fosters endosome maturation. Learn more about how the authors detected this mitochondria-endosome interaction using ECGreen for endosome labeling, and PlasMem Bright Red for plasma membrane labeling, which served as a negative control (please refer to Figures 5C - E and 5F - G).

Interaction between PI3K and the VDAC2 channel tethers Ras-PI3K-positive endosomes to mitochondria and promotes endosome maturation
Click here for the original article: Aya O Satoh, et. al., Cell Rep., 42, 112229 (2023)

Point of Interest

- VDAC2, a protein located on the outer membrane of mitochondria, interacts with PI3K, serving as a link between endosomes and mitochondria.

- This interaction facilitates clathrin-independent endocytosis.

- The binding of VDAC2 and PI3K triggers the maturation of endosomes that are connected to mitochondria.

- Besides its structural role in facilitating this association, VDAC2 also has a functional role in promoting endosome maturation at these contact points.

Related Techniques

Endocytosis Detection detection

ECGreen-Endocytosis Detection

Lysosomal function

Lysosomal Acidic pH Detection Kit -Green/Red and Green/Deep Red

Plasma Membrane Staining

PlasMem Bright Green / Red

Glycolysis/Oxidative phosphorylation Assay

Glycolysis/OXPHOS Assay Kit

Oxygen consumption rate assay

Extracellular OCR Plate Assay Kit

Related Applications

Fatty acid starvation induced by uptake inhibitor evoke reprogramming of cellular metabolism

Mitochondrial fatty acid β-oxidation and oxidative phosphorylation (OXPHOS) are crucial biochemical processes that metabolize fats and sugars to produce ATP, the cell's primary energy source. In this section, we underscored the significance of fatty acid starvation and energy pathways, with an emphasis on the fatty acid uptake inhibitor, FATP2. Here are the key findings from our experiments conducted on HeLa cells:

・Inhibition of fatty acid uptake results in reduced cell proliferation, though it does not lead to cell death. This was determined through the use of a Cell Counting Kit-8 and Fatty Acid Uptake Kit (Image 1).

・Fatty acid starvation shifts cellular metabolism from OXPHOS to glycolysis, as indicated by the Glycolysis/JC-1 MitoMP Assay Kit. (Image 2)

・When fatty acid uptake is inhibited, a compensatory increase in glucose and glutamine uptake occurs to preserve cell viability, as observed using the Glucose Assay Kit and Glutamine Assay Kit. (Image 3)

Products in Use
for Fatty Acid Uptake Assay
  ① Fatty Acid Uptake Assay Kit

for Cell Proliferation/Cytotoxicity Assay
  ② Cell Counting Kit-8

for Glycolysis Assay and Mitochondrial Membrane Potential Detection
  ③ Glycolysis/JC-1 MitoMP Assay Kit

for Glucose and Glutamine Consumption Assay
  ④ Glucose Assay Kit

  ⑤ Glutamine Assay Kit