Related Experiment Video
Updated: Sep 13, 2025

Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses
Published on: June 14, 2020
VDAC2 brake release: unleashing inflammation via IFNγ
Swapneel J Patel1, Zhijian J Chen2
1Department of Dermatology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
None:
Identification of therapeutic vulnerabilities in cancer remains a high priority for cancer research. A recent CRISPR/Cas9 screen identified that VDAC2 deletion in tumors enhanced their sensitivity to interferon-γ (IFNγ) through the release of mitochondrial DNA (mtDNA) and activation of the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway. These data suggest that VDAC2 inhibition could enhance antitumor therapies.
More Related Videos
Related Concept Videos
Inflammatory Response I: Vascular and Cellular
Inflammatory Response
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Inflammatory Response II: Inflammatory Exudate and Tissue Repair
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the...
Inflammation
Vascular Spasm
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The...

