This resource is a video abstract of a research paper created by …
This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:
"The molecular mechanisms behind diseases and malignancies were once considered to follow a basic paradigm. Cells use a network of protein-protein interactions to detect environmental changes, signal the nucleus, and then trigger a response through changes in gene expression. Recent evidence, however, suggests the products of protein breakdown, rather than the proteins alone, could play an important role. A new review from the Kastritis Laboratory outlines how the fatty acid metabolites acetyl-CoA, α-ketoglutarate, and palmitic acid, in particular help orchestrate cell signaling and communication. These metabolites are regulated by large enzymatic complexes, or “metabolons”; acetyl-CoA by the pyruvate dehydrogenase complex, α-ketoglutarate by the 2-oxoglutarate dehydrogenase complex and palmitic acid by fatty acid synthase..."
The rest of the transcript, along with a link to the research itself, is available on the resource itself.
This resource is a video abstract of a research paper created by …
This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:
"Cancers are complex diseases largely characterized by rapid cellular proliferation. This can be slowed by regulated cell death mechanisms like ferroptosis. Ferroptosis is triggered by extensive peroxidation of cell membrane phospholipids by reactive oxygen species (ROS), but ferroptosis can be inhibited by enzymes that undo peroxidation like GPX4. Another enzyme, DHODH, supports GPX4 and is vital to the production of pyrimidine nucleotides, critical building blocks for rapidly proliferating cells. In theory, this would make inhibiting DHODH a valuable therapeutic target for cancer by freeing up ferroptosis and hampering proliferation. However, this is complicated by the “Warburg effect,” which is common in some cancer cells. The Warburg effect is a shift away from using mitochondria for energy to other metabolic processes, which has knock-on effects..."
The rest of the transcript, along with a link to the research itself, is available on the resource itself.
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