Wednesday, October 19, 2011

Autophagy: Finding the Line Between Normal and Diseased

Autophagy is when a cell gets rid of intracellular components, such as organelles and proteins. The inability of autophagosomes to do work can lead to several diseases, including cancer, inflammatory diseases, and neurodegeneration. Autophagosomes are membrane-bound organelles that transport cellular components to lysosomes, fusing to become autolysosomes. Enzymes in the autolysosome then degrade the enveloped material, converting it to basic materials that can be reused in the cell.

As more research has been conducted on autophagy, it has been observed that there are several links between autophagy and human diseases. Some autophagic proteins, such as beclin-1, have tumor suppressing properties. Mice that lack the Beclin-1autophagy protein have shown more formation of tumors than those who have Beclin-1. Mutations in the genes of autophagosomes can lead to the accumulation of damaged DNA as well as genome instability. Observing autophagic pathways can be tricky because it can be difficult to distinguish them from normal pathways.

Autophagosomes are biologically important molecules because they function in homeostatic processes. These homeostatic mechanisms include helping the cell signal its homeostatic condition to the outside environment and modifying the cell's metabolic state to more effectively counter harmful external stimuli. Their activity is regulated by external conditions, such as nutrients and stress, and mTOR, which supervises cell signaling pathways involved in cellular metabolism. Researchers are looking to determine what function autophagosomes have on developmental processes in the hopes of producing disease therapies through their research. For more information, click here to access my article.

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