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Monash researchers have developed a key process in all human cells that contributes to diseases such as cancer and neurodegenerative diseases, as well as aging. The discovery reveals how cells effectively get rid of cellular junk food that, when accumulated, can lead to death and health problems badociated with aging.
Autophagy is the team cleaning the cell, used by cells to break down debris such as broken proteins, cell membrane fragments, viruses or bacteria. To capture this waste, the cells use specialized membranes to trap the cargo so that it is recycled into new parts and new energies. Without effective autophagy, the cells are smothered by their own damaged components, which can contribute to the development of many diseases, including diabetes, muscular dystrophy, Parkinson's disease and Alzheimer's disease.
The laboratory of Dr. Michael Lazarou of the Monash Biomedicine Institute of Discovery has released data today Nature Communications it distorted beliefs about how cells target their trash. Cells target different types of cargo using "autophagy receptors", which can bind cargo as well as enveloping membranes. Until recently, it was thought that these autophagy receptors were recruiting cargo membranes, but research conducted by Dr. Benjamin Padman of Lazarou Laboratory now shows that this is not the case.
Dr. Padman suppressed the ability of autophagic receptors to bind to membranes and found that this did not stop the autophagy process. In collaboration with Dr. Lan Nguyen, head of the Monash BDI Computer Network Modeling Laboratory, researchers have instead uncovered how cells boost autophagy rates.
"It completely changed my thinking," said Dr. Padman.
"Autophagy receptors did not recruit membranes, they recruited more autophagy receptors to speed things up," he said.
According to Dr. Padman, a number of treatments and therapies being developed globally aim to control the activity of these proteins, "which, according to our findings, do not work as we thought before. "
"The autophagy cleansing team is still working hard in our cells, but it can sometimes struggle to keep pace.If we could find drugs that target this amplification mechanism, we could help neuronal cells manage the accumulation of Huntington-related waste proteins and Alzheimer's disease, "said Dr. Padman.
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Material provided by Monash University. Note: Content can be changed for style and length.
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