"In the current study, Kalb and his collaborators aimed to investigate the role of RAD23, a protein that is involved in the identification and disposal of damaged or misfolded proteins. Under normal circumstances, elimination of misfolded proteins is essential for maintaining a healthy collection of proteins in cells, a process known as protein homeostasis, or proteostasis. Proteostasis is essential for physiological cell function, operating to balance the creation and destruction of proteins."
"First, Kalb and his team performed a genetic screen in C. elegans models of ALS and found that the protein RAD23 plays a dual role: it helps degrade some proteins while stabilizing others. His team showed that loss of RAD23 from cells accelerates the breakdown of several disease-linked proteins - including mutated forms of TDP43 and SOD - suggesting that physiological levels of RAD23 may actually hinder the cell's ability to clear harmful protein aggregates."
RAD23 acts as a cellular gatekeeper that identifies and helps dispose of damaged or misfolded proteins, contributing to proteostasis. RAD23 performs a dual role by promoting degradation of some substrates while stabilizing others. Loss of RAD23 accelerates breakdown of several disease-linked proteins, including mutated TDP43 and SOD, indicating that normal RAD23 levels can impede clearance of harmful aggregates. Proteostasis balances protein creation and destruction; its failure permits toxic aggregate accumulation implicated in ALS, Parkinson’s, Huntington’s, and Alzheimer’s. Two mammalian paralogs, RAD23A and RAD23B, are targets for genetic manipulation to assess therapeutic potential.
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