IndraLab

Statements


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"Knockdown of USP24 in cell lines and in human induced-pluripotent stem cells (iPSC) differentiated into dopaminergic neurons resulted in elevated ULK1 protein levels and increased autophagy flux in a manner independent of MTORC1 but dependent on the class III phosphatidylinositol 3-kinase (PtdIns3K) activity."

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"Knockdown of USP24 also led to increase in levels of the autophagosome associated lipidated form of LC3 (LC3-II) [30]), confirming increase in autophagy."

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"USP24 is another modulator of autophagy which may also influence PD progression as it can regulate dopaminergic neurite outgrowth, but the potential as a disease modulator is not evaluated yet."

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"Blocking lysosomal function with bafilomycin led to significant increase in accumulation of GFP-LC3 positive autophagosomes in USP24 knockdown cells, indicating that USP24 is negatively regulating autophagy flux without affecting lysosomal degradation)."

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"USP24 is implicated in Parkinson’s disease and increased autophagy , but expression data presented here indicate a role for USP24 in heart, nerve, and muscle tissue, but not adipose or brain tissues."