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Discussion CEP192 is a context-specific regulator of Aurora-A with a dual-site interaction mechanism Aurora-A depends on binding partners to stimulate its activation via autophosphorylation, and so we have previously described it as an incomplete kinase (Burgess et al, 2015)

Notably, NIT treatment was initiated 4 wks from the onset of trauma as a delayed intervention

Progressive destruction of articular cartilage is characteristic of OA, and the maintenance of tissue function of articular cartilage is dependent on its sole resident cell type, the chondrocyte

PMID: 34541734

It helps transport fatty acids into the mitochondria, where theyre converted into usable fuel