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The overexpression of DYRK1A in T21 brains may contribute directly to early-onset neurofibrillary degeneration through tau hyperphosphorylation and indirectly through the phosphorylation of alternative splicing factors (Wegiel et al
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Potential Research Applications: Injury recovery and soft tissue repair studies Tendon, ligament, and muscle healing models Anti-inflammatory and immune modulation research Angiogenesis and cellular regeneration investigations For laboratory research only
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