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A decrease in proteasomal activity appears to enhance the underlying condition of Huntingtons disease, Alzheimers disease, Parkinsons disease, and Prion disease

This suggests that direct COP1-p53 recognition may require additional cofactors, adaptors, or specific cellular signal conditions such as glucose induce assembly of CRL4 COP1 for p53 degradation, as suggested in Su et al 29

Conformational transitions of the pituitary adenylate cyclase-activating polypeptide receptor, a human class B GPCR

doi: 10.1111/jdi.13136 9 ElKGraySMCapozziMEKnuthERJinESvendsenBet al