HIGHLIGHTS
SUMMARY
The endogenous regulation of CK1δ, on the other hand, can be carried out through various mechanisms, including autophosphorylation or phosphorylation by other protein_kinases (Graves and Roach, 1995; Bischof et_al, 2013), interactions with other protein and/or cellular components, and subcellular sequestration (Milne et_al, 2001; Xu et_al, 2019). Homodimerization excludes ATP from the binding_site, thus inhibiting kinase activity (Longenecker et_al, 1998; Hirner et_al, 2012). The correlation between CK1δ activity and tau protein aggregates in various neurodegenerative diseases has been confirmed by co-immunoprecipitation studies, which highlight that the presence of CK1δ is associated with hyperphosphorylated . . .
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