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Published 2021 Nov 9
This facilitates K48-linked ubiquitination of OCTN2, accelerating its degradation via the autophagy-lysosome and endocytosis-lysosome pathways [104, 105]
This underscores that the problem in IR is not oxidative stress or other CS manifestations per se, but their unbalanced, dysfunctional progression
Because senile plaques started to form in mice older than 8 months of age, A in these plaques might not be extracted by SDS or GdnHCl (Kawarabayashi et al , 2001)
