Model for the dysregulation of BACE1 and α2,6-sialylation in AD. (IMAGE)
Caption
In AD patients, we propose the existence of highly expressed α2,6-sialylation catalyzed by ST6Gal-I. This ST6Gal-I-mediated α2,6-sialylation of BACE1 regulates BACE1 expression by affecting BACE1 ubiquitination (Ub) levels. Increased α2,6-sialylation on BACE1 enhances Aβ42 deposition, which is a feature of AD patients.
Credit
Kangkang Yang, Xueying Li, Minchao Lai, Weiwei Zhao, Wanli Song, Shaobin Chen, Wenzhe Li
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CC BY-NC-ND