report that a 50% global reduction of BIN1 protein levels resulting from a single Bin1 allele deletion in mice does not change BACE1 levels or localization in vivo nor does this reduction alter the production of endogenous murine Abeta in nontransgenic mice
these results indicate that BIN1 and DNM2 regulate muscle development and organization function through a common pathway and define BIN1 as a negative regulator of DNM2 in vitro and in vivo during muscle maturation.
Bin1 and CD2AP keep APP and BACE1 apart in early endosomes by distinct mechanisms in axon and dendrites. Individuals carrying variants of either factor would slowly accumulate Abeta in neurons increasing the risk for late-onset AD.
the depletion of BIN1 increases cellular BACE1 levels through impaired endosomal trafficking and reduces BACE1 lysosomal degradation resulting in increased Ab production. Our findings provide a mechanistic role of BIN1 in the pathogenesis of Alzheimer disease (AD) as a novel genetic regulator of BACE1 levels and Ab production
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