Population
Rat hepatoma cells and transiently transfected COS-1 cells expressing ApoB-17 (amino-terminal 17% of apoB)
Comparison
Structural perturbations of ApoB-17 via chemical… vs Wild-type ApoB-17
Design
Preclinical
Authors
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Disulfide bond 2 or 4 disruption spares apoB-17 lipid binding in vitro; leaves open alternative mechanisms for in vivo assembly impairment.
Disruption of native disulfide bonds in the alpha(1) domain of apoB does not impair its vesicle-binding properties in vitro, suggesting that these mutations block lipoprotein assembly in vivo through a different mechanism.
DeLozier et al. (2001) studied this question.
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