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Accumulation of neurotoxic amyloid-beta is a major hallmark of Alzheimer disease (AD\\\\; MIM 104300). 再加上，我们可以发Pigeon Homolog (Drosophila) 抗体 (47) 和 Pigeon Homolog (Drosophila) 蛋白 (6)和数多这个蛋白质的别的产品。
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GSAP cleavage via caspase-3 (显示 CASP3 ELISA试剂盒) is regulated and depend upon the availability of 5-Lipoxygenase (显示 ALOX5 ELISA试剂盒) in Alzheimer's disease.
gamma-secretase activating protein (GSAP) and imatinib have roles in the regulation of gamma-secretase activity and amyloid-beta generation
Protocols for recombinant bacterial expression and purification of potentially important protein GSAP are not successful in generating soluble forms of GSAP that contain well-ordered and homogeneous tertiary structure.
Aberrant regulation of gamma-secretase activating protein expression plays a key role in acceleration of gamma-cleavage of beta-secretase-cleaved C-terminal fragment of amyloid precursor protein (显示 APP ELISA试剂盒) and accumulation of Abeta (显示 APP ELISA试剂盒) in AD brains
A gamma-secretase activating protein (GSAP) that selectively increases amyloid-beta production via interactions with both gamma-secretase and its substrate, the amyloid precursor protein carboxy-terminal fragment.
Study reports discovery of a novel gamma-secretase activating protein (GSAP) that selectively increases amyloid-beta production through interactions with gamma-secretase and its substrate, the amyloid precursor protein (显示 APP ELISA试剂盒) carboxy-terminal fragment.
Accumulation of neurotoxic amyloid-beta is a major hallmark of Alzheimer disease (AD\; MIM 104300). Formation of amyloid-beta is catalyzed by gamma-secretase (see PSEN1\; MIM 104311), a protease with numerous substrates. PION, or GSAP, selectively increases amyloid-beta production through a mechanism involving its interaction with both gamma-secretase and its substrate, the amyloid-beta precursor protein (APP\; MIM 104760) C-terminal fragment (APP-CTF) (He et al., 2010
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