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1 B5 (serine protease inhibitor B5), and CSTB (cystatin B).
2 eletion of the lysosomal protease inhibitor, cystatin B.
3 s mouse model of EPM1 provides evidence that cystatin B, a non-caspase cysteine protease inhibitor, h
4 mutations in the gene (CSTB) encoding human cystatin B, a widely expressed cysteine protease inhibit
5 y form of cerebral amyloid angiopathy whilst cystatin B aggregates are found in cases of Unverricht-L
8 mined the structured core of human stefin B (cystatin B) amyloid fibrils using quenched hydrogen exch
9 ied the effects of diminishing expression of cystatin B, an endogenous inhibitor of cathepsins B, H a
10 over in TgCRND8 mice by genetically deleting cystatin B, an endogenous inhibitor of lysosomal cystein
13 evidence that mutations in the gene encoding cystatin B are responsible for the primary defect in pat
16 and three were successfully verified, namely cystatin B (CSTB), triosephosphate isomerase (TPI1), and
22 tation, were identified in the gene encoding cystatin B in EPM1 patients but were not present in unaf
24 of lipid accumulation in TgCRND8 by removing cystatin B inhibition on lysosomal proteases suggests th
27 m ROS was attenuated in an NPC cell model by cystatin B over-expression or pharmacological inhibition
28 5 of 266 evaluable proteins (angiopoietin 1, cystatin B, the latency-associated peptide of transformi