BACE knockout mice are healthy despite lacking the primary beta-secretase activity in brain: implications for Alzheimer's disease therapeutics.
By S. Roberds, John P. Anderson, G. Basi, M. Bienkowski, D. Branstetter, Karen S. Chen, S. Freedman, N. Frigon, D. Games, K. Hu and 22 more. Human Molecular Genetics, 2001
728 citations recorded by the source corpus.
Subfields: Computational Theory and Mathematics, Pharmacology, Physiology
View Paper: https://www.semanticscholar.org/paper/5642e45889fac00d824afc6c54e015e70ae38073
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Citations in the corpus
- Transcriptional Regulation of BACE1, the β-Amyloid Precursor Protein β-Secretase, by Sp1 (2004, background): “However, mice deficient in BACE1, having a marked reduction in A formation, develop normally without any detectable physiological defects (6, 30, 35 ), which makes BACE1 a superior therapeutic target.”
- Trafficking and proteolytic processing of APP. (2012, background): “BACE1 knockout mice are Cite this article as Cold Spring Harb Perspect Med 2012;2:a006270 3 w w w .p e rs p e c ti v e si n m e d ic in e .o rg viable and fertile and do not show any major behavioral, morphological, or developmental deficits (Cai et al. 2001; Roberds et al. 2001; Luo et al. 2003).”
- An Overview of APP Processing Enzymes and Products (2010, neutral): “A possible explanation for these findings and the seemingly discrepant results of Cai et al. (2000), Roberds et al. (2001) and Luo et al., (2001) is that cathepsins cleave wildtype (wt) human APP but not human APP that is mutated at the βsecretase cleavage site (mtAPP) as is the case in transgenic…”
- Can the pharmaceutical industry reduce attrition rates? (2004, result): “We have, in a similar manner, provided very strong evidence that inhibition of β-secretase inhibits the production of amyloid-β in knockout mic”