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β-Site Amyloid Precursor Protein (APP)-cleaving Enzyme 1 (BACE1)-deficient Mice Exhibit a Close Homolog of L1 (CHL1) Loss-of-function Phenotype Involving Axon Guidance Defects

Hitt, Brian, Riordan, Sean M., Kukreja, Lokesh, Eimer, William A., Rajapaksha, Tharinda W., Vassar, Robert·2012·Journal of Biological Chemistry
DOI 10.1074/jbc.m112.415505
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Crossref · 10.1074/jbc.m112.415505

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  • BACE1 is highly expressed in the nervous system and contributes to additional physiological processes besides its role in AD, e.g., through neuregulin-1 cleavage in myelination and CHL1 cleavage in axon targeting.

    “BACE1 is highly expressed in the nervous system and contributes to additional physiological processes besides its role in AD, e.g. through neuregulin-1 cleavage in myelination and CHL1 cleavage in axon targeting [7–12].”

    From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [11]

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Research works printed but not linked: 49

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Metadata

Authors
Hitt, B., Riordan, S. M., Kukreja, L., Eimer, W. A., Rajapaksha, T. W., & Vassar, R.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2012-11
Volume
287
Issue
46
Pages
38408-38425
ISSN
0021-9258
DOI
10.1074/jbc.m112.415505
Cited by
143
References
8
Language
en
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