Abstract:
:Deposition of amyloid beta protein in the brain is the major pathological feature of Alzheimer's disease. Amyloid beta protein is generated from beta-amyloid precursor protein by beta-secretase and gamma-secretase. Proteolytic processing of amyloid precursor protein at the beta site by BACE1 is essential to generate amyloid beta protein. BACE1, the major beta-secretase involved in cleaving amyloid precursor protein, has been identified as a type 1 membrane-associated aspartyl protease. In this study, we found that BACE1 gene expression is controlled by a TATA-less promoter. BACE1 gene expression is tightly regulated at the transcriptional level and the transcription factor Sp1 plays an important role in regulation of BACE1 to process amyloid precursor protein generating amyloid beta protein. Furthermore, we found that BACE1 protein is ubiquitinated, and the degradation of BACE1 proteins and amyloid precursor protein processing are regulated by the ubiquitin-proteasome pathway.
journal_name
Ann N Y Acad Scijournal_title
Annals of the New York Academy of Sciencesauthors
Zhou W,Qing H,Tong Y,Song Wdoi
10.1196/annals.1332.004subject
Has Abstractpub_date
2004-12-01 00:00:00pages
49-67eissn
0077-8923issn
1749-6632pii
1035/1/49journal_volume
1035pub_type
杂志文章abstract::Tick burdens cause direct damage to hosts and transmit several disease agents, the majority of which are secreted into feeding lesions through tick salivary glands. Reduced incidence of naturally transmitted tick-borne diseases was recently observed among cattle immunized with tick salivary gland extracts (TSGE). The ...
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journal_title:Annals of the New York Academy of Sciences
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journal_title:Annals of the New York Academy of Sciences
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