Amyloid $sZ-protein stimulates parallel increases in cellular levels of its precursor and amyloid precursor-like protein 2 (APLP2) in human cerebrovascular smooth muscle cells

Autor:	Gopal Thinakaran, Sangram S. Sisodia, William E. Van Nostrand, Lynda Ruffini, Susan M. Saporito-irwin
Rok vydání:	1997
Předmět:	Pathology medicine.medical_specialty biology Amyloid BACE1-AS P3 peptide Biochemistry of Alzheimer's disease Cell biology Internal Medicine biology.protein Amyloid precursor protein medicine Senile plaques Amyloid precursor protein secretase APLP2
Zdroj:	Amyloid. 4:54-60
ISSN:	1744-2818 1350-6129
DOI:	10.3109/13506129708995270
Popis:	The amyloid β-protein (Aβ) which accumulates in cerebral vascular and senile plaque deposits in the brains of patients with Alzheimer's disease (AD) is proteolytically derived from a larger precursor protein, the amyloid β-protein precursor (AβPP). AβPP is a member of a multigene family which includes amyloid precursor-like protein 2 (APLP2). Recently, we showed that Aβ1-42, but not the shorter Aβ1-40 induces cellular levels of AβPP in degenerating cultured human cerebrovascular smooth muscle (HCSM) cells. Here we report that Aβ1-42 stimulates a parallel increase in the cellular levels of APLP2 in cultured HCSM cells. in contrast, the levels of smooth muscle cell α-actin or total cellular protein did not appreciably change. These findings suggest a common regulatory mechanism for increased levels of HCSM cellular AJPP and APLP2 in response to pathologic Aβ1-42 induced stress.
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=doi_________::e36871e8caacec19c2feda4a6aa2b6e6 https://doi.org/10.3109/13506129708995270 Zobrazit plný text záznamu