Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1993-5-7
pubmed:abstractText
The beta/A4 region of the amyloid precursor protein (APP) accumulates in brains of victims of Alzheimer disease (AD) where it is a major component of senile plaques. We examined the pathophysiological consequences of overexpression of the beta/A4-C-terminal DNA in PC12 cells. Serum-free conditioned media (SFCM) from positive transfectants stimulated control PC12 cells to extend neurites and increase in size. Unlike the factor that affected cell size, neurite lengthening activity was significantly decreased after immunoabsorption with anti-beta/A4 monoclonal antibodies (MAb) and changes in pH. The data support the view that among the consequences of beta/A4-C-terminal DNA overexpression in PC12 cells is the release of factors that stimulate nontransfected cells to undergo morphological transformations that include differentiation to a neuronal phenotype. It is hypothesized that similar activities that may contribute to the molecular pathophysiology of the disorder may be present in the AD brain.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1044-7393
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
99-113
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:articleTitle
PC12 cells release stimulatory factors after transfection with beta/A4-C-terminal DNA of the Alzheimer amyloid precursor protein.
pubmed:affiliation
Massachusetts General Hospital, Department of Psychiatry, Boston.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't