Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1989-2-14
pubmed:abstractText
Among the major obstacles to clarifying molecular mechanisms involved in amyloid metabolism in Alzheimer disease has been the unavailability of laboratory models for this uniquely human disorder. The present studies were aimed at establishing genetically engineered cell lines that overexpress amyloid immunoreactivity and that may be relevant to amyloid accumulation in the Alzheimer disease brain. We used cloned amyloid cDNA that contains a region encoding A4 (beta-polypeptide) amino acids along with recently developed tumor virus vectors derived from simian virus 40 to prepare transformed cells. After transient and permanent transfection, a variety of cell types overexpressed A4 immunoreactivity that was detected by highly specific monoclonal antibodies. We observed that the use of an amyloid subdomain containing the A4 region, but lacking the sequence of a Kunitz-type protease inhibitor found in amyloid precursor protein variants, was sufficient to obtain cells that overproduced an A4 epitope. The transformed cells were readily propagated in culture and may provide an experimental medium to elucidate aspects of the molecular pathogenesis of Alzheimer disease. The cellular models may also serve as tools for deriving potentially useful therapeutic agents.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-1065897, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-176412, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-2457908, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-2881207, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-2893289, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-2893290, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-2893291, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-2893379, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-2949367, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-3035574, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-3159021, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-3357357, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-3374733, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-3810169, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-3930053, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-4357758, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-4748425, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-6246378, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-6260373, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-6267479, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-6375662, http://linkedlifedata.com/resource/pubmed/commentcorrection/2563163-6960240
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0027-8424
pubmed:author
pubmed:issnType
Print
pubmed:volume
86
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
337-41
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Overexpression of amyloid precursor protein A4 (beta-amyloid) immunoreactivity in genetically transformed cells: implications for a cellular model of Alzheimer amyloidosis.
pubmed:affiliation
Cancer Center, University of Rochester Medical School, NY 14642.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't