Linked Life Data

14678766

Source:http://linkedlifedata.com/resource/pubmed/id/14678766

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2003-12-17
pubmed:abstractText
alpha(2)-Macroglobulin (alpha(2)M) is an abundant plasma/extracellular space protein implicated in clearance of amyloid beta (Abeta), a key constituent of Alzheimer's disease (AD) plaques. alpha(2)M also regulates proteinase and growth factor activities. In recent years, there have been >30 genetic studies debating the controversial role of a five-base-pair intronic deletion in the A2M gene in late-onset AD. However, little is known about potential effects of the deletion upon alpha(2)M function. In this study, we examined the subunit and conformational structure of alpha(2)M in AD plasma samples, and its capacity to bind trypsin, transforming growth factor-beta1, and Abeta. Plasma from patients homozygous for the deletion (DD) showed normal alpha(2)M subunit size, conformation, and proteinase inhibitory activity. Interestingly, plasma alpha(2)M from two DD patients showed markedly increased TGF-beta1 binding. Moreover, methylamine-treated DD plasma samples showed modest, but significant, elevations in Abeta binding to alpha(2)M* compared with samples from patients lacking the deletion. These observations suggest a possible functional basis by which the A2M deletion may influence multifactorial AD pathogenesis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0969-9961
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
504-12
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Functional analysis of plasma alpha(2)-macroglobulin from Alzheimer's disease patients with the A2M intronic deletion.
pubmed:affiliation
Department of Pathology, University of Pittsburgh, Pittsburgh, PA 15213, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't