Linked Life Data

12490287

Source:http://linkedlifedata.com/resource/pubmed/id/12490287

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2002-12-19
pubmed:abstractText
During the in vivo maturation of erythrocytes, the number of CR1 per cell decreases by approximately two-thirds in 30 days. The CR1 loss is enhanced in several diseases such as SLE, AIDS, and particularly in factor I deficiency. Microvesicles enriched in CR1 and DAF are released from erythrocytes matured in vitro, leading to the same loss of both molecules. When comparing reticulocytes and erythrocytes, CR1 and DAF were lost similarly in 15 normal individuals, suggesting that vesiculation may be at the origin of CR1 loss in vivo. However, the enhanced loss of CR1 in 3 patients with factor I deficiency was contrasted with a normal loss of DAF, raising the possibility that, in this pathological condition, CR1 might be proteolytically cleaved, leaving small CR1 fragments on the erythrocytes. To answer this question, a rabbit polyclonal antibody was raised against the cytoplasmic (tail) domain of CR1, which recognised specifically CR1 of erythrocytes and urinary vesicles on Western blots. However, no CR1 fragments could be detected on erythrocytes of the factor I deficient patients although this antibody was able to recognise CR1 fragments after treatment of normal erythrocytes or urinary vesicles with elastase. These data suggest that cell surface domains rich in CR1, but not in DAF, are specifically lost in factor I deficiency.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1079-9796
pubmed:author
pubmed:issnType
Print
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
200-12
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
The mechanism of loss of CR1 during maturation of erythrocytes is different between factor I deficient patients and healthy donors.
pubmed:affiliation
Department of Research, University Hospital Basel, Basel, Switzerland. smiot@uhbs.ch
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't