Linked Life Data

8965676

Source:http://linkedlifedata.com/resource/pubmed/id/8965676

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1996-12-4
pubmed:abstractText
Adhesins and adhesin-related accessory proteins of the bacterial pathogen, Mycoplasma pneumoniae, are proline-rich in composition and mediate successful parasitism of host target cells. A specific class of peptidyl-proyl cis-trans isomerases (PPIs), called cyclophilins (Cyps), activate proline-rich proteins, and this enzymatic activity is inhibited by the drug, cyclosporin A (CsA). This study builds upon the connection between the structural/functional properties of the proline-rich proteins of M. pneumoniae and the mode of action of CsA to demonstrate that CsA reduces cytadherence capabilities of mycoplasmas, affects colony morphology and can be mycoplasmacidal. As a consequence of CsA treatment early passage mycoplasmas lacked the major adhesin, P1, explaining their cytadherence-negative phenotype. Three mycoplasma proteins with molecular masses of 160, 84 and 80 kDa were identified by CsA-affinity chromatography. A PCR cloned partial cyp gene of M. pneumoniae, which exhibited sequence homologies with prokaryotic and eukaryotic cyclophilins, was present in multiple copies. These results implicate the role of PPIs as important regulators of cytadherence, virulence and growth cycle events in mycoplasmas.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0882-4010
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
155-69
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Correlations between Mycoplasma pneumoniae sensitivity to cyclosporin A and cyclophilin-mediated regulation of mycoplasma cytadherence.
pubmed:affiliation
Department of Microbiology, University of Texas Health Science Center at San Antonio 78284-7758, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.