Linked Life Data

7852286

Source:http://linkedlifedata.com/resource/pubmed/id/7852286

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1995-3-15
pubmed:abstractText
The effects of thapsigargin (Tg), a specific inhibitor of Ca(2+)-ATPase of the endoplasmic reticulum (ER), on replication of Sendai virus (HVJ) in BALB3T3 cells were examined. In the presence of Tg, the cells infected with HVJ did not release viral particles to the culture medium. Tg inhibited almost completely the expression of viral envelope proteins, HN and F0, on the cell surface, although it did not affect the synthesis of viral proteins. Two other inhibitors of Ca(2+)-ATPase of the ER, 2,5-di(tert-butyl)-1,4-benzohydroquinone (BHQ) and cyclopiazonic acid (CPA), as well as Ca(2+)-ionophores such as A23187 and ionomycin, also inhibited the expression of HN protein on the cell surface. Tg seemed to inhibit the intracellular transport or maturation of the viral membrane proteins by perturbing intracellular distribution of Ca2+ ions. In the presence of Tg, HN protein remained sensitive to endoglycosidaseH (endoH) for 3 h after its synthesis. On the other hand, F0 protein became resistant to endoH and sensitive to neuraminidase even in the presence of Tg. These results indicate that the transport of HN protein is blocked at the ER or the cis-Golgi region, while that of F0 protein is blocked at the post-Golgi stage in the presence of Tg.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0021-924X
pubmed:author
pubmed:issnType
Print
pubmed:volume
116
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
649-56
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Transport of envelope proteins of Sendai virus, HN and F0, is blocked at different steps by thapsigargin and other perturbants to intracellular Ca2+.
pubmed:affiliation
Department of Physiological Chemistry, Tokyo Metropolitan Institute of Medical Science.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't