Linked Life Data

2925452

Source:http://linkedlifedata.com/resource/pubmed/id/2925452

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1989-5-3
pubmed:abstractText
Intracellular cleavage of Ii was evaluated in immunoprecipitates of radiolabeled Raji cells treated with protease inhibitors (leupeptin, antipain, chymostatin, and pepstatin) or blockers of endosomal function (chloroquine and monensin). Immunoprecipitates with anti-class II and anti-Ii(12-28) sera and VIC-Y1 MoAb revealed Ii cleavage products of 21,000 and 10,000 daltons (p21 and p10) only in leupeptin- and antipain-treated cells. Both p21 and p10 were judged to be N-terminal products because they were recognized with anti-Ii(12-28) and not with anti-Ii(183-193) or anti-Ii(192-211) sera. p10 might be derived from p21 because its intensity was increased in inverse proportion to p21 as a function of leupeptin or antipain concentration. p21, but not p10, was recognized by anti-class II antibody and thus might originate from class II-associated Ii. In pulse-chase studies, p21 and p10 appeared at 2 hr and later after Ii synthesis. p25, an Ii C-terminal fragment, was about 60% reduced by leupeptin or antipain. Intracellular proteolytic cleavage of class II-associated Ii appeared to follow two pathways leading either to N-terminal p21 and p10 or to C-terminal p25. Such cleavages might regulate or catalyze foreign antigen binding to class II.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0198-8859
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
153-63
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Inhibition by leupeptin and antipain of the intracellular proteolysis of Ii.
pubmed:affiliation
Department of Pharmacology, University of Massachusetts Medical School, Worcester 01655.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.