Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1990-7-31
pubmed:abstractText
Most B chronic lymphocytic leukemia (CLL) cells express on their surface the CD5 antigen which is an activation marker on normal B cells. To investigate the control of CD5 expression in B-CLL cells, we examined several inducing agents for their effects on CD5 mRNA expression. Northern blot analysis demonstrated that the expression of CD5 mRNA could be up- or down-regulated depending on the inducers used. Treatment with direct activators of protein kinase C (PKC), the phorbol ester phorbol 12-myristate 13-acetate (PMA) or the natural agent bryostatin 1 (Bryo), caused increased CD5 mRNA expression after 8-16 h of incubation. In contrast, exposure to the dual signals of a PKC activator (PMA or Bryo) plus the calcium ionophore A23187 led to down-regulation of CD5 mRNA expression. The molecular alterations at the RNA level were accompanied by morphological changes: PMA and/or Bryo induced cellular features of activation while PMA plus A23187 or Bryo plus A23187 mediated morphological changes indicative of differentiation to plasmacytoid cells. The data suggest that as a consequence of maturation differentiated B-CLL cells down-regulate CD5 expression by analogy with the normal ontogenic process in which plasma cells, the end-stage cells of normal B cell differentiation, are CD5-.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0014-2980
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1119-23
pubmed:dateRevised
2009-9-29
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Down-regulation of CD5 mRNA in B-chronic lymphocytic leukemia cells by differentiation-inducing agents.
pubmed:affiliation
Royal Free Hospital School of Medicine, Department of Haematology, London.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't