Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1994-1-25
pubmed:abstractText
The signalling mechanisms of the IL-2R remained an enigma until recent years. We now know that IL-2R are coupled to their own unique signalling pathways that complement rather than duplicate TCR signalling. The IL-2R beta- and gamma-chains are essential for signal coupling. Sequence comparisons indicate that portions of the extracellular and cytoplasmic domains of IL2R beta gamma molecules are homologous to several hematopoietic growth factor receptors, including erythropoietin. This may indicate that these receptors utilize common or related molecules in ligand binding or signal transduction. The cytoplasmic domain of the IL-2R beta-chain contains distinctive serine (S) and acidic (A) rich regions that participate in signalling. The overall scheme of IL-2R signalling is similar to other eukaryotic growth factors in that ligand binding activates a complicated and branching series of enzymatic steps that utilize protein tyrosine kinase (PTK) activation as a central component. More recent reports indicate that IL-2R are linked to additional membrane and cytosolic signalling molecules, including glycosylated phosphatidylinositol (GPI), phosphatidylinositol-3-kinase (PI3K), p74c-raf and p21ras. The regulation of these factors and their importance in IL-2 induced growth and differentiation awaits further study.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1044-5323
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
337-44
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Protein and lipid kinase activation cascades in interleukin-2 receptor signalling.
pubmed:affiliation
Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia 19104.
pubmed:publicationType
Journal Article, Review