Linked Life Data

7678037

Source:http://linkedlifedata.com/resource/pubmed/id/7678037

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1993-1-25
pubmed:abstractText
Activation of either dense tonsilar B lymphocytes or the B lymphoblastoid cell line T5-1 with Staphylococcus aureus, Cowan strain I, induced surface expression of insulin receptors. Addition of insulin to these activated cells resulted in subsequent phosphorylation of the B cell surface protein CD20, the functions to regulate B cell activation. The cytoplasmic domains of CD20 contain multiple serine and threonine residues, of which at least two are followed by acidic sequences typical of substrate sites favored by casein kinase II. Tryptic mapping of CD20 isolated from intact cells treated with insulin showed increased phosphorylation on peptides having similar migration to those phosphorylated by casein kinase II in vitro. Treatment of tonsilar B cells or T5-1 cells with phorbol esters or in vitro phosphorylation by purified protein kinase C did not result in phosphorylation of peptides phosphorylated by casein kinase II, suggesting that protein kinase C is not directly involved in CD20 phosphorylation in the response to insulin. Phosphorylation of CD20 cannot be triggered by insulin in resting B cells, as the insulin receptor is expressed only after entry into the G1 phase of the cell cycle. Thus, distinct regulation of activation pathways are available to resting as opposed to activated B lymphocytes.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
150
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
96-105
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Insulin regulates serine/threonine phosphorylation in activated human B lymphocytes.
pubmed:affiliation
Department of Microbiology, University of Washington, Seattle 98195.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.