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PMID: 3523754 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Interleukin-2 induction of T-cell G1 progression and c-myb expression.

Science (New York, N.Y.) ·Vol. 233 ·No. 4760 ·1986-07-11 ·Pages 203-6

Stern JB, Smith KA

Abstract

In studies to determine the biochemical mechanisms responsible for cell proliferation, synchronized T cells were used as a model for cellular growth control. By metabolic and morphologic criteria, it was found that activation of the T-cell antigen receptor rendered the cells responsive to interleukin-2 (IL-2), but did not move them through the cell cycle. Instead, IL-2 stimulated G1 progression to S phase, or lymphocyte "blastic transformation." During IL-2-promoted G1 progression, expression of the cellular proto-oncogene c-myb was induced transiently at six to seven times basal levels, maximal levels occurring at the midpoint of G1.

MeSH Terms
Animals Cell Cycle/drug effects Cell Division/drug effects Gene Expression Regulation/drug effects Humans Interleukin-2/pharmacology Mice Proto-Oncogene Mas Proto-Oncogene Proteins/biosynthesis Proto-Oncogenes/drug effects Receptors, Antigen, T-Cell/drug effects T-Lymphocytes/drug effects,growth & development
Chemicals
Interleukin-2 MAS1 protein, human Proto-Oncogene Mas Proto-Oncogene Proteins Receptors, Antigen, T-Cell
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Stern J B
Smith K A
Article Info
Journal
Science (New York, N.Y.)
Abbr.
Science
ISSN
0036-8075
Published
1986-07-11
Pages
203-6
Language
English
Region
United States
NLM ID
0404511
Subset
IM
Grants
NCI NIH HHS · CA 09367 · United States
NCI NIH HHS · CA-17643 · United States
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