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PMID: 11983158 Published · ppublish English Journal Article Review

Cytokine signaling in 2002: new surprises in the Jak/Stat pathway.

Cell ·Vol. 109 Suppl ·2002-04-00 ·Pages S121-31

O'Shea JJ, Gadina M, Schreiber RD

Abstract

The importance of Jak-Stat pathway signaling in regulating cytokine-dependent gene expression and cellular development/survival is well established. Nevertheless, advances continue to be made in defining Jak-Stat pathway effects on different cellular processes and in different organisms. This review focuses on recent advances in the field and highlights some of the most active areas of Jak-Stat pathway research.

MeSH Terms
Animals Carrier Proteins/metabolism Cytokines/metabolism DNA-Binding Proteins/chemistry,metabolism Gene Expression Regulation Humans Intracellular Signaling Peptides and Proteins Janus Kinase 1 Methylation Protein Inhibitors of Activated STAT Protein-Tyrosine Kinases/metabolism Proteins/metabolism Receptors, Cytokine/metabolism Repressor Proteins STAT1 Transcription Factor Signal Transduction Suppressor of Cytokine Signaling 1 Protein Suppressor of Cytokine Signaling Proteins Trans-Activators/chemistry,metabolism
Chemicals
Carrier Proteins Cytokines DNA-Binding Proteins Intracellular Signaling Peptides and Proteins Protein Inhibitors of Activated STAT Proteins Receptors, Cytokine Repressor Proteins SOCS1 protein, human STAT1 Transcription Factor STAT1 protein, human Suppressor of Cytokine Signaling 1 Protein Suppressor of Cytokine Signaling Proteins Trans-Activators Protein-Tyrosine Kinases JAK1 protein, human Janus Kinase 1
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
O'Shea John J
Molecular Immunology and Inflammation Branch, National Institutes of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20852, USA. [email protected]
Gadina Massimo
Schreiber Robert D
Article Info
Journal
Cell
Abbr.
Cell
ISSN
0092-8674
Published
2002-04-00
Pages
S121-31
Language
English
Region
United States
NLM ID
0413066
Subset
IM
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