Abstract
The protooncogene Pim-1 encodes serine/threonine protein kinases that are involved in cytokine-mediated cell proliferation and in lymphoma- and leukemogenesis. It is largely unknown how Pim-1 executes its biological effects. Here we show that Pim-1 physically interacts with heat shock protein 90 alpha and beta (Hsp90alpha and beta). The Hsp90-specific inhibitor geldanamycin (GA) induced a rapid degradation of Pim-1 and reduced its kinase activity. The expression of Hsp90alpha was regulated by a signal from the cytokine receptor gp130, as is Pim-1's expression. These results indicate that Hsp90 is coordinately regulated with Pim-1 and is involved in the stabilization and function of Pim-1.
Copyright 2001 Academic Press.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Amino Acid Sequence
-
Antigens, CD / metabolism
-
Base Sequence
-
Cell Line
-
Cytokine Receptor gp130
-
DNA Primers
-
DNA-Binding Proteins / metabolism
-
Gene Expression Regulation / physiology*
-
HSP90 Heat-Shock Proteins / physiology*
-
Membrane Glycoproteins / metabolism
-
Molecular Sequence Data
-
Protein Serine-Threonine Kinases*
-
Proto-Oncogene Proteins / genetics*
-
Proto-Oncogene Proteins c-pim-1
-
Reverse Transcriptase Polymerase Chain Reaction
-
STAT3 Transcription Factor
-
Signal Transduction
-
Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
-
Trans-Activators / metabolism
Substances
-
Antigens, CD
-
DNA Primers
-
DNA-Binding Proteins
-
HSP90 Heat-Shock Proteins
-
Membrane Glycoproteins
-
Proto-Oncogene Proteins
-
STAT3 Transcription Factor
-
Trans-Activators
-
Cytokine Receptor gp130
-
Protein Serine-Threonine Kinases
-
Proto-Oncogene Proteins c-pim-1