Gi proteins use a novel beta gamma- and Ras-independent pathway to activate extracellular signal-regulated kinase and mobilize AP-1 transcription factors in Jurkat T lymphocytes. [electronic resource]
Producer: 19990805Description: 19992-20001 p. digitalISSN:- 0021-9258
- Benzoquinones
- Calcium-Calmodulin-Dependent Protein Kinases -- metabolism
- Cyclic AMP-Dependent Protein Kinases -- metabolism
- DNA-Binding Proteins
- Enzyme Activation
- GTP-Binding Proteins -- metabolism
- Gene Expression Regulation
- Humans
- Jurkat Cells
- Lactams, Macrocyclic
- MAP Kinase Kinase 1
- Mitogen-Activated Protein Kinase Kinases
- Pertussis Toxin
- Phosphatidylinositol 3-Kinases -- metabolism
- Protein Serine-Threonine Kinases -- metabolism
- Protein-Tyrosine Kinases -- metabolism
- Proto-Oncogene Proteins -- metabolism
- Proto-Oncogene Proteins c-fos -- metabolism
- Quinones -- pharmacology
- RNA, Messenger -- metabolism
- Receptors, Opioid, delta -- metabolism
- Rifabutin -- analogs & derivatives
- Signal Transduction
- Transcription Factor AP-1 -- metabolism
- Transcription Factors
- Virulence Factors, Bordetella -- pharmacology
- beta-Adrenergic Receptor Kinases
- ets-Domain Protein Elk-1
- ras Proteins -- metabolism
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Publication Type: Journal Article; Research Support, Non-U.S. Gov't
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