The role of Jun, Fos and the AP-1 complex in cell-proliferation and transformation.
Phorbol ester-inducible genes contain a common cis element recognized by a TPA-modulated trans-acting factor
- P. Angel, M. Imagawa, M. Karin
- 19 June 1987
DNA Binding of the Glucocorticoid Receptor Is Not Essential for Survival
- H. Reichardt, K. Kaestner, G. Schütz
- 15 May 1998
AP-1 subunits: quarrel and harmony among siblings
- J. Hess, P. Angel, M. Schorpp-Kistner
- BiologyJournal of Cell Science
- 1 December 2004
AP-1-mediated regulation of processes such as proliferation, differentiation, apoptosis and transformation should be considered within the context of a complex dynamic network of signalling pathways and other nuclear factors that respond simultaneously.
The jun proto-oncogene is positively autoregulated by its product, Jun/AP-1
- P. Angel, K. Hattori, T. Smeal, M. Karin
- 2 December 1988
Altered endochondral bone development in matrix metalloproteinase 13-deficient mice
- D. Stickens, Danielle J. Behonick, Z. Werb
- Biology, EngineeringDevelopment
- 1 December 2004
The hypothesis that proper ECM remodeling is the dominant rate-limiting process for programmed cell death, angiogenesis and osteoblast recruitment during normal skeletal morphogenesis is supported.
Activation of protein kinase C decreases phosphorylation of c-Jun at sites that negatively regulate its DNA-binding activity
- W. J. Boyle, T. Smeal, T. Hunter
- Biology, ChemistryCell
- 8 February 1991
ATF‐2 is preferentially activated by stress‐activated protein kinases to mediate c‐jun induction in response to genotoxic agents.
- H. Dam, D. Wilhelm, I. Herr, A. Steffen, P. Herrlich, P. Angel
- Biology, ChemistryEMBO Journal
- 1 April 1995
The data demonstrate that distinct signal transduction pathways converge at c‐Jun/ATF‐2, whereby each subunit is individually addressed by a specific class of protein kinases, which allows fine tuned modulation of c‐jun expression by a large spectrum of extracellular signals.
S100A8 and S100A9 in inflammation and cancer.
- C. Gebhardt, J. Nemeth, P. Angel, J. Hess
- BiologyBiochemical Pharmacology
- 30 November 2006
Stimulation of c-Jun activity by CBP: c-Jun residues Ser63/73 are required for CBP induced stimulation in vivo and CBP binding in vitro.
- Andrew J. Bannister, T. Oehler, D. Wilhelm, P. Angel, T. Kouzarides
- Biology, Computer ScienceOncogene
- 21 December 1995
It is shown that CBP also stimulates the activity of both c-Jun and v-Jun in vivo, consistent with a mechanism by which CBP acts as a co-activator protein for Jun dependent transcription by interacting with the Jun N-terminal activation domain.