Unconventional Signalling Mechanisms Mediated by the Angiotensin II Type 1 Receptor in Cardiovascular Cell Types
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REVIEW ARTICLE
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Unconventional Signalling Mechanisms Mediated by the Angiotensin II Type 1 Receptor in Cardiovascular Cell Types Peiyong Zhai, Jonathan Galeotti and Junichi Sadoshima Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, University of Medicine & Dentistry of New Jersey, New Jersey Medical School, Newark, New Jersey, USA
Contents Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143 1. G Protein-Independent Signalling of the Angiotensin II Type 1 Receptor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144 2. Activation of Protein Kinases Through Sequence-Specific Signalling Mechanisms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145 2.1 Transactivation of Epidermal Growth Factor Receptor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146 2.2 Janus Kinases-Signal Transducers and Activators of Transcription (JAK-STAT) Pathway . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147 3. Direct Interaction with Intracellular Signalling Molecules . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147 4. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148
Abstract
Angiotensin II (Ang II) is an important effector of the renin-angiotensin system, which plays a critical role in mediating hypertension, cardiac hypertrophy and heart failure. These pathological effects of Ang II on the heart are primarily mediated by the Ang II type 1 (AT1) receptor, a seven transmembrane G protein-coupled receptor. The signalling mechanism of the AT1 receptor is traditionally described as dependent on heterotrimeric G proteins. However, accumulating lines of evidence have suggested that some aspects of AT1 receptor-mediated signalling apparently occur independently of G protein activation. The AT1 receptor also uses a part of its amino acid sequence, the YIPP (tyrosine [Y] isoleucine [I] proline [P] proline [P]) motif, in addition to conventional G protein-dependent mechanisms, to activate tyrosine kinases, such as the epidermal growth factor receptor and Janus kinases (JAK). The AT1 receptor also directly associates with other intracellular molecules, such as AT1 receptor-associated protein. Interaction between the AT1 receptor and these molecules affects the cellular functions of each. Such mechanisms, relying on the specific amino acid sequences of the AT1 receptor, provide the AT1 receptor with a unique modality to communicate with
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