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162 results on '"Shah, Bukhtiar H."'

5. GPCR-mediated transactivation of RTKs in the CNS: mechanisms and consequences

Author

Shah, Bukhtiar H. and Catt, Kevin J.

Subjects
Neurology -- Research, Health, Psychology and mental health
Abstract

G protein-coupled receptors (GPCRs) mediate cellular responses to a diverse array of extracellular messenger molecules. Recent studies have shown that GPCR-mediated signaling pathways include transactivation of receptor tyrosine kinases (RTKs), such as receptors for epidermal growth factor, platelet-derived growth factor, neurotrophins and fibroblast growth factor. Cross-communication between GPCRs and RTKs is a complex process, and utilizes sets of signaling molecules that are primarily determined by cell context and the types of receptors activated. The differential involvement of RTKs and downstream signaling pathways activated in response to GPCR-mediated stimulation elicits a variety of cellular effects during development, proliferation, differentiation, survival, repair and synaptic transmission in the CNS.

Published
2004

6. A central role of EGF receptor transactivation in angiotensin II-induced cardiac hypertrophy

Author

Shah, Bukhtiar H. and Catt, Kevin J.

Subjects
Heart diseases -- Research, Heart diseases -- Care and treatment, Pharmacology -- Research, Biological sciences, Chemistry, Pharmaceuticals and cosmetics industries
Abstract

In addition to their physiological roles in the cardiovascular system (CVS), G-protein-coupled receptor (GPCR) agonists such as noradrenaline, endothelin-1 and angiotensin II (Ang II) are known to be involved in the development of cardiac hypertrophy. Recent studies using targeted overexpression of the angiotensin A[T.sub.1] receptor in cardiomyocytes suggest that Ang II can directly promote the growth of cardiomyocytes via transactivation of the epidermal growth factor (EGF) receptor and subsequent activation of mitogen-activated protein kinases (MAPKs). This process is mediated by the production of heparin-binding EGF (HB-EGF) by metalloproteases. Blockade of the generation of HB-EGF by metalloprotease inhibitors, or abrogation of EGF receptor kinase activity by selective pharmacological inhibitors or antisense oligonucleotides, protects against Ang II-mediated cardiac hypertrophy. These approaches offer a potential therapeutic strategy to prevent cardiac remodeling and hypertrophy, and possibly prevent progression to heart failure.

Published
2003

21. Gonadotrophin-releasing hormone receptor agonist-mediated down-regulation of G(q)-alpha/G11-alpha (pertussis toxin-insensitive) G proteins in alpha-T3-1 gonadotroph cells reflects increased G protein turnover but not alterations in mRNA levels

Author

Shah, Bukhtiar H., MacEwan, David J., and Milligan, Graeme

Subjects
Gonadotropin releasing hormone -- Research, Hormone receptors -- Physiological aspects, G proteins -- Research, Science and technology
Abstract

Gonadotrophin-releasing hormone receptor agonist down-modulates pertussis toxin-insensitive G proteins G9-alpha and G11-alpha in alpha T3-1 pituitary gonadotrophs. Exposure to the agonist increases the turnover of G9 alpha and G11 alpha but not cause changes in mRNA levels. These results reflect enhanced proteolysis of the activated G proteins.

Published
1995

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