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We are now on the verge of viewing effector molecules and other regulatory sites as therapeutic targets for the amelioration of human and animal disease. The recognition, for example, that mutant proteins are frequently misrouted molecules, rather than functionally defective ones, changes our approach to "inborn errors of metabolism" and offers new approaches for pharmacological discovery, based on rescue of receptors, ion channels and enzymes with pharmacoperones. Ion channels, regulators of G-protein signaling and enzymes engaged in regulation, now present opportunities for drug development.
The state of our art also benefits by the availability of superior tools that allow measurement of interactions and afford unprecedented insight into the biomolecular interactions that present novel approaches to drug design.
List of contents
Molecular and functional diversity of the TRPC family of ion channels. TRPC channels and their role in ROCE/SOCE.- Functional Rescue of Misfolded Receptor Mutants.- Obesity-related mutations of leptin and melanocortin receptors.- cAMP- and cGMP-dependent control of lipolysis and lipid mobilization in humans: putative targets for fat cell management.- Central Neuropeptide Receptors Involved in Water Balance: Application to Apelin.- Targeting regulators of G protein signaling (RGS proteins) to enhance agonist specificity.- Dimeric GPCRs: what did we learn from the metabotropic glutamate receptors?.- Guiding principles applied in the design of GPCR-selective hypothalamic hormone agonists and antagonists.- Mutations in G proteins and G protein-coupled receptors in human endocrine diseases.- A molecular dissection of the glycoprotein hormone receptors.- Receptor Tyrosine Kinases as Targets for Cancer Therapy Development.- Targets for pituitary tumor therapy.- The endogenous cannabinoid system in the control of food intake and energy balance.
Summary
We are now on the verge of viewing effector molecules and other regulatory sites as therapeutic targets for the amelioration of human and animal disease. The recognition, for example, that mutant proteins are frequently misrouted molecules, rather than functionally defective ones, changes our approach to "inborn errors of metabolism" and offers new approaches for pharmacological discovery, based on rescue of receptors, ion channels and enzymes with pharmacoperones. Ion channels, regulators of G-protein signaling and enzymes engaged in regulation, now present opportunities for drug development.
The state of our art also benefits by the availability of superior tools that allow measurement of interactions and afford unprecedented insight into the biomolecular interactions that present novel approaches to drug design.
