By Allen M. Spiegel MD (auth.), Allen M. Spiegel MD (eds.)
More than a set of assessment articles, G Proteins, Receptors, and ailment summarizes intensive the nation of our wisdom this day bearing on not just how cells converse through G-protein-coupled sign transduction strategies, but in addition how defects in those proteins and their receptors could cause severe human ailment related to many various organ structures. Written via best investigators, each one bankruptcy describes intimately the constitution and serve as of a specific G protein or receptor, outlines attainable mutations, and discusses totally the molecular pathogenesis of linked ailments. Diagnostic and healing implications also are mentioned while relevant.
In its designated combination of state of the art uncomplicated technological know-how and scientific drugs, G Proteins, Receptors, and sickness deals deep insights into the physiological importance of this key sign transduction pathway, in addition to into the molecular foundation of illnesses starting from weight problems to malignancy. the elemental figuring out of the complicated sign transduction method completed the following presents an organization origin for destiny efforts to avoid and medication those diseases.
Read or Download G Proteins, Receptors, and Disease PDF
Similar nonfiction_10 books
Organic getting older because the time-depending normal decline of organic platforms linked to a gradually expanding mortality chance is a common phenomenom of serious importance. The underlying strategies are very advanced and counting on genetic and setting components. those components encode or impact a community of interconnected mobile pathways.
This e-book was once conceived with the item of offering to medical professionals and scientific scholars with a possible curiosity within the disciplines of orthopaedic surgical procedure, diagnostic radiology and orthopaedic pathology, a quantity which might include simple and crucial details touching on these issues of the skeleton during which a standard curiosity exists.
- Electromagnetic Radiation in Space: Proceedings of the Third ESRO Summer School in Space Physics, Held in Alpbach, Austria, from 19 July to 13 August, 1965
- Microbial Bioproducts
- Corneal Topography: Measuring and Modifying the Cornea
- Amor Mundi: Explorations in the Faith and Thought of Hannah Arendt
- Philipp Franz von Siebold and His Era: Prerequisites, Developments, Consequences and Perspectives
- Paramagnetic Organometallic Species in Activation/Selectivity, Catalysis
Additional resources for G Proteins, Receptors, and Disease
Coleman DE, Berghuis AM, Lee E, Linder ME, Gilman AG, Sprang SR Structures of active conformations of G ia1 and the mechanism of GTP hydrolysis. Science 1994;265: 1405-1412. 8. Wall MA, Coleman DE, Lee E, Ifiiguez-Lluhi JA, Posner BA, Gilman AG, Sprang SR The structure of the G-protein heterotrimer Gial~IY2' Cell 1995;83: 1047-1058. 9. Yamamoto S, Sippel KC, Berson EL, Dryja TP. Defects in the rhodopsin kinase gene in the Oguchi form of stationary night blindness. Nat Genet 1997;15:175-178. 10.
The severity of the AHO phenotype varies greatly between patients with Gs deficiency, with some patients showing few (11) or no (140) somatic features. Although Gs deficiency is presumed to have a major role in the pathogenesis of AHO, the role of downstream pathways (abnormal cAMP generation vs other Gs-coupled effector pathways) is poorly established. 40 Weinstein The most characterisitic feature of AHO is brachydactyly, which involves the phalanges of the hands and feet in either a symmetric or asymmetric manner.
Gnas maps within a region that is implicated as having one or more imprinted genes (71,72). Four major species of human Gas cDNA have been identified and appear to result from alternative splicing of a single gene (68,73). Two long and two short forms are the result of the splicing in or out of exon 3, respectively, and correspond to the long and short forms of Gas identified on immunoblots. Further heterogeneity is produced by the use of 2 alternative 3' splice sites for intron 3, resulting in the presence or absence of an extra CAG codon at the junction of the exon 3 and 4 coding sequences.
G Proteins, Receptors, and Disease by Allen M. Spiegel MD (auth.), Allen M. Spiegel MD (eds.)