By P.Michael Conn
Oregon future health Sciences Univ., Portland. built-in evaluate of membrane receptor-initiated cellphone signalling and nuclear receptor-initiated gene law. offers an in-depth remedy of cyclic AMP, protein kinases, and protein phosphatases. For scientific and base researchers.
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Extra resources for Principles of Molecular Regulation
Kjeldgaard M, Nyborg J, Clark FC. The GTP binding motif: variations on a theme. FASEB J 1996; 10:1347. Spiegel AM. Defects in G protein-coupled signal transduction in human disease. Annu Rev Physiol 1995; 58:143. Stern-Marr R, Benovic JL. Regulation of G protein-coupled receptors by receptor kinases and arrestins. Vitam Horm 1995; 51:193. Strader CD, Fung TM, Tota MR, Underwood D. Structure and function of G protein-coupled receptors. Annu Rev Biochem 1994; 63:101. Van Biesen T, Luttrell LM, Hawes BE, Lefkowitz RJ.
The Gα-subunits have a single, high-afﬁnity binding site for the guanine nucleotide that is comprised within a highly conserved amino acid sequence that forms a guanine nucleotide binding pocket. , in an “off” state). Receptor-promoted and Mg2+-dependent GDP➝GTP exchange within the Gα guanine nucleotide binding site leads to a conformational change of the subunit that causes G protein activation and dissociation of the trimeric complex into Gα–GTP and Gβγ (“on” state), allowing their interaction with and activation of different effector enzymes or ion channels (Fig.
Down-regulation of the Gαi and Gαq/11 proteins has also been documented. Further, this desensitization is not apparently mediated by changes at the transcriptional or translational levels but rather by the enhancement in turnover of the speciﬁc G proteins that occurs upon receptor activation. Another mechanism by which the activity of G proteins may be regulated is that mediated through phosducin. This phosphoprotein was originally puriﬁed from retina as a complex with the Gβγ-subunit (β1γ1) of transducin as well as from the pineal gland.