Regular ArticleAn Intramolecular Contact in Gα Transducin That Participates in Maintaining Its Intrinsic GDP Release Rate☆
References (32)
- et al.
J. Biol. Chem.
(1996) - et al.
J. Biol. Chem.
(1990) - et al.
FEBS Lett.
(1986) - et al.
J. Biol. Chem.
(2000) - et al.
J. Biol. Chem.
(1997) Anal. Biochem.
(1976)- et al.
J. Biol. Chem.
(1987) - et al.
J. Biol. Chem.
(1999) - et al.
J. Biol. Chem.
(1999) - et al.
Biochem. Biophys. Res. Commun.
(1984)
Neuroscience
Biochem. Biophys. Acta
Curr. Opin. Neurobiol.
Biochemistry
Biochemistry
Cited by (8)
How do Receptors Activate G Proteins?
2007, Advances in Protein ChemistryCitation Excerpt :C‐terminal truncations in Gαo and Gαi2 resulted in reduced affinity for GDP because of impaired interactions with the N‐terminus (Denker et al., 1992, 1995). A hydrophobic interaction between the N‐terminus and α5 helix in Gαt stabilizes the GDP‐bound state (Natochin et al., 2000), and a salt bridge between the N‐terminus and β3 strand in Gαt has also been implicated in maintaining such a low rate of basal nucleotide exchange in this Gαi family member (Thomas et al., 2001). This interaction connects the N‐terminus to Switch II via the β3‐strand.
Mutations affecting G-protein subunit α<inf>11</inf> in hypercalcemia and hypocalcemia
2013, New England Journal of MedicineCitation Excerpt :Such studies might help to clarify the effects of mutant Gα11 on renal calcium excretion. Somatic GNA11 gain-of-function mutations involving the Arg183 and Gln209 residues have been described in patients with uveal melanomas.25,31 However, these patients were not reported to have hypocalcemia,31 and the two patients with autosomal dominant hypocalcemia type 2 who had Gα11 mutants with gain of function did not have ophthalmologic abnormalities.
Nucleotide binding switches the information flow in RAS GTPases
2011, PLoS Computational BiologyA perspective on more effective GPCR-targeted drug discovery efforts
2008, Expert Opinion on Drug DiscoveryReceptor-mediated activation of heterotrimeric G-proteins: Current structural insights
2007, Molecular PharmacologyMechanism of the receptor-catalyzed activation of heterotrimeric G proteins
2006, Nature Structural and Molecular Biology
- ☆
This work was supported by NIH Grants EY06062 and EY10291.
- 1
To whom correspondence should be addressed at Department of Pharmacology, Vanderbilt University Medical Center, 442 Robinson Research Building, Nashville, TN 37232. Fax: (615) 343-1084. E-mail: [email protected].