A Usual G-Protein-Coupled Receptor in Unusual Membranes.
Tucson, United States. In Angew Chem Int Ed Engl, Feb 2016
We reveal a new allosteric mode of rhodopsin activation incurred by the non-biological membranes: the cationic membrane drives a transition from the inactive MI to the activated MII state in the absence of high [H(+) ] or negative spontaneous curvature.
Loss of neurogenesis in Hydra leads to compensatory regulation of neurogenic and neurotransmission genes in epithelial cells.
Genève, Switzerland. In Philos Trans R Soc Lond B Biol Sci, Feb 2016
By crossing these results with cell-type-specific transcriptomics, we identified epithelial genes up-regulated upon loss of neurogenesis: transcription factors (Dlx, Dlx1, DMBX1/Manacle, Ets1, Gli3, KLF11, LMX1A, ZNF436, Shox1), epitheliopeptides (Arminins, PW peptide), neurosignalling components (CAMK1D, DDCl2, Inx1), ligand-ion channel receptors (CHRNA1, NaC7), G-Protein Coupled Receptors and FMRFRL.
How Can Mutations Thermostabilize G-Protein-Coupled Receptors?
Duarte, United States. In Trends Pharmacol Sci, Jan 2016
The data indicate that receptors are stabilized through a combination of factors, including an increase in receptor rigidity, a decrease in collective motion, reduced stress at specific residues, and the presence of ordered water molecules.