Newest Articles
Co-ion driven transporter kineticsAlthough high-resolution structures are now available for many ion-coupled, or secondary, transporters, the mechanisms by which coupling is achieved remain to be determined. Lolkema and Slotboom derive new mathematical models that can be used to analyze transport data and determine kinetic mechanisms.
P2X receptor intracellular terminiThe intracellular amino and carboxyl termini of the P2X1 receptor associate to form a cytoplasmic cap on the open state. Fryatt et al. use cysteine-reactive cross linking and molecular modeling to demonstrate structural organization of the intracellular termini in the apo and desensitized states.
Investigating an epileptogenic mutationJGP study examines how a mutation in KCNQ3 affects channel behavior.
Antagonist-induced cooperative AMPA receptor gatingGlutamate activates individual subunits of AMPA receptors in a stepwise manner. Shi et al. reveal that two noncompetitive antagonists disrupt this gating pattern and that their binding sites at the boundary between the transmembrane and extracellular linker domains is a tunable locus for gating.
Substrate specificity of the voltage-sensing phosphataseCiona intestinalis voltage-sensing phosphatase (VSP) has lipid 5- and 3-phosphatase activity, but 3-phosphatase is evident only at high VSP concentrations. Using kinetic modeling including endogenous lipid metabolizing enzymes and VSP phosphatase activities, Kruse et al. show how apparent activation of 3-phosphatase at high concentrations arises.
Fluorescence improvement with melaninXenopus laevis oocytes are used to study membrane proteins because of their ability to translate exogenous mRNA, but their high intrinsic fluorescence limits fluorescence recordings. Lee and Bezanilla present two methods to increase the amount of melanin and reduce background fluorescence in oocytes.
β-MHC enhances length-dependent activationThe expression of β-myosin heavy chain (β-MHC) in the guinea pig heart increases during postnatal development. Reda et al. show that this increase in β-MHC enhances length-mediated increases in myofilament Ca2+ sensitivity and sarcomere length–dependent changes in contractile function.
Batrachotoxin activation of NaChBac and NavSp1Batrachotoxin (BTX) causes paralysis and death by activating “pseudosymmetric” eukaryotic sodium (Nav) channels. Finol-Urdaneta et al. investigate its action on the prokaryotic homotetrameric homologues NaChBac and NavSp1, revealing use-dependent facilitation of activation, and inhibition of deactivation, caused by BTX binding to the symmetric pore.
Impaired myofilament energetics in HCMHypertrophic cardiomyopathy (HCM) is caused by mutations in sarcomeric proteins, but the pathogenic mechanism is unclear. Piroddi et al. find impairment of cross-bridge kinetics and energetics in human sarcomeres with a TNNT2 mutation, suggesting that HCM involves inefficient ATP utilization.
How a mutation undermines cardiac functionJGP paper explores how a mutated troponin T causes cardiac hypertrophy.
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Current Issue
February 4, 2019
Volume 151, No. 2
