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Species | Coeli M B LopesSummaryAffiliation: University of Rochester Country: USA Publications
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Publications
Alterations in conserved Kir channel-PIP2 interactions underlie channelopathiesCoeli M B Lopes
Department of Physiology and Biophysics, Mount Sinai School of Medicine, New York University, New York, NY 10029, USA
Neuron 34:933-44. 2002..We find basic residues that interact with PIP(2), two of which have been associated with Andersen's and Bartter's syndromes. We show that several naturally occurring mutants decrease channel-PIP(2) interactions, leading to disease...- Protein kinase A modulates PLC-dependent regulation and PIP2-sensitivity of K+ channelsCoeli M B Lopes
Department of Medicine, Cardiovascular Research Institute, University of Rochester, Rochester, New York 14642, USA
Channels (Austin) 1:124-34. 2007..Our results suggest that PKA phosphorylation of these channels affects Gq-coupled receptor inhibition through modulation of the channel sensitivity to PIP2... 
Use of mutant-specific ion channel characteristics for risk stratification of long QT syndrome patientsChristian Jons
Cardiology Division, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
Sci Transl Med 3:76ra28. 2011..Our results indicate that genotype and biophysical phenotype analysis may be useful for risk stratification of LQT1 patients and suggest that slow channel activation is associated with an increased risk of cardiac events...- PKA and PKC partially rescue long QT type 1 phenotype by restoring channel-PIP2 interactionsAlessandra Matavel
Cardiovascular Research Institute, Department of Medicine, University of Rochester, Rochester, NY, USA
Channels (Austin) 4:3-11. 2010..Our data indicates that stimulation by PKA and PKC can partially rescue LQT1 mutant channels with weakened response to PIP(2) by strengthening channel interactions with PIP(2)... 
Ion channel mechanisms related to sudden cardiac death in phenotype-negative long-QT syndrome genotype-phenotype correlations of the KCNQ1(S349W) mutationSamuel Horr
Cardiology Division, Department of Medicine, Cardiovascular Research Institute Department of Nephrology, University of Rochester Medical Center, Rochester, New York, USA
J Cardiovasc Electrophysiol 22:193-200. 2011....- Molecular basis of decreased Kir4.1 function in SeSAME/EAST syndromeDavid M Williams
Department of Medicine, Nephrology Division, University of Rochester, Rochester, New York 14642, USA
J Am Soc Nephrol 21:2117-29. 2010..In conclusion, perturbed pH gating may underlie the loss of channel function for the disease-associated mutant Kir4.1 channels and may have important physiologic consequences... - PKC activation and PIP(2) depletion underlie biphasic regulation of IKs by Gq-coupled receptorsAlessandra Matavel
Cardiovascular Research Institute, Department of Medicine, University of Rochester, 601 Elmwood Ave, Box CVRI, Rochester, NY 14642, USA
J Mol Cell Cardiol 46:704-12. 2009..Our results indicate that the depletion of membrane PIP(2) underlies receptor-mediated inhibition of IKs and that phosphorylation by PKC of the KCNE1 subunit underlies the GqPCR-mediated channel activation... - Adrenergic signaling controls RGK-dependent trafficking of cardiac voltage-gated L-type Ca2+ channels through PKD1Bong Sook Jhun
Department of Medicine, Aab Cardiovascular Research Institute, University of Rochester, Rochester, NY, USA
Circ Res 110:59-70. 2012..ObjecTIVE: To determine if Rem1 function is physiologically regulated by adrenergic signaling and thus impacts voltage-gated L-type calcium channel (VLCC) activity in the heart... - A novel mitochondrial K(ATP) channel assayAndrew P Wojtovich
Department of Pharmacology, University of Rochester Medical Center, 601 Elmwood Ave, Rochester, NY 14642, USA
Circ Res 106:1190-6. 2010..The validity of current methods to assay mK(ATP) activity is disputed... - PIP(2) activates KCNQ channels, and its hydrolysis underlies receptor-mediated inhibition of M currentsHailin Zhang
Department of Physiology and Biophysics, Mount Sinai School of Medicine, New York University, New York, NY 10029, USA
Neuron 37:963-75. 2003..Finally, native or recombinant channels inhibited by muscarinic agonists can be activated by PIP(2). Our data strongly suggest that PIP(2) acts as a membrane-diffusible second messenger to regulate directly the activity of KCNQ currents... - PI(4,5)P2 regulates the activation and desensitization of TRPM8 channels through the TRP domainTibor Rohacs
Department of Physiology and Biophysics, Mount Sinai School of Medicine, One Gustave L Levy Place, Box 1218, New York, New York 10029, USA
Nat Neurosci 8:626-34. 2005..These data suggest that the TRP domain of these channels may serve as a PI(4,5)P(2)-interacting site and that regulation by PI(4,5)P(2) is a common feature of members of the TRP channel family... - PIP2 hydrolysis underlies agonist-induced inhibition and regulates voltage gating of two-pore domain K+ channelsCoeli M B Lopes
Department of Physiology and Biophysics, Mount Sinai School of Medicine, New York, NY 10029, USA
J Physiol 564:117-29. 2005..Our results suggest that PIP2 is a common gating molecule for K+ channel families despite their distinct structures and physiological properties... - Sorcin regulates excitation-contraction coupling in the heartMarian B Meyers
Department of Medicine and Pediatrics, New York University School of Medicine, New York, New York, 10016, USA
J Biol Chem 278:28865-71. 2003..Together, these data indicate that sorcin modulates intracellular Ca2+ cycling and Ca2+ influx pathways in the heart... - Specificity of activation by phosphoinositides determines lipid regulation of Kir channelsTibor Rohacs
Department of Physiology and Biophysics, Mount Sinai School of Medicine of New York University, New York, NY 10029, USA
Proc Natl Acad Sci U S A 100:745-50. 2003..1 channel decreasing phosphoinositide specificity allow activation by LC acyl-CoA. Our data demonstrate that differences in phosphoinositide specificity determine the modulation of Kir channel activity by distinct regulatory lipids...