R
Richard M. Epand
Researcher at McMaster University
Publications - 521
Citations - 26937
Richard M. Epand is an academic researcher from McMaster University. The author has contributed to research in topics: Membrane & Peptide. The author has an hindex of 80, co-authored 515 publications receiving 25125 citations. Previous affiliations of Richard M. Epand include Brigham Young University & University of Edinburgh.
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Anomalous swelling in phospholipid bilayers is not coupled to the formation of a ripple phase.
TL;DR: The present results should facilitate theory by showing that the formation of the phase below T(M) is not related to critical phenomena above T(T), and both monomethyl and dimethyl DMPE undergo transitions into a gel phase rather than a rippled phase below M.
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A comparison of membrane properties and composition between cell lines selected and transfected for multi-drug resistance.
TL;DR: The results indicate that the properties of the plasma membrane from resistant cells are altered compared with their parental cell line, particularly the surface hydrophobicity.
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The tryptophan-rich region of HIV gp41 and the promotion of cholesterol-rich domains.
TL;DR: It is suggested that the difference between HIV-1 and HIV-2 in their requirements for glycosphingolipids in determining their tropism is related to their difference in partitioning to cholesterol-rich domains in biological membranes.
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A conserved MADS-box phosphorylation motif regulates differentiation and mitochondrial function in skeletal, cardiac, and smooth muscle cells
Wajihah Mughal,Lucas Nguyen,S Pustylnik,S C da Silva Rosa,S Piotrowski,Donald Chapman,Min Du,Nezeka S. Alli,Jörg Grigull,Andrew J. Halayko,Michel Aliani,Matthew K. Topham,Richard M. Epand,Grant M. Hatch,Troy J. Pereira,Stephanie M. Kereliuk,John C. McDermott,Christof Rampitsch,Vernon W. Dolinsky,Joseph W. Gordon +19 more
TL;DR: This work identifies a conserved phosphorylation motif within the MEF2 and SRF Mcm1 Agamous Deficiens SRF (MADS)-box that regulates miR-133a expression and mitochondrial function in response to a lipotoxic signal, and shows that rodents exposed to gestational diabetes during fetal development display muscle diacylglycerol accumulation.