B. M. Miller

Most-cited papers

1. Kinetic Analysis of Drosophila Muscle Myosin Isoforms Suggests a Novel Mode of Mechanochemical Coupling*

   B. M. Miller, M. Nyitrai, S. Bernstein, M. Geeves

   2003Journal of Biological Chemistry35 citations Open access

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2. A variable domain near the ATP-binding site in Drosophila muscle myosin is part of the communication pathway between the nucleotide and actin-binding sites.

   B. M. Miller, M. Bloemink, M. Nyitrai, S. Bernstein +1 more

   2007Journal of Molecular Biology27 citations Open access

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3. Reaction of aminosulfur trifluorides with alcohols: inversion vs. retention

   D. Shellhamer, A. A. Briggs, B. M. Miller, Jeanie M. Prince +2 more

   199621 citations

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4. COOH-terminal truncation of flightin decreases myofilament lattice organization, cross-bridge binding, and power output in Drosophila indirect flight muscle.

   B. Tanner, Mark S. Miller, B. M. Miller, P. Lekkas +3 more

   2011American Journal of Physiology - Cell Physiology18 citations Open access

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5. An alternative domain near the nucleotide-binding site of Drosophila muscle myosin affects ATPase kinetics.

   B. M. Miller, Shuxing Zhang, J. A. Suggs, D. Swank +3 more

   2005Journal of Molecular Biology18 citations

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6. Functional Effects of Nemaline Myopathy Mutations on Human Skeletal α-Actin*

   B. M. Miller, K. Trybus

   2008Journal of Biological Chemistry15 citations Open access

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7. and power output in Drosophila indirect flight muscle binding, myofilament lattice organization, cross-bridge COOH-terminal truncation of flightin decreases

   T. Irving, D. Maughan, J. Vigoreaux, B. Tanner +3 more

   20110 citations

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8. A C-terminal Truncation of Flightin Slows Actomyosin Cycling, Elevates Passive Tension, and Decreases Power Output in Drosophila Flight Muscle Fibers

   B. Tanner, Mark S. Miller, B. M. Miller, P. Lekkas +2 more

   20100 citations Open access

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9. P-192 Mitochondrial DNA (mtDNA) deletions in human oocytes

   J. Barritt, B. M. Miller, G. VanTuyle, D. Matt

   19970 citations Open access

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