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James A. Spudich

Stanford University, Palo Alto, CA 
"James Spudich"

Cross-listing: Chemistry Tree


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Arthur Kornberg grad student 1968 Stanford
 (The nature and origin of bacterial spore proteins)


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Rona Giffard grad student Stanford (Neurotree)
Stephen J. Kron grad student
Jung-Chi Liao grad student (E-Tree)
Arturo D. Lozanne grad student 1982-1988 Stanford
Holly V. Goodson grad student 1995 Stanford
Coleen T. Murphy grad student 1993-1999
William M. Shih grad student 2000 Stanford (Chemistry Tree)
Ji-Hong Zang grad student 2000 Stanford
Daniel Hostetter grad student 2004 Stanford
Thomas J. Purcell grad student 2004 Stanford
David Altman grad student 2006 Stanford
Stephani S. Dean grad student 2006 Stanford
Nathan C. Geething grad student 2008 Stanford
Benjamin Spink grad student 2008 Stanford
L. Stirling S. Churchman grad student 2000-2008 Stanford
Sarah Rice post-doc (Neurotree)
Matthias Rief post-doc Stanford (Physics Tree)
Sivaraj Sivaramakrishnan post-doc Stanford
Matthew L. Springer post-doc Stanford
Margaret Titus post-doc Stanford
Debanjan Bhowmik post-doc 2019- Stanford University Medical School (Chemistry Tree)
Douglas N. Robinson post-doc 1997-2001 Stanford University Medical School
Ronald S. Rock post-doc 1999-2004 Stanford
Zev D. Bryant post-doc 2007 Stanford (Chemistry Tree)
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Sarkar SS, Trivedi DV, Morck MM, et al. (2020) The hypertrophic cardiomyopathy mutations R403Q and R663H increase the number of myosin heads available to interact with actin. Science Advances. 6: eaax0069
Adhikari AS, Trivedi DV, Sarkar SS, et al. (2019) β-Cardiac myosin hypertrophic cardiomyopathy mutations release sequestered heads and increase enzymatic activity. Nature Communications. 10: 2685
Trivedi DV, Adhikari AS, Sarkar SS, et al. (2017) Hypertrophic cardiomyopathy and the myosin mesa: viewing an old disease in a new light. Biophysical Reviews
Nag S, Trivedi DV, Sarkar SS, et al. (2017) The myosin mesa and the basis of hypercontractility caused by hypertrophic cardiomyopathy mutations. Nature Structural & Molecular Biology
Kawana M, Sarkar SS, Sutton S, et al. (2017) Biophysical properties of human β-cardiac myosin with converter mutations that cause hypertrophic cardiomyopathy. Science Advances. 3: e1601959
Sung J, Mortensen KI, Spudich JA, et al. (2017) How to Measure Load-Dependent Kinetics of Individual Motor Molecules Without a Force-Clamp. Methods in Enzymology. 582: 1-29
Adhikari AS, Kooiker KB, Sarkar SS, et al. (2016) Early-Onset Hypertrophic Cardiomyopathy Mutations Significantly Increase the Velocity, Force, and Actin-Activated ATPase Activity of Human β-Cardiac Myosin. Cell Reports. 17: 2857-2864
Mortensen KI, Sung J, Spudich JA, et al. (2016) How to Measure Separations and Angles Between Intramolecular Fluorescent Markers. Methods in Enzymology. 581: 147-185
Homburger JR, Green EM, Caleshu C, et al. (2016) Multidimensional structure-function relationships in human β-cardiac myosin from population-scale genetic variation. Proceedings of the National Academy of Sciences of the United States of America
Spudich JA, Aksel T, Bartholomew SR, et al. (2016) Effects of hypertrophic and dilated cardiomyopathy mutations on power output by human β-cardiac myosin. The Journal of Experimental Biology. 219: 161-7
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