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James A. Spudich

Affiliations:

Stanford University, Palo Alto, CA

Area:

myosin

Website:

http://spudlab.stanford.edu/

Google:

"James Spudich"

Bio:

http://chemistry.library.nd.edu/resources/genealogy/chemistry/documents/SpudichJA.pdf

Cross-listing: Chemistry Tree

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Parents

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

Children

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)

Collaborators

BETA: Related publications

Publications

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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