Zobrazeno 1 - 10
of 56
pro vyhledávání: '"Donald A. Winkelmann"'
Autor:
Michael S. Woody, Michael J. Greenberg, Bipasha Barua, Donald A. Winkelmann, Yale E. Goldman, E. Michael Ostap
Publikováno v:
Nature Communications, Vol 9, Iss 1, Pp 1-11 (2018)
Omecamtiv mecarbil (OM) is a positive cardiac inotrope in clinical trials for the treatment of heart failure whose mechanism of action is incompletely understood. Here the authors show that OM inhibits myosin's working stroke and prolongs actomyosin
Externí odkaz:
https://doaj.org/article/a390d9a0840145559f69f13c5f0635e6
Autor:
Aaron Snoberger, Bipasha Barua, Jennifer L Atherton, Henry Shuman, Eva Forgacs, Yale E Goldman, Donald A Winkelmann, E Michael Ostap
Publikováno v:
eLife, Vol 10 (2021)
Hypertrophic cardiomyopathies (HCMs) are the leading cause of acute cardiac failure in young individuals. Over 300 mutations throughout β-cardiac myosin, including in the motor domain, are associated with HCM. A β-cardiac myosin motor mutation (R71
Externí odkaz:
https://doaj.org/article/a7523ab1d3fc41fc9e768c62b8590538
Publikováno v:
eLife, Vol 8 (2019)
Key steps of cardiac mechanochemistry, including the force-generating working stroke and the release of phosphate (Pi), occur rapidly after myosin-actin attachment. An ultra-high-speed optical trap enabled direct observation of the timing and amplitu
Externí odkaz:
https://doaj.org/article/7e6497584f8c4b5f9f10fe21aaa0176a
Autor:
Aaron Snoberger, Yale E. Goldman, Eva Forgacs, Henry Shuman, E. Michael Ostap, Bipasha Barua, Jennifer L. Atherton, Donald A. Winkelmann
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::46ec188b006e3329b1e7b86aabad699f
https://doi.org/10.7554/elife.63691.sa2
https://doi.org/10.7554/elife.63691.sa2
Autor:
E. Michael Ostap, Aaron Snoberger, Eva Forgacs, Donald A. Winkelmann, Henry Shuman, Bipasha Barua, Yale E. Goldman, Jennifer L. Atherton
Hypertrophic cardiomyopathies (HCMs) are the leading cause of acute cardiac failure in young individuals. Over 300 mutations throughout β-cardiac myosin, including in the motor domain, are associated with HCM. A β-cardiac myosin motor mutation (R71
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::d76fa6fc6ee63399d57cd7e26d13486b
https://doi.org/10.1101/2020.10.02.323782
https://doi.org/10.1101/2020.10.02.323782
Autor:
Aaron Snoberger, Eva Forgacs, Jennifer L. Atherton, Donald A. Winkelmann, Bipasha Barua, E. Michael Ostap, Henry Shuman, Yale E. Goldman
Publikováno v:
eLife
eLife, Vol 10 (2021)
eLife, Vol 10 (2021)
Hypertrophic cardiomyopathies (HCMs) are the leading cause of acute cardiac failure in young individuals. Over 300 mutations throughout β-cardiac myosin, including in the motor domain, are associated with HCM. A β-cardiac myosin motor mutation (R71
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f2d3f7a7f40e22f9890f6339fa9fa08b
https://pubmed.ncbi.nlm.nih.gov/33605878
https://pubmed.ncbi.nlm.nih.gov/33605878
Publikováno v:
PLoS ONE, Vol 3, Iss 5, p e2137 (2008)
Myosin folding and assembly in striated muscle is mediated by the general chaperones Hsc70 and Hsp90 and a myosin specific co-chaperone, UNC45. Two UNC45 genes are found in vertebrates, including a striated muscle specific form, Unc45b. We have inves
Externí odkaz:
https://doaj.org/article/d89417009d3d46788d48e776bccb5f43
Publikováno v:
eLife, Vol 8 (2019)
eLife
eLife
Key steps of cardiac mechanochemistry, including the force-generating working stroke and the release of phosphate (Pi), occur rapidly after myosin-actin attachment. An ultra-high-speed optical trap enabled direct observation of the timing and amplitu
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::109459997520687eab365de1116d8d5d
https://doi.org/10.7554/elife.49266
https://doi.org/10.7554/elife.49266
Publikováno v:
Biophysical Journal. 118:436a
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::f0f4dc6dc187e7a8e2bfb2ec28aa0864
https://doi.org/10.1016/j.bpj.2019.11.2445
https://doi.org/10.1016/j.bpj.2019.11.2445