Zobrazeno 1 - 10
of 25
pro vyhledávání: '"Steven Marston"'
Autor:
Steven Marston, Jose Renato Pinto
Publikováno v:
Frontiers in Cardiovascular Medicine, Vol 9 (2023)
In cardiac muscle the action of adrenaline on β1 receptors of heart muscle cells is essential to adjust cardiac output to the body’s needs. Adrenergic activation leads to enhanced contractility (inotropy), faster heart rate (chronotropy) and faste
Externí odkaz:
https://doaj.org/article/9fca58cdcc864f24a93439b01119edc7
Autor:
Steven Marston
Publikováno v:
Frontiers in Physiology, Vol 12 (2022)
Contractility, the generation of force and movement by molecular motors, is the hallmark of all muscles, including striated muscle. Contractility can be studied at every level of organization from a whole animal to single molecules. Measurements at s
Externí odkaz:
https://doaj.org/article/4359269beec7446cb50584da67c31c4a
Autor:
O’neal Copeland, Andrew Messer, Andrew Jabbour, Corrado Poggesi, Sanjay Prasad, Steven Marston
Publikováno v:
Frontiers in Physiology, Vol 11 (2020)
In previous studies of septal heart muscle from HCM patients with hypertrophic obstructive cardiomyopathy (HOCM, LVOT gradient 50–120 mmHg) we found that the level of phosphorylation of troponin I (TnI) and myosin binding protein C (MyBP-C) was ext
Externí odkaz:
https://doaj.org/article/07f6047762bf4133aae2b9b6a732267e
Autor:
Steven Marston, Cecile Montgiraud, Alex B Munster, O'Neal Copeland, Onjee Choi, Cristobal Dos Remedios, Andrew E Messer, Elisabeth Ehler, Ralph Knöll
Publikováno v:
PLoS ONE, Vol 10, Iss 9, p e0138568 (2015)
BackgroundStudies of the functional consequences of DCM-causing mutations have been limited to a few cases where patients with known mutations had heart transplants. To increase the number of potential tissue samples for direct investigation we perfo
Externí odkaz:
https://doaj.org/article/21b7a55348dd474487eea475a9a01194
Autor:
Steven Marston, Jose Renato Pinto
In cardiac muscle the action of adrenaline on β1 receptors of heart muscle cells is essential to adjust cardiac output to the body’s needs. Adrenergic activation leads to enhanced contractility (inotropy), faster heart rate (chronotropy) and faste
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8d6a29abe1880e69b442d01d89b3426a
http://hdl.handle.net/10044/1/102631
http://hdl.handle.net/10044/1/102631
Autor:
Steven Marston
Publikováno v:
Journal of Muscle Research and Cell Motility.
Ca2+ acts on troponin and tropomyosin to switch the thin filament on and off, however in cardiac muscle a more graded form of regulation is essential to tailor cardiac output to the body’s needs. This is achieved by the action of adrenaline on β1
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9d1419b5c385f0e257c980ec112bc064
https://doi.org/10.1007/s10974-022-09630-4
https://doi.org/10.1007/s10974-022-09630-4
Autor:
Steven Marston, Victor Tsang, Shapour Jalilzadeh, C Redwood, K J Livesey, William J. McKenna, Adam Jacques, O'Neal Copeland, Hugh Watkins, S Carballo
Publikováno v:
U39
Rationale: Most sarcomere gene mutations that cause hypertrophic cardiomyopathy are missense alleles that encode dominant negative proteins. The potential exceptions are mutations in the MYBPC3 gene (encoding cardiac myosin-binding protein-C [MyBP-C]
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2b241e31478d1906680f9915fa89e48d
https://doi.org/10.1161/circresaha.109.202440
https://doi.org/10.1161/circresaha.109.202440
Publikováno v:
Biochemical Journal. 328:211-218
Caldesmon interaction with smooth muscle myosin and its ability to cross-link actin filaments to myosin were investigated by the use of several bacterially expressed myosin-binding fragments of caldesmon. We have confirmed the presence of two functio
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::59888569867d18dbec918423a6ac6b97
https://doi.org/10.1042/bj3280211
https://doi.org/10.1042/bj3280211
Autor:
Steven, Marston, O'Neal, Copeland, Katja, Gehmlich, Saskia, Schlossarek, Lucie, Carrier, Lucie, Carrrier
Publikováno v:
Journal of Muscle Research and Cell Motility
Journal of Muscle Research and Cell Motility; Vol 33
Journal of Muscle Research and Cell Motility; Vol 33
It is well established that MYBPC3 mutations are the most common cause of hypertrophic cardiomyopathy, accounting for about half of identified mutations. However, when compared with mutations in other myofibrillar proteins that cause hypertrophic car
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0fde9fff960c1fbcf8fd121d839ad4ef
http://ora.ox.ac.uk/objects/uuid:69633860-6b4d-4750-8ece-cf2a73e3bfbf
http://ora.ox.ac.uk/objects/uuid:69633860-6b4d-4750-8ece-cf2a73e3bfbf
Autor:
Nigel F, Clarke, Biljana, Ilkovski, Sandra, Cooper, Valentina A, Valova, Phillip J, Robinson, Ikuya, Nonaka, Juan-Juan, Feng, Steven, Marston, Kathryn, North
Publikováno v:
Annals of neurology. 61(6)
Mutations in ACTA1 have been associated with a variety of changes in muscle histology that likely result from fundamental differences in the way that ACTA1 mutations disrupt muscle function. Recently, we reported three patients with congenital fiber
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::f12b7ecf0766fb2e5161a4c1f74ef92a
https://pubmed.ncbi.nlm.nih.gov/17387733
https://pubmed.ncbi.nlm.nih.gov/17387733