|
|
第3回ＣＯＥ(自己組織系物理)ワークショップ ［通算第17回］（慈恵医大「医学研究の基礎を語り合う集い」との共催）
| 筋収縮・制御 |
| 日 時 |
2005年10月24日(月) 16:30-18:30 |
| 会 場 |
慈恵医大：大学一号館６階会議室 |
| 講 師 |
Prof. Sarah Hitchcock-DeGregori
Department
of Neuroscience and Cell Biology, UMDNJ-Robert Wood Johnson
Medical School, Piscataway, New Jersey, USA
Prof. Richard L. Moss
Department of Physiology, University of
Wisconsin Medical School, Madison, Wisconsin, USA
|
| 紹介教員 |
石渡信一 |
|
| [プログラム] |
| 16:30-17:30 |
Prof. Sarah Hitchcock-DeGregori
"Tropomyosin: A regulator of actin
filament dynamics and contractile function"
Abstract: Tropomyosin is well known for its role in
stabilizing actin filaments and cooperatively regulating muscle
contraction with myosin and troponin. More recently it has
been shown to regulate the rate of protrusion of migrating
cells. We have been using structural and functional
approaches to understand how tropomyosin, a coiled coil protein,
carries out these functions. We have shown that the coiled
coil flexibility, as well as specific surface residues are
needed for tropomyosin to bind to actin. The solution
structure of the overlap region of striated muscle tropomyosin
illustrates the importance of flexibility of the carboxyl
terminus for complex formation. Finally, we are investigating
the isoform specificity of tropomyosin in regulating dynamics of
the actin filament, alone and with the pointed end capping
protein, tropomodulin.
|
| |
| 17:30-18:30 |
Prof. Richard L. Moss
"The
paradox of hyper-contractility and cardiac insufficiency in HCM:
Insights from the cMyBP-C null mouse"
Abstract: Hypertrophic cardiomyopathies frequently present a hypercontractile cardiac
phenotype, but assessment of cardiac function in some cases
reveals cardiac insufficiency.
Our work on the cardiac MyBP-C null mouse indicates that stroke
volume is reduced and the
period of systolic ejection is much shorter than normal, but the
rate of cross-bridge cycling
is increased. The increase in rate of cycling can explain
reduced ejection if the
accelerated
cycling leads to an earlier end to systolic ejection. Evidence
will be presented in support
of this working hypothesis. |
 |
