Arg92Leu-cTnT Alters the cTnC-cTnI Interface Disrupting PKA-Mediated Relaxation
These data show that the early diastolic dysfunction observed in a subset of HCM is attributable to allosterically mediated structural changes at the cTnC-cTnI interface that impair accessibility of PKA, thereby blunting β-adrenergic responsiveness and identifying a potential molecular target for therapeutic intervention.
Authors
- Anne M. Murphy (ORCID: https://orcid.org/0000-0001-9254-3202)
- Jesús Jiménez (ORCID: https://orcid.org/0000-0001-5399-8538)
- Cyonna Gibson
- Matthew M. Klass (ORCID: https://orcid.org/0000-0003-2215-4345)
- Melissa L. Lynn (ORCID: https://orcid.org/0000-0002-1107-4027)
- Romi L. Castillo (ORCID: https://orcid.org/0000-0002-9383-7365)
- Catherine Vasquez (ORCID: https://orcid.org/0009-0004-7267-4079)
- Jil C. Tardiff (ORCID: https://orcid.org/0000-0003-4291-4882)
- Andrew Kim
- Anthony P. Baldo
Institutions
- University of Arizona (US)
- Johns Hopkins University (US)
- Sandia National Laboratories California (US)
- Washington University in St. Louis (US)
- Johns Hopkins Medicine (US)
- Sandia National Laboratories (US)
- Department of Physiological Sciences (RU)
Publication Details
- Journal
- Circulation Research
- Published
- 2024-09-27
- DOI
- https://doi.org/10.1161/circresaha.124.325223
- Citations
- 1
- Primary Topic
- Cardiomyopathy and Myosin Studies
- Type
- article
- Field-Weighted Citation Impact
- 0.40