ArticleThe Journal of biological chemistry2011
Cardiac troponin T, a sarcomeric AKAP, tethers protein kinase A at the myofilaments.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 54 citations in OpenAlex.
- A framework to map cAMP signalling nanodomains: phosphodiesterase-centred phosphoproteome-interactome networks (pPINs) in cardiac myocytes.Journal of molecular endocrinology · 2026Review
- Nanodomain cAMP signaling in cardiac pathophysiology: potential for developing targeted therapeutic interventions.Physiological reviews · 2025Review
- Integrative Genetic Approach Facilitates Precision Strategies for Acute Myocardial Infarction.Genes · 2023Review
- Regulation of cardiac function by cAMP nanodomains.Bioscience reports · 2023Review
- Cardiac troponin T and autoimmunity in skeletal muscle aging.GeroScience · 2022Article
- Hitting the Detection Limit in cAMP Signaling.Function (Oxford, England) · 2022Article
- Regulation of Cardiac PKA Signaling by cAMP and Oxidants.Antioxidants (Basel, Switzerland) · 2021Review
- Review
- AKAP Signaling Islands: Venues for Precision Pharmacology.Trends in pharmacological sciences · 2020Review
- Protein Kinase A Catalytic and Regulatory Subunits Interact Differently in Various Areas of Mouse Brain.International journal of molecular sciences · 2020Article
- Troponin destabilization impairs sarcomere-cytoskeleton interactions in iPSC-derived cardiomyocytes from dilated cardiomyopathy patients.Scientific reports · 2020Article
- Imaging cAMP nanodomains in the heart.Biochemical Society transactions · 2019Review
- A Microwell Cell Capture Device Reveals Variable Response to Dobutamine in Isolated Cardiomyocytes.Biophysical journal · 2019Article
- Whole-Cell cAMP and PKA Activity are Epiphenomena, Nanodomain Signaling Matters.Physiology (Bethesda, Md.) · 2019Review
- Identification of risk genes associated with myocardial infarction based on the recursive feature elimination algorithm and support vector machine classifier.Molecular medicine reports · 2018Article
- Cardiac troponin T and fast skeletal muscle denervation in ageing.Journal of cachexia, sarcopenia and muscle · 2017Article
- Mast cells regulate myofilament calcium sensitization and heart function after myocardial infarction.The Journal of experimental medicine · 2016Article
- TNNT1, TNNT2, and TNNT3: Isoform genes, regulation, and structure-function relationships.Gene · 2016Review
- Effects of a myofilament calcium sensitizer on left ventricular systolic and diastolic function in rats with volume overload heart failure.American journal of physiology. Heart and circulatory physiology · 2014Article
- Decreased polycystin 2 expression alters calcium-contraction coupling and changes β-adrenergic signaling pathways.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Efficient and specific phosphorylation of PKA substrates, elicited in response to β-adrenergic stimulation, require spatially confined pools of PKA anchored in proximity of its substrates. PKA-dependent phosphorylation of cardiac sarcomeric proteins has been the subject of intense investigations. Yet, the identity, composition, and function of PKA complexes at the sarcomeres have remained elusive. Here we report the identification and characterization of a novel sarcomeric AKAP (A-kinase anchoring protein), cardiac troponin T (cTnT). Using yeast two-hybrid technology in screening two adult human heart cDNA libraries, we identified the regulatory subunit of PKA as interacting with human cTnT bait. Immunoprecipitation studies show that cTnT is a dual specificity AKAP, interacting with both PKA-regulatory subunits type I and II. The disruptor peptide Ht31, but not Ht31P (control), abolished cTnT/PKA-R association. Truncations and point mutations identified an amphipathic helix domain in cTnT as the PKA binding site. This was confirmed by a peptide SPOT assay in the presence of Ht31 or Ht31P (control). Gelsolin-dependent removal of thin filament proteins also reduced myofilament-bound PKA-type II. Using a cTn exchange procedure that substitutes the endogenous cTn complex with a recombinant cTn complex we show that PKA-type II is troponin-bound in the myofilament lattice. Displacement of PKA-cTnT complexes correlates with a significant decrease in myofibrillar PKA activity. Taken together, our data propose a novel role for cTnT as a dual-specificity sarcomeric AKAP.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.