ArticleFEBS letters2012
Familial hypertrophic cardiomyopathy related E180G mutation increases flexibility of human cardiac α-tropomyosin.
Article in FEBS letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Creatine Kinase Equilibration and ΔGInternational journal of molecular sciences · 2023Article
- Mouse Models of Cardiomyopathies Caused by Mutations in Troponin C.International journal of molecular sciences · 2023Review
- Computational and biophysical determination of pathogenicity of variants of unknown significance in cardiac thin filament.JCI insight · 2021Article
- Loss of crossbridge inhibition drives pathological cardiac hypertrophy in patients harboring the TPM1 E192K mutation.The Journal of general physiology · 2021Article
- Moving beyond simple answers to complex disorders in sarcomeric cardiomyopathies: the role of integrated systems.Pflugers Archiv : European journal of physiology · 2019Review
- Sarcomere gene variants act as a genetic trigger underlying the development of left ventricular noncompaction.Pediatric research · 2018Article
- HCM and DCM cardiomyopathy-linked α-tropomyosin mutations influence off-state stability and crossbridge interaction on thin filaments.Archives of biochemistry and biophysics · 2018Article
- Biophysical Derangements in Genetic Cardiomyopathies.Heart failure clinics · 2018Review
- The structural basis of alpha-tropomyosin linked (Asp230Asn) familial dilated cardiomyopathy.Journal of molecular and cellular cardiology · 2017Article
- Investigating the effects of tropomyosin mutations on its flexibility and interactions with filamentous actin using molecular dynamics simulation.Journal of muscle research and cell motility · 2016Article
- Predicting Effects of Tropomyosin Mutations on Cardiac Muscle Contraction through Myofilament Modeling.Frontiers in physiology · 2016Article
- N-acetylcysteine reverses diastolic dysfunction and hypertrophy in familial hypertrophic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2015Article
- Pathogenesis associated with a restrictive cardiomyopathy mutant in cardiac troponin T is due to reduced protein stability and greatly increased myofilament Ca2+ sensitivity.Biochimica et biophysica acta · 2015Article
- Energy landscapes reveal the myopathic effects of tropomyosin mutations.Archives of biochemistry and biophysics · 2014Article
- Maladaptive modifications in myofilament proteins and triggers in the progression to heart failure and sudden death.Pflugers Archiv : European journal of physiology · 2014Review
- Decreasing tropomyosin phosphorylation rescues tropomyosin-induced familial hypertrophic cardiomyopathy.The Journal of biological chemistry · 2013Article
- Tropomyosin de-phosphorylation in the heart: what are the consequences?Journal of muscle research and cell motility · 2013Review
- Nuclear tropomyosin and troponin in striated muscle: new roles in a new locale?Journal of muscle research and cell motility · 2013Review
- Alpha-tropomyosin mutations in inherited cardiomyopathies.Journal of muscle research and cell motility · 2013Review
- Conserved Asp-137 is important for both structure and regulatory functions of cardiac α-tropomyosin (α-TM) in a novel transgenic mouse model expressing α-TM-D137L.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
α-Tropomyosin (αTm) is central to Ca(2+)-regulation of cardiac muscle contraction. The familial hypertrophic cardiomyopathy mutation αTm E180G enhances Ca(2+)-sensitivity in functional assays. To investigate the molecular basis, we imaged single molecules of human cardiac αTm E180G by direct probe atomic force microscopy. Analyses of tangent angles along molecular contours yielded persistence length corresponding to ~35% increase in flexibility compared to wild-type. Increased flexibility of the mutant was confirmed by fitting end-to-end length distributions to the worm-like chain model. This marked increase in flexibility can significantly impact systolic and possibly diastolic phases of cardiac contraction, ultimately leading to hypertrophy.
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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.