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Journal Abstract Search

354 related items for PubMed ID: 29626422

  • 1. HCM and DCM cardiomyopathy-linked α-tropomyosin mutations influence off-state stability and crossbridge interaction on thin filaments.
    Farman GP, Rynkiewicz MJ, Orzechowski M, Lehman W, Moore JR.
    Arch Biochem Biophys; 2018 Jun 01; 647():84-92. PubMed ID: 29626422
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  • 2. Hypertrophic cardiomyopathy caused by a novel alpha-tropomyosin mutation (V95A) is associated with mild cardiac phenotype, abnormal calcium binding to troponin, abnormal myosin cycling, and poor prognosis.
    Karibe A, Tobacman LS, Strand J, Butters C, Back N, Bachinski LL, Arai AE, Ortiz A, Roberts R, Homsher E, Fananapazir L.
    Circulation; 2001 Jan 02; 103(1):65-71. PubMed ID: 11136687
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  • 7. Cardiomyopathy-associated mutations in tropomyosin differently affect actin-myosin interaction at single-molecule and ensemble levels.
    Kopylova GV, Shchepkin DV, Nabiev SR, Matyushenko AM, Koubassova NA, Levitsky DI, Bershitsky SY.
    J Muscle Res Cell Motil; 2019 Dec 02; 40(3-4):299-308. PubMed ID: 31643006
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  • 14. A comparison of muscle thin filament models obtained from electron microscopy reconstructions and low-angle X-ray fibre diagrams from non-overlap muscle.
    Poole KJ, Lorenz M, Evans G, Rosenbaum G, Pirani A, Craig R, Tobacman LS, Lehman W, Holmes KC.
    J Struct Biol; 2006 Aug 02; 155(2):273-84. PubMed ID: 16793285
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  • 15. Familial dilated cardiomyopathy mutations uncouple troponin I phosphorylation from changes in myofibrillar Ca²⁺ sensitivity.
    Memo M, Leung MC, Ward DG, dos Remedios C, Morimoto S, Zhang L, Ravenscroft G, McNamara E, Nowak KJ, Marston SB, Messer AE.
    Cardiovasc Res; 2013 Jul 01; 99(1):65-73. PubMed ID: 23539503
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  • 16. Dilated cardiomyopathy mutations in three thin filament regulatory proteins result in a common functional phenotype.
    Mirza M, Marston S, Willott R, Ashley C, Mogensen J, McKenna W, Robinson P, Redwood C, Watkins H.
    J Biol Chem; 2005 Aug 05; 280(31):28498-506. PubMed ID: 15923195
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