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Items: 1 to 20 of 140

1.

Altered interactions between cardiac myosin binding protein-C and α-cardiac actin variants associated with cardiomyopathies.

Chow ML, Shaffer JF, Harris SP, Dawson JF.

Arch Biochem Biophys. 2014 May 15;550-551:28-32. doi: 10.1016/j.abb.2014.04.003. Epub 2014 Apr 13.

2.

COOH-terminal truncated cardiac myosin-binding protein C mutants resulting from familial hypertrophic cardiomyopathy mutations exhibit altered expression and/or incorporation in fetal rat cardiomyocytes.

Flavigny J, Souchet M, Sébillon P, Berrebi-Bertrand I, Hainque B, Mallet A, Bril A, Schwartz K, Carrier L.

J Mol Biol. 1999 Nov 26;294(2):443-56.

PMID:
10610770
3.

E258K HCM-causing mutation in cardiac MyBP-C reduces contractile force and accelerates twitch kinetics by disrupting the cMyBP-C and myosin S2 interaction.

De Lange WJ, Grimes AC, Hegge LF, Spring AM, Brost TM, Ralphe JC.

J Gen Physiol. 2013 Sep;142(3):241-55. doi: 10.1085/jgp.201311018.

4.

Functional characterization of the human α-cardiac actin mutations Y166C and M305L involved in hypertrophic cardiomyopathy.

Müller M, Mazur AJ, Behrmann E, Diensthuber RP, Radke MB, Qu Z, Littwitz C, Raunser S, Schoenenberger CA, Manstein DJ, Mannherz HG.

Cell Mol Life Sci. 2012 Oct;69(20):3457-79. doi: 10.1007/s00018-012-1030-5. Epub 2012 May 29.

PMID:
22643837
5.

The myosin-binding protein C motif binds to F-actin in a phosphorylation-sensitive manner.

Shaffer JF, Kensler RW, Harris SP.

J Biol Chem. 2009 May 1;284(18):12318-27. doi: 10.1074/jbc.M808850200. Epub 2009 Mar 5.

6.

C0 and C1 N-terminal Ig domains of myosin binding protein C exert different effects on thin filament activation.

Harris SP, Belknap B, Van Sciver RE, White HD, Galkin VE.

Proc Natl Acad Sci U S A. 2016 Feb 9;113(6):1558-63. doi: 10.1073/pnas.1518891113. Epub 2016 Feb 1.

7.

The cMyBP-C HCM variant L348P enhances thin filament activation through an increased shift in tropomyosin position.

Mun JY, Kensler RW, Harris SP, Craig R.

J Mol Cell Cardiol. 2016 Feb;91:141-7. doi: 10.1016/j.yjmcc.2015.12.014. Epub 2015 Dec 21.

8.

Effects of troponin T cardiomyopathy mutations on the calcium sensitivity of the regulated thin filament and the actomyosin cross-bridge kinetics of human β-cardiac myosin.

Sommese RF, Nag S, Sutton S, Miller SM, Spudich JA, Ruppel KM.

PLoS One. 2013 Dec 18;8(12):e83403. doi: 10.1371/journal.pone.0083403. eCollection 2013.

9.

Subdomain location of mutations in cardiac actin correlate with type of functional change.

Mundia MM, Demers RW, Chow ML, Perieteanu AA, Dawson JF.

PLoS One. 2012;7(5):e36821. doi: 10.1371/journal.pone.0036821. Epub 2012 May 8.

10.

Modulation of thin filament activation of myosin ATP hydrolysis by N-terminal domains of cardiac myosin binding protein-C.

Belknap B, Harris SP, White HD.

Biochemistry. 2014 Oct 28;53(42):6717-24. doi: 10.1021/bi500787f. Epub 2014 Oct 20.

11.

The A31P missense mutation in cardiac myosin binding protein C alters protein structure but does not cause haploinsufficiency.

van Dijk SJ, Bezold Kooiker K, Mazzalupo S, Yang Y, Kostyukova AS, Mustacich DJ, Hoye ER, Stern JA, Kittleson MD, Harris SP.

Arch Biochem Biophys. 2016 Jul 1;601:133-40. doi: 10.1016/j.abb.2016.01.006. Epub 2016 Jan 9.

PMID:
26777460
12.

Using baculovirus/insect cell expressed recombinant actin to study the molecular pathogenesis of HCM caused by actin mutation A331P.

Bai F, Caster HM, Rubenstein PA, Dawson JF, Kawai M.

J Mol Cell Cardiol. 2014 Sep;74:64-75. doi: 10.1016/j.yjmcc.2014.04.014. Epub 2014 Apr 30.

13.

Pathogenic properties of the N-terminal region of cardiac myosin binding protein-C in vitro.

Govindan S, Sarkey J, Ji X, Sundaresan NR, Gupta MP, de Tombe PP, Sadayappan S.

J Muscle Res Cell Motil. 2012 May;33(1):17-30. doi: 10.1007/s10974-012-9292-y. Epub 2012 Apr 17.

14.

Do cardiac actin mutations lead to altered actomyosin interactions?

Dahari M, Dawson JF.

Biochem Cell Biol. 2015 Aug;93(4):330-4. doi: 10.1139/bcb-2014-0156. Epub 2015 Mar 18.

PMID:
26194323
15.

[Abnormal tropomyosin function in ATPase cycle in hypertrophic and dilated cardiomyopathies].

Borovikov IuS, Karpicheva OE, Rysev NA, Redwood CS.

Ross Fiziol Zh Im I M Sechenova. 2013 Jan;99(1):73-80. Russian.

PMID:
23659058
16.

Genetic mutations and mechanisms in dilated cardiomyopathy.

McNally EM, Golbus JR, Puckelwartz MJ.

J Clin Invest. 2013 Jan;123(1):19-26. doi: 10.1172/JCI62862. Epub 2013 Jan 2. Review.

17.

Determination of the critical residues responsible for cardiac myosin binding protein C's interactions.

Bhuiyan MS, Gulick J, Osinska H, Gupta M, Robbins J.

J Mol Cell Cardiol. 2012 Dec;53(6):838-47. doi: 10.1016/j.yjmcc.2012.08.028. Epub 2012 Sep 11.

18.

In vivo definition of cardiac myosin-binding protein C's critical interactions with myosin.

Bhuiyan MS, McLendon P, James J, Osinska H, Gulick J, Bhandary B, Lorenz JN, Robbins J.

Pflugers Arch. 2016 Oct;468(10):1685-95. doi: 10.1007/s00424-016-1873-y. Epub 2016 Aug 27.

19.

A gain-of-function mutation in the M-domain of cardiac myosin-binding protein-C increases binding to actin.

Bezold KL, Shaffer JF, Khosa JK, Hoye ER, Harris SP.

J Biol Chem. 2013 Jul 26;288(30):21496-505. doi: 10.1074/jbc.M113.474346. Epub 2013 Jun 19.

20.

Ablation of cardiac myosin binding protein-C disrupts the super-relaxed state of myosin in murine cardiomyocytes.

McNamara JW, Li A, Smith NJ, Lal S, Graham RM, Kooiker KB, van Dijk SJ, Remedios CGD, Harris SP, Cooke R.

J Mol Cell Cardiol. 2016 May;94:65-71. doi: 10.1016/j.yjmcc.2016.03.009. Epub 2016 Mar 26.

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