S. V. van Dijk

发表

Mutations in MYH7 reduce the force generating capacity of sarcomeres in human familial hypertrophic cardiomyopathy.

S. Heymans, F. T. ten Cate, C. D. dos Remedios, 2013, Cardiovascular research.

Renal Damage Susceptibility and Autoregulation in Rf-1 and Rf-5 Congenic Rats

H. Jacob, J. Lazar, P. Specht, 2005, Nephron Experimental Nephrology.

Building a Professional Identity and an Academic Career Track in Translational Medicine

N. Rosenblum, A. Domenighetti, V. Melotte, 2019, Front. Med..

The development of familial hypertrophic cardiomyopathy: from mutation to bedside

A. van Rossum, T. Germans, J. van der Velden, 2011, European journal of clinical investigation.

Normal cardiac contraction in mice lacking the proline-alanine rich region and C1 domain of cardiac myosin binding protein C.

S. Harris, C. Witt, S. V. van Dijk, 2015, Journal of molecular and cellular cardiology.

A piece of the human heart: variance of protein phosphorylation in left ventricular samples from end-stage primary cardiomyopathy patients

C. D. dos Remedios, J. van der Velden, G. Stienen, 2009, Journal of Muscle Research and Cell Motility.

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

R. Cooke, R. Graham, Amy Li, 2016, Journal of molecular and cellular cardiology.

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

A. Kostyukova, D. Mustacich, S. Harris, 2016, Archives of biochemistry and biophysics.

Sarcomeric dysfunction in heart failure.

W. Paulus, D. Duncker, J. van der Velden, 2008, Cardiovascular research.

Point mutations in the tri-helix bundle of the M-domain of cardiac myosin binding protein-C influence systolic duration and delay cardiac relaxation.

S. Harris, S. Mazzalupo, S. V. van Dijk, 2018, Journal of molecular and cellular cardiology.

Cardiac Myosin-Binding Protein C Mutations and Hypertrophic Cardiomyopathy: Haploinsufficiency, Deranged Phosphorylation, and Cardiomyocyte Dysfunction

F. T. ten Cate, C. D. dos Remedios, L. Carrier, 2009, Circulation.

Absence of an Interaction between the Rf-1 and Rf-5 QTLs Influencing Susceptibility to Renal Damage in Rats

H. Jacob, J. Lazar, P. Specht, 2006, Nephron Experimental Nephrology.

Synergistic QTL interactions between Rf-1 and Rf-3 increase renal damage susceptibility in double congenic rats.

H. Jacob, J. Lazar, P. Specht, 2006, Kidney international.

Interaction between Rf-1 and Rf-4 quantitative trait loci increases susceptibility to renal damage in double congenic rats.

H. Jacob, J. Lazar, P. Specht, 2005, Kidney international.

Contractile Dysfunction Irrespective of the Mutant Protein in Human Hypertrophic Cardiomyopathy With Normal Systolic Function

E. R. Paalberends, F. T. ten Cate, C. D. dos Remedios, 2012, Circulation. Heart failure.

HIV-1 Can Persist in Aged Memory CD4+ T Lymphocytes With Minimal Signs of Evolution After 8.3 Years of Effective Highly Active Antiretroviral Therapy

D. Baarle, C. Boucher, N. Vrisekoop, 2009, Journal of acquired immune deficiency syndromes.

Hypertrophic cardiomyopathy in purpose-bred cats with the A31P mutation in cardiac myosin binding protein-C

S. Harris, J. Stern, Y. Ueda, 2023, Scientific reports.

Sarcomeric dysfunction in heart failure.

W. Paulus, D. Duncker, J. van der Velden, 2008, Cardiovascular research.