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activin expression haplotype nurr 1 lesion receptor figure tgf -β1 study follistatin factor disease artery nr 4a haplotypes protein restenosi macrophage nr 4a formation analysis response association erasmus mc patient table model level free-activin binding assay nr 4a gene growth reference lesion formation aortic stent atherosclerotic receptor nurr 1 carotid nurr 1 gene experiment aorta function assay calcification atherosclerotic lesions muscle cells control nurr 1 expression activin receptors effect neointima atherosclerosi analyses atherogenesi online-only data supplement systolic blood pressure frequency injury hybridization proliferation heart disease score section muscle pathway circulation nurr 1 overexpression erasmu antibody nurr 1 knockdown downloaded library activin-a phosphorylation circ.ahajournals.org artery smcs tgf -β extracellular neointimal smcs activation vries cj
4 Most Recent Publications
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Activin A induces a non-fibrotic phenotype in smooth muscle cells in contrast to TGF-β
(Article)
Groenendijk, B.C.W. Benus, G.F.J.D. Horrevoets, A.J.G. Vries, C.J.M. de Klous, A. Pacheco, Y.M. Volger, O.L. Fledderus, J.O. Ferreira, V. Engelse, M.A. Pannekoek, H. Dijke, P. ten |
2011-01-15
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Nuclear receptor nurr1 is expressed in and is associated with human restenosis and inhibits vascular lesion formation in mice involving inhibition of smooth muscle cell proliferation and inflammation
(Article)
Bonta, P.I. Pols, T.W.H. Pannekoek, H. Biessen, E.A.L. Bot, I. Vries, C.J.M. de Tiel, C.M. van Vos, M. Arkenbout, E.K. Rohlena, J. Koch, K. Maat, M.P.M. de Tanck, M.W.T. Winter, R.J. de |
2010-05-11
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Haplotypes of the NR4A2/NURR1 gene and cardiovascular disease: The Rotterdam study
(Article)
Kardys, I. Tiel, C.M. van Vries, C.J.M. de Pannekoek, H. Uitterlinden, A.G. Hofman, A. Witteman, J.C.M. Maat, M.P.M. de |
2009-03-01
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Human activin-A is expressed in the atherosclerotic lesion and promotes the contractile phenotype of smooth muscle cells
(Article)
Engelse, M.A. Neele, J.M. Achterberg, T.A.E. van Aken, B.E. van Schaik, R.H.N. van Pannekoek, H. Vries, C.J. de |
1999-01-01
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