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	题名	作者	年代	出处	被引量
1	BMP-9 signals via ALK1 and inhibits bFGF-induced endothelial cellprolifer-ation and VEGF-stimulated angiogenesis显示文摘	Scharpfenecker M van Dinther M Liu Z		0，，：	1
2	ALK2 R206H Mutation Linked to Fibrodysplasia Ossificans Progressiv a Confers Constitutive Activity to the BMP Type I Receptor and Sensitizes Mesenchymal Cells to BMP-Induced Osteoblast Differentiation and Bone Formation显示文摘	Maarten van Dinther Nils Visser David JJ de Gorter		0，，06：	1
3	ALK2 R206H Mutation Linked to Fibrodysplas-ia Ossificans Progressiv a Confers Constitutive Activity to the BMP Type I Receptor and Sensitizes Mesenchymal Cells to BMP-Induced Osteoblast Differentiation and Bone Formation显示文摘	Maarten van Dinther Nils Visser David JJ de Gorter		0，，06：	1
4	Anti-sclerostin Antibody Inhibits Internalization of sclerostin and sclerostin-Mediated Antagonism of Wnt/LRP6 Signaling显示文摘	van Dinther M Zhang J Weidauer SE	2013	PLoS One2013，8，62：	1
5	BMP-9 signals via ALK1 and inhibits bFGF-induced endothelial cellproliferation and VEGF-stimulated angiogenesis显示文摘	Scharpfenecker M van Dinther M Liu Z		0，，：	1
6	BMP-9 signals via ALK1 and inhibits bFGF-induced endothelial cell proliferation and VEGF-stimulated angiogenesis 显示文摘	Scharpfenecker M van Dinther M Liu Z	2007	J Cell Sci2007，120，6：	1
7	Autocrine bone morphogenetic protein-9 signals through activin receptor-like kinase-2/Smadl/Smad4 to promote ovarian cancer cell proliferation显示文摘	HERRERA B VAN DINTHER M TEN DIJKE P	2009	Cancer Res2009，69，24：	1
8	ALK2 R206H mutation linked to fibrodysplasia ossificans progressiva confers constitutive activity to the BMP type I receptor and sensitizes mesenchymal ceils to BMP-induced osteoblast differentiation and bone formation 显示文摘	van Dinther M Visser N de Gorter D J	2010	J Bone Miner Res2010，25，6：	1
9	Anti-Sclerostinantibody inhibits internalization of Sclerostin and Sclerostin-mediatedantagonism of Wnt/LRP6 signaling显示文摘	Van Dinther M Zhang J Weidauer SE	2013	PLoS One2013，8，62：	1
10	Improved three-step de-embedding method to accurately account for the influence of pad parasitics in silicon on-wafer RF test-structures显示文摘	Vandamme E Schreurs D van Dinther C	2001	IEEE Trans Electron Devices2001，48，4：	1
11	The tumor suppressor Smad4 is required for transforming growth factor beta-induced epithelial to mesenchymal transition and bone metastasis of breast cancer cells显示文摘	DECKERS M VAN DINTHER M BUIJS J		0，，04：	1
12	The tumor suppressor Smad4 is required for transforming growth factor beta-induced epithelial to mesenchymal transition and bone metastasis of breast cancer cells显示文摘	Deckers M van Dinther M Buijs J	2006	Cancer Res2006，66，4：	1
13	Anti-Sclerostin antibody inhibits internalization of Sclerostin and Sclerostin-mediated antagonism of Wnt/LRP6 signaling显示文摘	van Dinther M Zhang J Weidauer SE		0，，04：	1
14	VprBP mitigates TGF-β and Activin signaling by promoting Smurf1-mediated type Ⅰ receptor degradation显示文摘The transforming growth factor-β(TGF-β)family controls embryogenesis,stem cell differentiation,and tissue homeostasis.However,how post-translation modifications contribute to fine-tuning of TGF-βfamily signaling responses is not well understood.Inhibitory(I)-Smads can antagonize TGF-β/Smad signaling by recruiting Smurf E3 ubiquitin ligases to target the active TGF-βreceptor for proteasomal degradation.A proteomic interaction screen identified Vpr binding protein(VprBP)as novel binding partner of Smad7.Mis-expression studies revealed that VprBP negatively controls Smad2 phosphorylation,Smad2–Smad4 interaction,as well as TGF-βtarget gene expression.VprBP was found to promote Smad7–Smurf1–TβRI complex formation and induce proteasomal degradation of TGF-βtype I receptor(TβRI).Moreover,VprBP appears to stabilize Smurf1 by suppressing Smurf1 poly-ubiquitination.In multiple adult and mouse embryonic stem cells,depletion of VprBP promotes TGF-βor Activin-induced responses.In the mouse embryo VprBP expression negatively correlates with mesoderm marker expression,and VprBP attenuated mesoderm induction during zebrafish embryogenesis.Our findings thereby uncover a novel regulatory mechanism by which Smurf1 controls the TGF-βand Activin cascade and identify VprBP as a critical determinant of embryonic mesoderm induction.	Yihao Li Chao Cui Feng Xie Szymon Kietbasa Hailiang Mei Maarten van Dinther Hans van Dam Andreas Bauer Long Zhang Peterten Dijke	2020	Journal of Molecular Cell Biology2020，12，2：	1
15	Biphasic effects of transforming growth factorβon bone morphogenetic protein-induced osteoblast differentiation显示文摘	de Gorter DJ van Dinther M Korchynskyi O		0，，：	1
16	Autocrine bone morphogenetic protein-9 signals through activin receptor-like kinase-2/Smad1/Smad4 to promote ovarian cancer cell proliferation显示文摘	Herrera B van Dinther M ten Dijke P	2009	Cancer Res2009，69，24：	1
17	Design and synthesis of a novel synthetic NAPAP-pentasaecharide conjugate displaying a dual antithrombotic action 显示文摘	Buijsman RC Basten JEM Dinther TG van	1999	Bioorg Med Chem Lett1999，9，：	1
18	Design and synthesis of a novel synthetic NAPAP- pentasaccharide conjugate displaying a dual antithrombotic action显示文摘	Buijsman R C Basten J E M van Dinther T G	1999	Bioorg Med Chem Lett1999，9，14：	1
19	The tumor suppressor Smad4 is required for transforming growth factor beta-induced epithelial to mesenchymal transition and bone metastasis of breast cancer cells 显示文摘	Deckers M van Dinther M Buijs J	2006	Cancer Research2006，66，4：	1
20	Autocrine bone morphogenetic protein-9 signals through activin receptor-like kinase-2/Smad1/Smad4 to promote ovarian cancer cell proliferation显示文摘	HERRERA B VAN DINTHER M TEN DIJKE P	2009	Cancer Res2009，69，24：	1

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