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Midory Thorikay

Researcher at Leiden University Medical Center

Publications -  14
Citations -  1501

Midory Thorikay is an academic researcher from Leiden University Medical Center. The author has contributed to research in topics: Angiogenesis & Transforming growth factor. The author has an hindex of 9, co-authored 13 publications receiving 1351 citations. Previous affiliations of Midory Thorikay include Netherlands Cancer Institute.

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Endoglin promotes endothelial cell proliferation and TGF‐β/ALK1 signal transduction

TL;DR: The results indicate a pivotal role for endoglin in the balance of ALK1 and ALK5 signalling to regulate endothelial cell proliferation and blocks TGF‐β‐induced growth arrest by indirectly reducing T GF‐β/ALK5 signalling.
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Elucidation of Smad Requirement in Transforming Growth Factor-β Type I Receptor-induced Responses

TL;DR: Mutation in the L45 loop region did not affect the binding of inhibitory Smads but did abrogate the weak binding of X-linked inhibitor of apoptosis protein and Disabled-2 to ALK5, which suggests that the L 45 loop in the kinase domain is important for docking of other binding proteins.
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Genetic and pharmacological targeting of activin receptor-like kinase 1 impairs tumor growth and angiogenesis

TL;DR: It is demonstrated, by genetic and pharmacological means, that the TGF-β and BMP9 receptor activin receptor-like kinase (ALK) 1 represents a new therapeutic target for tumor angiogenesis and offers mechanistic insight for the forthcoming clinical development of drugs blocking ALK1 in oncology.
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ALK1 Opposes ALK5/Smad3 Signaling and Expression of Extracellular Matrix Components in Human Chondrocytes†

TL;DR: This work examined ALK1 expression and its regulation of TGF‐β signaling and responses in human chondrocytes and identified ALK2 as a second type I T GF‐β receptor.
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Anti-human Activin Receptor-like Kinase 1 (ALK1) Antibody Attenuates Bone Morphogenetic Protein 9 (BMP9)-induced ALK1 Signaling and Interferes with Endothelial Cell Sprouting

TL;DR: The data suggest that both the VEGF/VEGF receptor and the BMP9/ALK1 pathways are essential for stimulating angiogenesis, and targeting both pathways simultaneously may be an attractive strategy to overcome resistance to antiangiogenesis therapy.