The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.
Activin Receptor-like Kinase (ALK)1 Is an Antagonistic Mediator of Lateral TGFβ/ALK5 Signaling
Open accessAbstract
Transforming growth factor-beta (TGFbeta) regulates the activation state of the endothelium via two opposing type I receptor/Smad pathways. Activin receptor-like kinase-1 (ALK1) induces Smad1/5 phosphorylation, leading to an increase in endothelial cell proliferation and migration, while ALK5 promotes Smad2/3 activation and inhibits both processes. Here, we report that ALK5 is important for TGFbeta/ALK1 signaling; endothelial cells lacking ALK5 are deficient in TGFbeta/ALK1-induced responses. More specifically, we show that ALK5 mediates a TGFbeta-dependent recruitment of ALK1 into a TGFbeta receptor complex and that the ALK5 kinase activity is required for optimal ALK1 activation. TGFbeta type II receptor is also required for ALK1 activation by TGFbeta. Interestingly, ALK1 not only induces a biological response opposite to that of ALK5 but also directly antagonizes ALK5/Smad signaling.
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“and expression of angiogenic factors, including VEGF-A262,268.”
From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [268]
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Cites
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- Hendrix, 2002, Transendothelial function of human metastatic melanoma cells, Cancer Res., 62, 665
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Targeting the TGFβ signalling pathway in disease
Akhurst, R. J., & Hata, A. (2012) · Nature Reviews Drug Discovery · doi:10.1038/nrd3810 · Cited by 1,466
Spatial proteogenomics reveals distinct and evolutionarily conserved hepatic macrophage niches
Guilliams, M., Bonnardel, J., Haest, B., Vanderborght, B., Wagner, C., Remmerie, A., Bujko, A., Martens, L., Thoné, T., Browaeys, R., et al. (2022) · Cell · doi:10.1016/j.cell.2021.12.018 · Cited by 985
TGFβ biology in cancer progression and immunotherapy
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Metadata
- Authors
- Goumans, M.-J., Valdimarsdottir, G., Itoh, S., Lebrin, F., Larsson, J., Mummery, C., Karlsson, S., & ten Dijke, P.
- Affiliations
- The Netherlands Cancer Institute (NL)
- Skåne University Hospital (SE)
- Hubrecht Institute for Developmental Biology and Stem Cell Research (NL)
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2003-10
- Volume
- 12
- Issue
- 4
- Pages
- 817-828
- ISSN
- 1097-2765 (ISSN-L)
- OpenAlex
- W1978999523
- Cited by
- 689
- References
- 36
- Citations by year
- 2026: 9 · 2025: 17 · 2024: 23 · 2023: 21 · 2022: 21 · 2021: 27 · 2020: 27 · 2019: 23 · 2018: 22 · 2017: 22 · 2016: 26 · 2015: 36 · 2014: 29 · 2013: 46 · 2012: 40
- FWCI
- 10.23
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Molecular Cell (publishedVersion)
- PubMed (publishedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Kruppel-like factors research
- Keywords
- ALK1, ALK5, TGF-beta signaling, Smad1/5, Smad2/3, endothelial cells, TGFBR2, receptor complex assembly, kinase activity
- MeSH terms
- Receptor, Transforming Growth Factor-beta Type I, Receptor, Transforming Growth Factor-beta Type II, Animals, Cell Division, Cell Movement, DNA-Binding Proteins, Humans, Mutation, Phosphoproteins, Repressor Proteins, Transcription Factors, Signal Transduction, Trans-Activators, Transforming Growth Factor beta, Protein Serine-Threonine Kinases, Receptors, Transforming Growth Factor beta, COS Cells, Activin Receptors, Type I, Activin Receptors, Type II, Endothelial Cells, Cell Line, Tumor, Macromolecular Substances, Smad Proteins, Inhibitor of Differentiation Protein 1, Smad1 Protein, Smad5 Protein
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