Acquisition of the contractile phenotype by murine arterial smooth muscle cells depends on the Mir143/145 gene cluster.
By T. Boettger, Nadine Beetz, S. Kostin, J. Schneider, M. Krüger, L. Hein, Thomas Braun. Journal of Clinical Investigation, 2009
662 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/aa876abf5f688d9978b227ead78ba108e5be6540
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
- E. Olson
- Stefanie Dimmeler
- A. Zeiher
- Joshua T. Mendell
- Danish H Sayed
- M. Abdellatif
- C. Urbich
- Eva van Rooij
In Molecular Biology
- Stefanie Dimmeler
- E. Olson
- A. Zeiher
- C. Urbich
- Joshua T. Mendell
- Thomas Braun
- Danish H Sayed
- M. Abdellatif
Citations in the corpus
- MicroRNAs in development and disease. (2011, background): “It is induced by platelet-derived growth factor (PDGF), which is known to stimulate VSMC switching and proliferation during angiogenesis and neointimal formation (133, 378).”
- Linking actin dynamics and gene transcription to drive cellular motile functions (2010, positive): “miR-145 knockdown in cultured cells was reported to block smooth muscle gene activation by myocardin, pointing to this miRNA as an essential cofactor of myocardi”
- Atheroprotective communication between endothelial cells and smooth muscle cells through miRNAs (2012, background): “miRNAs also regulate SMC functions, and, in particular, the cluster comprising miR-143 and miR-145 (miR-143/145) has been described to be of crucial importance for proper SMC functio”
- MicroRNAs in stress signaling and human disease (2012, background): “However, contractility of the blood vessels of these mice is compromised, suggesting a subtle shift toward a less differentiated phenotype (Boettger et al., 2009).”