Smad1/5 is acetylated in the dorsal aortae of the mouse embryo before the onset of blood flow, driving early arterial gene expression
Our findings highlight the importance of the acetyl-CoA production in the cell and provide a novel control mechanism of Smad1/5 signalling involving protein acetylation. As disturbed canonical Smad1/5 signalling is involved in several vascular conditions, our results offer new insights in treatment options for circumventing canonical Smad1/5 signalling.
Authors
- Max Nobis (ORCID: https://orcid.org/0000-0002-1861-1390)
- An Zwijsen (ORCID: https://orcid.org/0000-0002-8583-1721)
- Bart Ghesquière (ORCID: https://orcid.org/0000-0003-1547-1705)
- Ljuba C. Ponomarev (ORCID: https://orcid.org/0000-0003-0721-168X)
- Colinda L. G. J. Scheele (ORCID: https://orcid.org/0000-0001-8999-5451)
- Elizabeth A. V. Jones (ORCID: https://orcid.org/0000-0002-2006-7064)
- Margo Daems (ORCID: https://orcid.org/0000-0002-6961-644X)
- Aernout Luttun (ORCID: https://orcid.org/0000-0001-7902-9524)
- Rita Simões-Faria
Institutions
- Maastricht University (NL)
- VIB-KU Leuven Center for Cancer Biology (BE)
- KU Leuven (BE)
Publication Details
- Journal
- Cardiovascular Research
- Published
- 2024-09-10
- DOI
- https://doi.org/10.1093/cvr/cvae201
- Citations
- 3
- Primary Topic
- Congenital heart defects research
- Type
- article
- Field-Weighted Citation Impact
- 0.70
Funders
- Fonds Wetenschappelijk Onderzoek
- KU Leuven