Publications by authors named "Mar Garcia-Colomer"
Background: Cavernous cerebral malformations can arise because of mutations in the , , or genes, and lack of has also been reported to induce these malformations in mice. However, the role of the CCM3 (cerebral cavernous malformation 3)-associated kinases in cavernoma development is not known, and we, therefore, have investigated their role in the process.
Methods: We used a combination of an in vivo approach, using mice genetically modified to be deficient in the CCM3-associated kinases STK24 and STK25 (serine/threonine kinases 24 and 25), and the in vitro model of human endothelial cells in which expression of and was inhibited by RNA interference.
Cerebral cavernous malformations (CCMs) are vascular malformations that can be the result of the deficiency of one of the CCM genes. Their only present treatment is surgical removal, which is not always possible, and an alternative pharmacological strategy to eliminate them is actively sought. We have studied the effect of the lack of one of the CCM genes, CCM3, in endothelial and non-endothelial cells.
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- CCM3/PDCD10 is a gene associated with cerebral cavernous malformations (CCM) that interacts with GCKIII protein kinases (MST3, SOK1, MST4).
- GCKIII proteins have similar effects as CCM3 in endothelial cells and in animal models like zebrafish, indicating their likely role in CCM development.
- The study introduces an in vitro kinase assay for GCKIII proteins to explore their regulation in endothelial and other cell types under various conditions.