@article{discovery10085773,
          volume = {10},
            year = {2019},
           title = {tmem33 is essential for VEGF-mediated endothelial calcium oscillations and angiogenesis},
          number = {1},
           month = {February},
         journal = {Nature Communications},
            note = {{\copyright} The Author(s) 2019. This article is licensed under a Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/).},
       publisher = {Springer Nature},
          author = {Savage, AM and Kurusamy, S and Chen, Y and Jiang, Z and Chhabria, K and MacDonald, RB and Kim, HR and Wilson, HL and van Eeden, FJM and Armesilla, AL and Chico, TJA and Wilkinson, RN},
             url = {https://doi.org/10.1038/s41467-019-08590-7},
        abstract = {Angiogenesis requires co-ordination of multiple signalling inputs to regulate the behaviour of endothelial cells (ECs) as they form vascular networks. Vascular endothelial growth factor (VEGF) is essential for angiogenesis and induces downstream signalling pathways including increased cytosolic calcium levels. Here we show that transmembrane protein 33 (tmem33), which has no known function in multicellular organisms, is essential to mediate effects of VEGF in both zebrafish and human ECs. We find that tmem33 localises to the endoplasmic reticulum in zebrafish ECs and is required for cytosolic calcium oscillations in response to Vegfa. tmem33-mediated endothelial calcium oscillations are critical for formation of endothelial tip cell filopodia and EC migration. Global or endothelial-cell-specific knockdown of tmem33 impairs multiple downstream effects of VEGF including ERK phosphorylation, Notch signalling and embryonic vascular development. These studies reveal a hitherto unsuspected role for tmem33 and calcium oscillations in the regulation of vascular development.},
            issn = {2041-1723},
        keywords = {Angiogenesis, Calcium signalling, Zebrafish}
}