Francis P.G. van Horck

Learn More
The small GTP-binding protein Rho has been implicated in the control of neuronal morphology. In N1E-115 neuronal cells, the Rho-inactivating C3 toxin stimulates neurite outgrowth and prevents actomyosin-based neurite retraction and cell rounding induced by lysophosphatidic acid (LPA), sphingosine-1-phosphate, or thrombin acting on their cognate G(More)
Neuronal cells undergo rapid growth cone collapse, neurite retraction, and cell rounding in response to certain G protein-coupled receptor agonists such as lysophosphatidic acid (LPA). These shape changes are driven by Rho-mediated contraction of the actomyosin-based cytoskeleton. To date, however, detection of Rho activation has been hampered by the lack(More)
In N1E-115 cells, neurite retraction induced by neurite remodelling factors such as lysophosphatidic acid, sphingosine 1-phosphate and semaphorin 3A require the activity of phosphatidylinositol 4-phosphate 5-kinases (PIP5Ks). PIP5Ks synthesise the phosphoinositide lipid second messenger phosphatidylinositol(4,5)bisphosphate [PtdIns(4,5)P₂], and(More)
ent substrates [9]. The Type I family, which is composed of three isoforms [3], is a PtdIns(4)P-5-kinase and has been shown to act downstream of both Rac-[10] and RhoA-dependent [4] pathways in the regulation of the actin cytoskeleton [6, 7, 11]. To investigate the role of [12], we used the Type II␣ PIPkinase, which is also able to synthesize PtdIns(4,5)P 2(More)
  • 1