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A possible role for p190RhoGAP in PKCepsilon-induced morphological effects
Ulrika Trollér1, Arathi Raghunath, Christer Larsson
1Lund University, Department of Laboratory Medicine, Molecular Medicine, Entrance 78, 3rd Floor, Malmö University Hospital, UMAS, SE-205 02, Malmö, Sweden.
Cellular Signalling
|November 26, 2003
Summary
Protein kinase C epsilon (PKCε) and p190RhoGAP both induce cell shape changes. This study suggests p190RhoGAP acts downstream of PKCε, mediating its effects on cell morphology without direct interaction.
Area of Science:
- Cell Biology
- Molecular Biology
- Neuroscience
Background:
- Protein kinase C epsilon (PKCε) is known to induce neurite outgrowth and stress fiber loss.
- The regulatory domain (RD) of PKCε and p190RhoGAP induce similar cellular processes, including neurite outgrowth in neuroblastoma cells.
Purpose of the Study:
- To investigate the potential downstream relationship between PKCε and p190RhoGAP.
- To determine if p190RhoGAP mediates the morphological effects induced by PKCε.
Main Methods:
- Co-localization studies of PKCε and p190RhoGAP in fibroblasts and neuroblastoma cells.
- Analysis of protein association using co-immunoprecipitation in response to TPA and NGF treatments.
- Experiments involving overexpression of PKCε and p190RhoGAP in CHO cells.
Main Results:
- PKCε and p190RhoGAP co-localize at membrane ruffles and show increased association in TPA-treated fibroblasts and neuroblastoma cells.
- NGF treatment decreases the interaction between PKCε and p190RhoGAP in SH-SYSY/TrkA cells.
- Overexpressed PKCε and p190RhoGAP do not directly interact, as shown by co-precipitation experiments.
Conclusions:
- p190RhoGAP is likely involved in mediating the morphological effects of PKCε.
- The interaction between PKCε and p190RhoGAP is regulated by cellular stimuli like TPA and NGF.
- PKCε may regulate p190RhoGAP activity through indirect mechanisms to influence cell morphology.