Other Publications (1)
Articles by Takrima Haque in JoVE
Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons Matthew Laaper1,2, Takrima Haque1, Ruth S. Slack3, Arezu Jahani-Asl1,2,4 1Lady Davis Institute for Medical Research, Jewish General Hospital, 2Integrated Program in Neuroscience, McGill University, 3Department of Cellular and Molecular Medicine, University of Ottawa, 4Department of Oncology, Faculty of Medicine, McGill University This protocol describes a simple method for isolating and culturing primary mouse cerebral granule neurons (CGNs) from 6-7 day old pups, efficient transduction of CGNs for loss and gain of function studies, and modelling NMDA-induced neuronal excitotoxicity, low-potassium-induced cell death, DNA-damage, and oxidative stress using the same culture model.
Other articles by Takrima Haque on PubMed
Control of Glioblastoma Tumorigenesis by Feed-forward Cytokine Signaling Nature Neuroscience. | Pubmed ID: 27110918 EGFRvIII-STAT3 signaling is important in glioblastoma pathogenesis. Here, we identified the cytokine receptor OSMR as a direct target gene of the transcription factor STAT3 in mouse astrocytes and human brain tumor stem cells (BTSCs). We found that OSMR functioned as an essential co-receptor for EGFRvIII. OSMR formed a physical complex with EGFRvIII, and depletion of OSMR impaired EGFRvIII-STAT3 signaling. Conversely, pharmacological inhibition of EGFRvIII phosphorylation inhibited the EGFRvIII-OSMR interaction and activation of STAT3. EGFRvIII-OSMR signaling in tumors operated constitutively, whereas EGFR-OSMR signaling in nontumor cells was synergistically activated by the ligands EGF and OSM. Finally, knockdown of OSMR strongly suppressed cell proliferation and tumor growth of mouse glioblastoma cells and human BTSC xenografts in mice, and prolonged the lifespan of these mice. Our findings identify OSMR as a critical regulator of glioblastoma tumor growth that orchestrates a feed-forward signaling mechanism with EGFRvIII and STAT3 to drive tumorigenesis.