Publications by authors named "Viviane Egler"
Article Synopsis
- - The EGFR pathway activates signaling processes through RAS and PI3K, but glioblastoma requires simultaneous activation of RAS and AKT for development in mice; blocking EGFR alone does not kill human glioblastoma cells, indicating other pathways are involved.
- - Combination therapies using specific protein kinase inhibitors on glioblastoma cells did not cause cell death, but simultaneous targeting of ERK and PI3K led to rapid cell death, highlighting their importance in cell survival.
- - The study suggests that using drug combinations to reduce both ERK and AKT activity could be an effective strategy to overcome resistance in certain glioblastoma cases.
The nuclear receptor PPARgamma is implicated in the control of cell proliferation and apoptosis. However, the molecular mechanisms by which it controls these processes remain largely elusive. We show here that PPARgamma activation in the presence of the retinoblastoma protein (RB) results in the arrest of cells at the G1 phase of the cell cycle, whereas in the absence of RB, cells accumulate in G2/M, endoreduplicate, and undergo apoptosis.
View Article and Find Full Text PDFThe retinoblastoma protein (RB) has previously been shown to facilitate adipocyte differentiation by inducing cell cycle arrest and enhancing the transactivation by the adipogenic CCAAT/enhancer binding proteins (C/EBP). We show here that the peroxisome proliferator-activated receptor gamma (PPARgamma), a nuclear receptor pivotal for adipogenesis, promotes adipocyte differentiation more efficiently in the absence of RB. PPARgamma and RB were shown to coimmunoprecipitate, and this PPARgamma-RB complex also contains the histone deacetylase HDAC3, thereby attenuating PPARgamma's capacity to drive gene expression and adipocyte differentiation.
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