Transcription profiling time series of mouse melanocytes transfected with an inducible version of the oncogenic receptor Xmrk, starved for 72 h and afterwards stimulated with EGF
ABSTRACT: Signaling pathways specifically induced by the oncogenic receptor Xmrk can be elucidated by comparing gene expression in cells with the activated receptor to gene expression in cells with the non-activated receptor. Mouse melanocytes transfected with an inducible version of the oncogenic receptor Xmrk, were starved for 72 h and afterwards stimulated with EGF. We compared cells stimulated for 15 minutes, 1 h, 2 h, 4 h, 8 h or 24 h, respectively, to unstimulated cells.
BACKGROUND: Melanoma is an aggressive tumor with increasing incidence. To develop accurate prognostic markers and targeted therapies, changes leading to malignant transformation of melanocytes need to be understood. In the Xiphophorus melanoma model system, a mutated version of the EGF receptor Xmrk (Xiphophorus melanoma receptor kinase) triggers melanomagenesis. Cellular events downstream of Xmrk, such as the activation of Akt, Ras, B-Raf or Stat5, were also shown to play a role in human melano ...[more]
Project description:Aim: identification of differentially expressed genes after LIN-9 depletion.<br> <br> hTERT immortalized human BJ fibroblasts were infected with pMSCV-Blasticidin based retroviruses encoding a shRNA which targets human LIN-9 and the empty vector respectively.<br> After 4 days of selection total RNA was isolated. Cy3 and Cy5 labelled cDNA probes were generated using the CyScribe Post-labelling Kit (Amersham Biosiences).
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Project description:Analysis of Retinoblastoma protein (Rb) (Hs.408528) dependent transcriptional changes following siRNA mediated ablation of the RET finger protein/ Tripartite protein (RFP/TRIM27) (Hs.440382). Common reference design, two biological replicates with two technical replicates each.
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Project description:Induction of apoptosis by the tumor suppressor p53 is known to protect from Myc-driven lymphomagenesis. The p53 family member p73 is also a pro-apoptotic protein, which is activated in response to oncogenes like Myc. We therefore investigated whether p73 provides a similar protection from Myc-driven lymphomas as p53. To generate B-cell lymphomas with defined genetic alterations in p53 or p73, we crossed the Eµ-Myc transgenic to mice heterozygous for germ-line deletions in p53 (p53+/) or p73 (p73+/-). Lymphomas which have spontaneously developed in Eµ-Myc transgenic animals with the genotypes p53+/+, p53+/-, p73+/+, p73+/- or p73-/- were isolated when the animals were moribund and further processed for gene expression profiling with 22.5K cDNA microarrays.
Project description:SH-EP cells were depleted for ZBTB4; Transfection of the cells were performed by oligofectamin RNAimax (Invitrogen) with siRNA smart pool (Dharmacon RNA Technologies); total RNA was isolated using RNAeasy Mini Kit (QIAGEN), preamplified, labeled with Cy3 and Cy5, respectively, and hybridized to cDNA-microarrays