Project description:Classical NF-κB activity can be inhibited by overexpression of the IκBα super repressor (SR). To determine the role of MyoD in rhabdomyosarcoma cells with NF-kB inhibited, ablated MyoD expression with CRISPR/cas9 editing and clonal selection of RH30-SR cell lines to compare differences in expression following deletion
Project description:Classical NF-κB activity can be inhibited by overexpression of the IκBα super repressor (SR). To determine the role of NF-κB in rhabdomyosarcoma cells, we overexpressed the IκBα SR in RH30 rhabdomyosarcoma cells. IκBα SR was overexpressed in RH30 cells. RH30 vector cells were used as control group.
Project description:We used human Affymetrix microarrays to identify the up- or down-regulated gene expressions from MDA-MB-231 cells infected with control vector or Flag-SR-IkBa Experiment Overall Design: The pattern of gene expression from MDA-MB-231 cells transduced with retroviruses were analysed by RNA extraction and hybridization on Affymetrix microarrays. From expression profiles, we identified NF-kB target genes, and uncovered a novel and specific role of a gene in osteolytic bone metastasis.
Project description:To study the role of MyoD in RMS biology, we examined chromatin status changes in the absence of MyoD by CRISPR/Cas9 targeted gene editing
Project description:ChIP-seq analysis of SNAIL binding sites in RH30 cells was performed to discover novel SNAIL binding sites in rhabdmyosarcoma cells.
Project description:The effect of the Smac mimetic BV6 on the transcriptional regulation in the alveolar rhabdomyosarcoma cell line RH30 was investigated by bulk RNA-sequencing. To this end, RH30 cells were treated with 5 µM BV6 for 24 h, or left untreated. Here, a regulation of several NF-κB target genes could be observed.
Project description:The activation of NFkB pathway is commonly observed in many neurodegenerative disease and contributes to the disease pathogenesis. However, with hundreds of target genes expressed in the brain, the mechanism of NFkB signaling transduction pathway is bearly understood. We were interested in revealing the downstream mediators of NFkB in the brain and chose the IkBa-dificient model as our tool. IkBa is the essential negative regulator of NFkB activity and deletioon of IkBa induced NFkB hyperactivation. We used Nestin-Cre to conditionally knockout IkBa in the brain cells of neural lineage and performed the microarray to give us candidate genes.
Project description:We used human Affymetrix microarrays to identify the up- or down-regulated gene expressions from MDA-MB-231 cells infected with control vector or Flag-SR-IkBa Keywords: microarray