ABSTRACT: Identification of PARD3 signature on PARD3 deficient H157 cell line, reconstituting the expression of PARD3 gene, with a wt and a mutant form.
Project description:To development our gene expression approach, we have employed whole genome microarray expression profiling as a discovery platform to identify genes potentialy regulated by the polarity protein PAR3. Human SCC cell line, NCI-H157 (H157), has a big deletion at PARD3 locus and showed no PAR3 protein expression. This cell line was used as a model in which we restored the expression of PAR3 (wt or mutant form). Afterwards, this model was used to identify PARD3 signature on Human SCC. There are triplicates of each sample. We compare the effects in gene expression between the different situations: no PARD3 expression in the cell, expression of the mutant form of PARD3 gene and expression of the PARD3 wt form in the cells.
Project description:We used microarrays to explore the expression profile from cells expressing wild type and UHRF1 S674A mutant. HeLa cells expressing UHRF1 WT and S674A mutant showed similar gene expression pattern without significant affecting the transcription of DNA repari genes. UHRF1 was depleted in HeLa cells by shRNA treatment. Total RNA was purified and used to determine the global gene transcription profiles by microarray assays. The UHRF1-related genes expression profiles were compared among control cells, UHRF1-depleted cells, UHRF1 WT reconstituting cells and UHRF1 S674A mutant reconstituting cells.
Project description:To development our gene expression approach, we have employed whole genome microarray expression profiling as a discovery platform to identify genes potentialy regulated by the polarity protein PAR3. Human SCC cell line, NCI-H157 (H157), has a big deletion at PARD3 locus and showed no PAR3 protein expression. This cell line was used as a model in which we restored the expression of PAR3 (wt or mutant form). Afterwards, this model was used to identify PARD3 signature on Human SCC.
Project description:- Six samples from the DEV cell line: 2 controls, 2 transduced with IL4R WT and 2 transduced with IL4R mutant (I242N)
- This DEV cell line is not commercially available and was acquired from a colleague in the Netherlands
Project description:We report the application of MeRIP sequencing technology for high-throughput profiling of m6A methylome in breast cancer cells. Comparison of m6A methylome between METTL3-WT and METTL3-K177Q reconstituting cells revealed the following findings: 1) Significant global alteration of methylation sites due to K177Q mutation (termed as KQ-m6A signature). 2) GO analysis of the differential m6A-MeRIP candidates enriched pathways involved in chromatin modification, RNA splicing, DNA damage, cell cycle, and autophagy, consistent with a critical role of m6A-mediated nuclear biological activities and highlighted generally recognized cellular events associated with tumorigenesis. 3) we dissected potential mechanistic clues explaining the attenuated invasive phenotype in METTL3K177Q reconstituting cells.
Project description:In order to determine the cell potency, by identification of genes responsible for pluri/multi potency, we performed a global gene expression profiling of MDSC isolated from five week old male wild type(WT), C57Bl6J and another hypertrophied musculature mouse genotype called myostatin null (Mstn-/-) mice using microarray analysis and compared this gene expression to that of a standard mouse ES cell line W4. Muscle derived stem cells (MDSC) were isolated from WT and Mstn null mice using an established preplate technique and compared with the gene expression signature of standard mouse ES cell line W4
Project description:Transcriptome analysis by RNAseq of human CD34+ hematopoietic stem and progenitor cells transduced with empty vector control(MIT), AML1-ETO (AE), wildtype FOXO1 (F WT) or FOXO1 DNA binding deficient mutant (F DB). We find wildtype FOXO1 partially recapitulates gene signature of AML1-ETO
