Project description:The goal of this study was to apply Next Generation Sequencing analyses to identify genes and pathways regulated by the FOXK1 and FOXK2 transcription factor in HeLa cells and to see whether reconstitution of FOXK1 WT and mutants can rescue the altered gene regulation in FOXK1 KO cells. Gene Ontology (GO) analysis did not uncover any dysregulated DNA damage–related pathways upon FOXKs KO. We found that cells reconstituted with any of the three FOXK1 mutants could largely rescue dysregulated gene expression in FOXK1 KO cells, similar to cells reconstituted with WT FOXK1. These suggesting that FOXK1's role in DNA damage response is not by direct transcriptional regulation of DNA damage related pathways and all the three FOXK1 mutants could not affect transcription.
Project description:In order to identify the function of the tumor suppressor CYLD in liver, we generate a liver specific disruption of this gene in mouse (liver specific CYLD KO mice). In our analysis it was revealed that these mice initially develop fibrosis and finally they develop spontaneous liver cancer after 1 year of age. We performed CGH analysis in 8 different tumor foci from the tumor livers of 4 different CYLD liver specific KO animals, in comparison to wild type reference liver DNA. From every tumor liver, two cancer foci was microdissected. Cancer foci samples with IDs: DS-071_01 and DS-071_02 are from liver specific CYLD KO animal #1, DS-071_03 and DS-071_04 are from liver specific CYLD KO animal #2, DS-071_05 and DS-071_06 are from liver specific CYLD KO animal #3, DS-071_07 and DS-071_08 are from liver specific CYLD KO animal #4. Liver genomic DNA from cancer samples and from a reference wild type liver was extracted (Qiagen) and CGH analysis was performed to determine DNA copy number changes (IMGM Laboratories, Germany). This analysis revealed a large number of amplifications and deletions ranging from 0,62Mb to 14,8Mb in all chromosomes.
Project description:The goal of this study was to apply next-generation sequencing (NGS) analyses to identify genes and pathways regulated by the Foxk1 transcription factor in the liver and to see the effects of liver-specific Foxk1 deficiency in the diet-induced non-alcoholic steatohepatitis (NASH) model. Transcriptome and ChIP-seq analysis revealed that liver Foxk1 promotes the pathogenesis of NASH by regulating the expression of a series of molecules involved in hepatic lipid metabolism in an mTORC1-dependent manner.
Project description:The goal of this study was to apply next-generation sequencing (NGS) analyses to identify genes and pathways regulated by the Foxk1 transcription factor in the liver and to see the effects of liver-specific Foxk1 deficiency in the diet-induced non-alcoholic steatohepatitis (NASH) model. Transcriptome and ChIP-seq analysis revealed that liver Foxk1 promotes the pathogenesis of NASH by regulating the expression of a series of molecules involved in hepatic lipid metabolism in an mTORC1-dependent manner.
Project description:To identify genes regulated by FXR in mouse liver, we compared gene expression profiles in livers of FXR+/+ (wt) and liver-specific FXR KO (lKO) mice
Project description:We used microarray to study the global transcriptomic changes in the livers of SIRT7 KO mice, which develop spontaneous nonalcoholic fatty liver disease.
Project description:To explore the potential targets of Bmi1 in the liver development of hepatic carcinogenesis, we assayed the gene expression level in the liver of Bmi1 knockout mice. We isolated the liver tissue of Bmi1 WT and KO mice around 6-8 weeks. Then we extracted total RNA and run the microarray detection. Gene expression in Bmi1 KO mouse livers was compared with that in Bmi1 WT mouse livers to screen potential targets of Bmi1.
Project description:Transcriptional Profiling of mouse liver tissues comparing normal tissues, livers arising from transgene expression after hepatocy transplantation using the comparative hepatocyte growth assay, and livers with transgene turned off for 4 and 12 weeks. Experimental groups: Control normal liver; Endstage liver tumors, livers with transgene turned off for 4 weeks, and livers with transgene turned off for 12 weeks.
Project description:D3, D5 and D10 EBs from iHA-Foxk1 and Foxk1 KO cells were harvested for RNA and submitted for sequencing to understand the transcriptional profile of these cells during differentiation in the presence and absence of FOXK1
