Project description:Baz2B protein was shown to form a chromatin remodelig complex mit Snf2H or Snf2L catalytic subunits. It is known that chromatin remodeling proteins regulate diffferent DNA-templated processes, therefore we wanted to know whether Baz2B plays a role in transcription regulation. We used microarrays to detail the global expression of transcripts in Hap1 parental cell line and compare them to Baz2B-KO. We found up- and down-regulated trasncripts that could be associated with the decreased cellular proliferation in Baz2B-KO cell line
Project description:We analysed the global effect of CHD3-KO and SENP1-KO HAP1 cell lines compared to control cell line, on chromatin accessibility using ATAC-seq.
Project description:The impact of NatC subunits NAA30, NAA35 and NAA38 on the human proteome (protein abundance). Analysis of HAP1 WT, NAA30 KO, NAA35 KO and NAA38 KO cells
Project description:Purpose: The aim of the experiment was to eludicate differentialy expressed genes (DEGs) upon treatment with alkylating agent MMS between WT and MED13 deficient HAP1 cells. Results: After bioinformatic processing, at ≥2-fold change and an FDR≤0.1, 446 DEGs were identified in MED13 KO cells when compared to WT. Upon the MMS treatment 394 DEGs were identified in MED13 KO cells, of which 229 were common with untreated MED13 KO cells. Conclusions: Common DEGs represented genes directly regulated by MED13.
Project description:Adipose Triglyceride Lipase (ATGL) and Monoglyceride Lipase (MGL) are two enzymes that contribute to intracellular neutral lipolysis by breaking down triglycerides stored within lipid droplets. Recently, lipid droplet accumulation has been described as a novel hallmark of cancer. While lipid metabolism has been investigated in cancer in recent decades, the role of lipid hydrolysis and its enzymes have not been in the focus of cancer research. We and others have found that lipid hydrolysis enzymes might play an important role in the development and progression of lung cancer. To this end, we chose four different non-small cell lung cancer cell lines and employed CRISPR-Cas9 gene editing to knock out either ATGL (ATGL-KO) or MGL (MGL-KO), and a non-targeting control (NTC) was employed to generate a control cell line within each parental cell type. We then performed label free quantitative proteomics to identify differences between the generated cell lines and confirmed ATGL-KO in ATGL-KO cell lines as well as MGL-KO in MGL-KO cell lines. Furthermore, dihydroorotate dehydrogenase (DHODH), an enzyme that is important in some cancer, was upregulated in some, but not all, of the NSCLC cancer cell lines lacking either one of the two lipases.
Project description:We performed a genome-scale screen for suppressors of interferon stimulated gene (ISG) expression in human haploid cells (HAP1). Ubiquitin specific peptidase 14 (USP14) was a significant hit. In order to validate USP14 as a regulator of ISG expression, we created knockouts of USP14 in HAP1 cells using CRISPR-Cas9 and performed RNA-seq on coding RNA from USP14 KO and WT cells. This data was used to determine if ISGs were upregulated in USP14 KO HAP1 cells.
Project description:We performed a genome-scale screen for suppressors of interferon stimulated gene (ISG) expression in human haploid cells (HAP1). DEAD-box helicase 6 (DDX6) was a significant hit. In order to validate DDX6 as a regulator of ISG expression, we created knockouts of DDX6 in HAP1 cells using CRISPR-Cas9 and performed RNA-seq on coding RNA from DDX6 KO and WT cells. This data was used to determine if ISGs were upregulated in DDX6 KO HAP1 cells.