Project description:This dataset presents ChIP-seq profiles of STAT1 wild-type (STAT1-WT) and lactylation-deficient mutant (STAT1-K193R) in MGC803 gastric cancer cells. The study aims to investigate the impact of STAT1-K193 lactylation on chromatin binding patterns. Comparative analysis of STAT1 occupancy between the two cell lines provides insights into the regulatory roles of STAT1 post-translational modification in gastric cancer progression.
Project description:Glycomic analysis of total N-glycan species released from ErbB2 isolated from WT and ST6GAL1 K.O. ErbB2-positive gastric cancer cells (NCI-N87)
Project description:To understand the basis behind the defective survival/expansion of Stat1-/- CD4+ T cells in Rag1-/- mice, we analyzed the gene expression of WT and Stat1-/- CD4+ T cells pre- and post-transfer into these mice by RNAseq.
Project description:Using ChIP-Seq analysis we define genes induced in macrophages through transcriptional activation by STAT1 and search for the gain of function in mutant Stat1Y701F compared to the Stat1-/- mice.
Project description:STAT1 ChIP DNA was isolated from HeLaS3 cells following Interferon-alpha stimulation for 30 min and from HeLaS3 cells left untreated. These two STAT1 ChIP DNA samples were combined and compared in the ENCODE regions on NimbleGen ENCODE arrays. Keywords: ChIP-chip
Project description:STAT1 ChIP-chip performed on Human Hela S3 Cells for three different platforms. Nimblegen ENCODE arrays which comprise 50mer oligonucleotides spaces every 38bps (overlapping by 12nts) (5 biological replicates), custom maskless array tiling most of ENCODE with 50mer oligonucleotides end-to-end (3 biological replicates) and custom maskless array tiling most of ENCODE with 36mer oligonucleotides end-to-end (2 biological replicates). The chromatin-immunoprecipitation protocol is the same for all samples, however the labelling and hybridization protocols differ between Nimblegen and custom maskless arrays. Keywords = Transcription Factor Binding, STAT1, ChIP-chip, Human, Genome Tiling Arrays Keywords: other
Project description:Purpose: Sox2 expression marks gastric stem and progenitor cells, raising important questions regarding the genes regulated by Sox2 and the role of Sox2 itself during stomach homeostasis and disease. The goal of this study is to determine the function of and the genes regulated by Sox2 in the stomach. Methods: Sox2 ChIP-enriched DNA and input DNA was isolated from gastric glands of adult antrum from Sox2 KO and Sox2 WT mice. DNA was purified and genomic libraries were prepared as described (Sulahian et al., 2014), using four micrograms of goat anti-SOX2 (AF2018, R&D). Libraries were sequenced (50 bp, single-end reads) on an Illumina Hi-Seq 2000 instrument. Results: Sox2 is dispensiable for gastric stem cell self-renewal and epithelial homeostasis, however modulates the expression of wnt, intestinal and cancer related genes Examination of Sox2 targets in the stomachs of Sox2 WT and Sox2 KO mice.
Project description:Colonization of the human stomach with cag pathogenicity island (PAI)-positive H. pylori strains is associated with increased gastric cancer risk compared to colonization with cag PAI-negative strains. To evaluate the contributions of the Cag type IV secretion system (T4SS) and CagA (a secreted bacterial oncoprotein) to gastric molecular alterations relevant for carcinogenesis, we infected Mongolian gerbils with a Cag T4SS-positive wild-type (WT) H. pylori strain, one of two Cag T4SS mutant strains (∆cagT or ∆cagY), or a ∆cagA mutant for 12 weeks. Histologic staining revealed a biphasic distribution of gastric inflammation severity (either minimal or severe) in WT-infected animals and minimal inflammation in mutant-infected animals. Atrophic gastritis (a premalignant condition), dysplasia, and gastric adenocarcinoma were only detected in WT-infected animals with high inflammation scores. Transcriptional profiling and analyses of micro-extracted tryptic peptides (LC-MS/MS and imaging mass spectrometry) revealed more than a thousand molecular alterations in gastric tissues from WT-infected animals with high inflammation scores compared to uninfected tissues and few alterations in tissues from other groups of infected animals. Proteins with altered abundance in animals with severe Cag T4SS-induced inflammation mapped to multiple pathways, including the complement/coagulation cascade and proteasome pathway. Proteins exhibiting markedly increased abundance in tissues from H. pylori-infected animals with severe inflammation included calprotectin components, lysozyme, lactoferrin, superoxide dismutase, eosinophil peroxidase, proteins involved in proteasome activation, STAT1, TrpRS, GBP2, and IIGP1. These results demonstrate key roles for CagA and Cag T4SS activity in promoting gastric mucosal inflammation, transcriptional alterations, and proteomic alterations relevant to gastric carcinogenesis.
Project description:Genome-wide DNA methylation profiling of gastric tumors and matched gastric non-malignant samples. The Illumina HumanMethylation27 BeadChip was used to obtain DNA methylation profiles across 27,578 CpGs in 203 gastric tumors and 94 matched non-malignant gastric samples. Bisulphite-converted DNA from the 203 gastric tumors and 94 matched gastric non-malignant samples was hybridized to the Illumina HumanMethylation27 BeadChip.