Project description:The CrdR-ChIP profiling is comparing H. pylori gDNA without crdR interaction as control and CrdR interact with H. pylori gDNA (WT vs crdR). The goal was determine the crdR binding site on H. pylori genome, it provide possible crdR-regulated genes. 2 samples: H. pylori 26695 is control, and CrdR is experiment.
Project description:EGF is one of the most well-characterized growth factors and plays a crucial role in cell proliferation and differentiation. EGFR has been extensively explored as a therapeutic target against multiple types of cancers, such as lung cancer and glioblastoma. Recent studies have established a connection between deregulated EGF signaling and metabolic reprogramming, especially rewiring in aerobic glycolysis, which is also known as the Warburg effect and recognized as a hallmark in cancer. Pyruvate kinase M2 (PKM2) is a rate-limiting enzyme controlling the final step of glycolysis and serves as a major regulator of the Warburg effect. We previously showed that PKM2 T405/S406 O-GlcNAcylation, a critical mark important for PKM2 detetramerization and activity, was markedly upregulated by EGF. However, the mechanism by which EGF regulates PKM2 O-GlcNAcylation still remains uncharacterized. Here we demonstrated that EGF promoted O-GlcNAc transferase (OGT) binding to PKM2 by stimulating OGT Y976 phosphorylation. As a consequence, PKM2 O-GlcNAcylation and detetramerization were upregulated, leading to a significant decrease in PKM2 activity. Moreover, other than PKM2, the association of additional phosphotyrosine binding proteins, including STAT1, STAT3, STAT5, PKCδ and p85, which are reported factors bearing O-GlcNAcylation, with OGT was also enhanced when Y976 was phosphorylated. Together, EGF-dependent Y976 phosphorylation is critical for OGT-PKM2 interaction and we propose that this post-translational modification might be important for the substrate selection by OGT.
Project description:There are two transcription profiles. The first profiling is comparing control untreated H. pylori with H. pylori with NO treatment. And the second profiling is comparing knockout-crdS in H. pylori untreated with knockout-crdS with NO treatment. The goal was determine the effects of NO-responsive gene and crdS-regulated genes on H. pylori gene expression. Four-condition experiment, wild-type H. pylori untreated (WT –NO), H. pylori with NO treatment (WT +NO), knockout-crdS in H. pylori untreated (ΔcrdS -NO), ΔcrdS with NO treatment (ΔcrdS +NO)
Project description:Methylated modifications of genome are common events in carcinogenesis and is involved in the tumorigenesis and progression of various cancers including gastric cancer Methylated DNA immunoprecipitation (MeDIP) combined with a human miRNA tiling microarray analysis demonstrated that there are much methylation differention between gastric cancers and adjacent controls microRNA gene methylation comparison of 3 pairs of gastric cancer and controls
Project description:Data for the third YPIC Challenge. A synthetic peptide was analyzed using HR-MS. The peptide contains a codeword/phrase/sentence. Can you decrypt it? Get your best mates and try to crack the challenge!
Project description:Introduction: Angong Niuhuang Wan (AGNHW), developed in the Qing dynasty (18th century) for treating consciousness disturbances caused by severe infections, has already been used to treat brain edema caused by ischemia-reperfusion. However, it remains unclear whether AGNHW can ameliorate vascular-origin brain edema caused by lipopolysaccharides (LPS).This study explores the ameliorative effects of AGNHW on cerebrovascular edema in mice caused by LPS, as well as its potential mechanisms.Mice were divided into four groups: Control, LPS 26 h, LPS 48 h, and LPS + AGNHW_M. Enriched phosphorylated peptides were extracted from mouse brain tissues at the corresponding time points and subjected to phosphoproteomic analysis.
Project description:3 sets of CFZ-exposed bacteria were compared to 3 sets of bacteria treated with vehicle (DMSO) for 24 hours in an aerated drug killing model.
Project description:The Purpose of this series of experiments is to identify copy number variations, duplications, and deletions in human induced pluripotent stem (hiPSC) cell lines. Genomic DNA of different human induced pluripotent stem cell lines are extracted and hybridized to NimbleGen CGH microarray, using genomic DNA of hESC H1 or H9 as common reference. Difference between different stem cell lines will be revealed.
Project description:B1 cells account for the majority of B cell population in the peritoneal cavity, and are essential for the innate immune responses and maintaining the homeostasis. The origin of the B1 cells and how to form the B1 cells pool in the postnatal life remain unknown. And the heterogeneity of B1 cells can largely affect the functions of B1 cells. Until now, nobody has performed the single cell RNA-seq of peritoneal B cells. In order to reveal the characteristics of peritoneal B cells, we have performed the scRNA-seq and scBCR-seq of the peritoneal B cells of mouse from different stages.
Project description:Phosphoglycerate mutase 1 (PGAM1) is a key-node enzyme that diverts the metabolic intermediates from glycolysis into its shunts to support macromolecule biosynthesis for rapid and sustainable cell proliferation. It is prevalent that PGAM1 activity is upregulated in various tumors; however, the underlying mechanism remains unclear. Here, we unveil that pyruvate kinase M2 (PKM2) moonlights as a histidine kinase in a phosphoenolpyruvate (PEP)-dependent manner to catalyze PGAM1 H11 phosphorylation, that is essential for PGAM1 activity. Moreover, the dimeric or monomeric PKM2 in tumor cells phosphorylates PGAM1 more efficiently than the tetrameric one. In response to epidermal growth factor (EGF), Src signaling triggered PGAM1 Y119 phosphorylation is a prerequisite for PKM2 binding and the subsequent H11 phosphorylation of PGAM1, which constitutes the discrepancy between tumor cells and normal ones. A PGAM1-derived pY119-containing cell-permeable peptide or Y119 mutation disrupts the interaction of PGAM1 with PKM2 and its H11 phosphorylation, and eventually dampens the glycolysis shunts and tumor growth. We not only identifes a histidine kinase function of PKM2, but also illustrates an enzymes-cross-talk regulatory mode during metabolic reprogramming.