Project description:KYSE410 cells were treated with PBS, TNFα, IL1β, and LPS respectively and mRNA expression profiles were assayed by Nimblegen gene expression microarray human HG18 (12x135K) Investigation of the critical gene participating various inflammatory stimuli in the process of ESCC progression.
Project description:KYSE410 cells were tranfected with NOX5 plasmid in the presence or absence of HIF-1α inhibitor-BAY87-2243 and mRNA expression of tumor-promoting molecules were assayed by RiboArray Human mRNA Array investigation of the critical gene participating in the process of NOX5/HIF-1α-mediated ESCC progression.
Project description:Memory T cells are critical to protect us from recurring infections. Their instantaneous reactivity to pathogens is empowered by persistent expression of cytokine mRNA. How aberrant protein production of this pre-formed mRNA is prevented in the absence of infection, however, remains unresolved. We show that protein production in memory T cells is blocked through a 3’untranslated region (3’UTR)-mediated process, and that AU-rich elements (AREs) are key herein. Germ-line deletion of AREs leads to chronic IFN- production in bona fide memory T cells. Strikingly, the aberrant protein production does not result from increased mRNA levels and/or half-life. Rather, AREs block the recruitment of cytokine mRNA to ribosomes, a process that is mediated by the ARE-binding protein ZFP36L2. Thus, AREs are crucial elements for translational repression that allow murine and human memory T cells to contain pre-formed cytokine mRNAs, while preventing undesirable protein production in the absence of infection.
Project description:KYSE410 cells were treated with 10 uM defactinib for 4 hours and 24 hours,and KYSE410 cells were collected for gene expression analysis using Agilent SurePrint G3 Human Gene Expression v3 (8×60K) Microarray. Investigation of the critical gene of KYSE410 cells treated by defactinib.
Project description:We used microarrays to detail the gene expression profiles of KYSE410 cell line to identify distinct up and down-regulated genes during treatment with cisplatin. KYSE410 cell line were treated with 20 nM YM155 for 6 hrs and selected for RNA extraction and hybridization on Affymetrix microarrays. We sought to gene expression profiles of KYSE 410 cell line treated with cisplatin.
Project description:Effective T cell responses against infections and tumors depend on the production of effector molecules, including the key pro-inflammatory cytokines IFN-γ, TNF-α and IL-2. Recent studies revealed that post-transcriptional events determine the magnitude and duration of cytokine production in T cells, a feature that is largely defined by RNA-binding proteins (RBPs). However, to date the interplay of RBPs with cytokine mRNA, and their mode of action are ill-defined. Here we employed an RNA-aptamer-based capture assay from human T cell lysates to map RBP interactions with the full length 3’untranslated regions of IFNG, TNF and IL2. We found that RBPs binding can be both promiscuous and cytokine-specific. Furthermore, the RBP binding landscape rapidly alters upon T cell activation. Genetic deletion of confirmed mRNA interactors uncovered RBP-specific activity in primary T cells in response to target cells. Thus, RBPs are critical determinants of fast but tightly controlled cytokine production in T cells.
Project description:MDA-MB-231 cells were treated with PBS, LPS, IL1b, TNFa, IL6, and TGFb respectively and expression profile were assayed by Arraystar human lncRNA array 2.0