Project description:Aryl hydrocarbon receptor (AHR) activation by tryptophan (Trp) catabolites enhances tumor malignancy and suppresses anti-tumor immunity. Hitherto, indoleamine-2,3-dioxygenase 1 (IDO1) or tryptophan- 2, 3-dioxygenase (TDO2) are recognized as the main Trp-catabolizing enzymes (TCEs) responsible for the generation of AHR agonists. Here, the ability of the aromatic L-amino acid oxidase, interleukin 4 induced 1 (IL4I1), to activate the AHR was investigated using IL4I1 knockout CAS-1 glioblastoma cells.
Project description:The objective of this study was to analyze AHR activation through aromatic amino acid metabolism. To this end, glioblastoma cells were exposed to aromatic amino acid derived metabolites and their ability to activate AHR was analysed. In addition, AHR activation was evaluated in glioblastoma cells expressing IL4I1, an aromatic amino acid degrading enzyme, with or without shRNA mediated knockdown of AHR.
Project description:The objective of this study was to analyze AHR activation through aromatic amino acid metabolism. To this end, glioblastoma cells were exposed to aromatic amino acid derived metabolites and their ability to activate AHR was analysed. In addition, AHR activation was evaluated in glioblastoma cells expressing IL4I1, an aromatic amino acid degrading enzyme, with or without shRNA mediated knockdown of AHR.
Project description:The objective of this study was to analyze AHR activation through aromatic amino acid metabolism. To this end, glioblastoma cells were exposed to aromatic amino acid derived metabolites and their ability to activate AHR was analysed. In addition, AHR activation was evaluated in glioblastoma cells expressing IL4I1, an aromatic amino acid degrading enzyme, with or without shRNA mediated knockdown of AHR.
Project description:The objective of this study was to analyze AHR activation through aromatic amino acid metabolism. To this end, glioblastoma cells were exposed to aromatic amino acid derived metabolites and their ability to activate AHR was analysed. In addition, AHR activation was evaluated in glioblastoma cells expressing IL4I1, an aromatic amino acid degrading enzyme, with or without shRNA mediated knockdown of AHR.
Project description:To study the function of AMD-associated gene POLDIP2 in retinal pigment epithelial (RPE) cells, we used CRISPR/Cas to knockout POLDIP2 in the human RPE cell line ARPE19. We then performed RNA-seq to profile the transcriptome of wildtype ARPE19 and POLDIP2 knockout.
Project description:We compared gene expression profile between healthy-donor peripheral monocytes and glioblastoma-patient peripheral monocytes as well as glioblastoma-patient peripheral monocytes with matched tumor-infiltrating myeloid cells.