You will be shown an abstract from a biomedical research paper. Given this abstract, your task is to extract all unique entities of the following types: ["RNA", "CellLine", "Protein", "DNA", "CellType"].

Please return the output as a JSON object of the format: {"DNA" : ["TAL1", ...], "RNA": ["mRNAs", ...], "CellLine": ["T cells", ...], "CellType": ["monocytes", ...], "Protein": ["IL-2", ...]}. The keys should be entity types and values should be lists of extracted entities belonging to the corresponding type. If you cannot find entities belonging to a specific type, the value should be [].

Only output the JSON object and do not include any additional text.

Abstract:

The AP-1 site at-150 bp, but not the NF-kappa B site, is likely to represent the major target of protein kinase C in the interleukin 2 promoter. Stimulation of T cells with antigen results in activation of several kinases, including protein kinase C (PKC), that may mediate the later induction of activation-related genes. We have examined the potential role of PKC in induction of the interleukin 2 (IL-2) gene in T cells stimulated through the T cell receptor / CD3 complex. We have previously shown that prolonged treatment of the untransformed T cell clone Ar-5 with phorbol esters results in downmodulation of the alpha and beta isozymes of PKC, and abrogates induction of IL-2 mRNA and protein. Here we show that phorbol ester treatment also abolishes induction of chloramphenicol acetyltransferase activity in Ar-5 cells transfected with a plasmid containing the IL-2 promoter linked to this reporter gene. The IL-2 promoter contains binding sites for nuclear factors including NFAT-1, Oct, NF-kappa B, and AP-1, which are all potentially sensitive to activation of PKC. We show that induction of a trimer of the NFAT and Oct sites is not sensitive to phorbol ester treatment, and that mutations in the NF-kappa B site have no effect on inducibility of the IL-2 promoter. In contrast, mutations in the AP-1 site located at-150 bp almost completely abrogate induction of the IL-2 promoter, and appearance of an inducible nuclear factor binding to this site is sensitive to PKC depletion. Moreover, cotransfections with c-fos and c-jun expression plasmids markedly enhance induction of the IL-2 promoter in minimally stimulated T cells. Our results indicate that the AP-1 site at-150 bp represents a major, if not the only, site of PKC responsiveness in the IL-2 promoter.
{"CellLine": ["T cell clone Ar - 5", "minimally stimulated T cells", "Ar - 5 cells", "T cells"], "CellType": ["T cells"], "DNA": ["plasmid", "AP - 1 site", "reporter gene", "NFAT and Oct sites", "IL - 2 promoter", "interleukin 2 promoter", "NF - kappa B site", "AP - 1", "IL - 2", "interleukin 2 (IL - 2) gene", "binding sites", "the interleukin 2 (IL - 2) gene", "- 150 bp"], "Protein": ["kinases", "nuclear factors", "protein", "alpha and beta isozymes", "chloramphenicol acetyltransferase", "PKC", "T cell receptor / CD3 complex", "NFAT - 1", "protein kinase C", "interleukin 2", "AP - 1", "protein kinase C (PKC)", "NF - kappa B", "Oct", "IL - 2", "inducible nuclear factor"], "RNA": ["IL - 2 mRNA"]}