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:

Regulation of c-jun expression during induction of monocytic differentiation by okadaic acid. The present work has examined the effects of okadaic acid, an inhibitor of type 1 and 2A protein phosphatases, on the regulation of c-jun expression during monocytic differentiation of U-937 leukemia cells. The results demonstrate that okadaic acid treatment is associated with induction of a differentiated monocyte phenotype characterized by: (a) growth arrest; (b) increases in Mac-1 cell surface antigen expression; (c) down-regulation of c-myc transcripts; and (d) induction of tumor necrosis factor gene expression. This induction of monocytic differentiation was associated with transient increases in c-jun mRNA levels, which were maximal at 6 h. Similar effects were obtained for the c-fos gene. Run-on analysis demonstrated detectable levels of c-jun transcription in U-937 cells and that this rate is increased approximately 40-fold following okadaic acid exposure. c-jun mRNA levels were superinduced in cells treated with both okadaic acid and cycloheximide, whereas inhibition of protein synthesis had little, if any, effect on okadaic acid-induced c-jun transcription. The half-life of c-jun mRNA was similar (45-50 min) in both untreated and okadaic acid-induced cells. In contrast, treatment with both okadaic acid and cycloheximide was associated with stabilization (t 1 / 2 = 90 min) of c-jun transcripts. Taken together, these findings indicate that the induction of c-jun transcription by okadaic acid is controlled primarily by a transcriptional mechanism. Since previous studies have demonstrated that the c-jun gene is autoinduced by Jun / AP-1, we also studied transcription of c-jun promoter (positions-132 / + 170) -reporter gene constructs with and without a mutated AP-1 element. (ABSTRACT TRUNCATED AT 250 WORDS)
{"CellLine": ["okadaic acid", "U - 937 leukemia cells", "U - 937 cells", "okadaic acid - induced cells"], "CellType": [], "DNA": ["c - fos gene", "c - jun promoter (positions - 132 / + 170) - reporter gene constructs", "c - jun", "tumor necrosis factor gene", "c - jun gene", "c - jun promoter", "AP - 1 element"], "Protein": ["Jun / AP - 1", "Mac - 1 cell surface antigen", "c - myc transcripts", "type 1 and 2A protein phosphatases", "tumor necrosis factor", "c - jun transcripts"], "RNA": ["c - jun mRNA"]}