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:

Reduced susceptibility to HIV-1 infection of ethyl-methanesulfonate-treated CEM subclones correlates with a blockade in their protein kinase C signaling pathway. We have described the isolation of chemically induced CEM subclones that express CD4 receptors and bind soluble gp120, yet show a markedly reduced susceptibility to infection with HIV-1. Two subclones were found to have an abnormal response to the protein kinase C (PKC) activator PMA. PMA treatment induced CD3 and CD25 (IL-2R) receptors on the parental line and on other ethyl-methanesulfonate-derived subclones, but not on these two mutants. Direct assays of PKC activity were conducted. Total cellular PKC enzymatic activity was found to be normal in these subclones. PMA-induced CD4 down-modulation occurred normally. In addition, activation of c-raf kinase was normal. Since HIV-1 long terminal repeat contains two functional nuclear factor kB (NF-kB) regulatory elements, we studied the ability of PMA to induce NF-kB binding activity by different assays. Chloramphenicol acetyl transferase (CAT) assays using the HIV-1 (-139) long terminal repeat-CAT construct showed no PMA induction of CAT activity in these subclones (unlike the parental line and other subclones). Okadaic acid, an inhibitor of phosphatases 1 and 2A, did not overcome the defect in these subclones. Gel retardation assays, using a 32P-probe containing the HIV-1 NF-kB probe and nuclear extracts from PMA-treated cells, showed significantly reduced induction of nuclear NF-kB binding proteins in these two subclones compared with wild type CEM and a control subclone. Deoxycholate treatment of cytoplasmic extracts from these subclones released much reduced NF-kB binding proteins from their cytoplasmic pools. Thus, reduced levels of PKC-induced nuclear NF-kB activity in two T cell subclones did not affect their normal cell growth, but correlated with a pronounced reduction in their susceptibility to HIV-1 infection.
{"CellLine": ["ethyl - methanesulfonate - treated CEM subclones", "CEM subclones", "ethyl - methanesulfonate - derived subclones"], "CellType": ["PMA - treated cells"], "DNA": ["nuclear factor kB (NF - kB) regulatory elements", "HIV - 1 (- 139) long terminal repeat - CAT construct", "HIV - 1 long terminal repeat"], "Protein": ["NF - kB", "phosphatases 1 and 2A", "NF - kB binding proteins", "c - raf kinase", "wild type CEM", "nuclear NF - kB binding proteins", "CD4 receptors", "CAT", "CD4", "PKC", "CD3 and CD25 (IL - 2R) receptors", "gp120", "CEM", "Chloramphenicol acetyl transferase", "protein kinase C"], "RNA": []}