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:

Modulation of normal erythroid differentiation by the endogenous thyroid hormone and retinoic acid receptors: a possible target for v-erbA oncogene action. The v-erbA oncogene, a mutated version of the thyroid hormone receptor alpha (c-erbA / TR-alpha), inhibits erythroid differentiation and constitutively represses transcription of certain erythrocyte genes, suggesting a normal function of the proto-oncogene c-erbA in erythropoiesis. Here we demonstrate that the endogenous thyroid hormone receptor alpha (c-erbA / TR-alpha) and the closely related retinoic acid receptor alpha (RAR-alpha) play a role in the regulation of normal erythroid differentiation. Retinoic acid (RA) distinctly modulated the erythroid differentiation program of normal erythroid progenitors and erythroblasts reversibly transformed by a conditional tyrosine kinase oncogene. When added pulsewise to immature cells, differentiation was accelerated while more mature cells underwent premature cell death. Thyroid hormone (T3) alone caused similar but weaker effects. Interestingly, T3 strongly enhanced the action of RA, suggesting cooperative action of the two receptors in modulating erythroid differentiation. Expression of the human RAR-alpha in receptor-negative erythroblasts conferred RA-induced regulation of differentiation to the otherwise unresponsive cells, thus showing that the RAR-alpha is essential for the RA effect. Likewise, enhanced expression of exogenous c-erbA / TR-alpha in erythroblasts rendered them susceptible to modulation of differentiation by T3, suggesting a similar function of both receptors.
{"CellLine": ["erythroblasts", "receptor - negative erythroblasts"], "CellType": ["immature cells", "mature cells", "unresponsive cells", "normal erythroid progenitors", "erythroblasts"], "DNA": ["erythrocyte genes", "proto - oncogene c - erbA", "tyrosine kinase oncogene", "The v - erbA oncogene", "v - erbA oncogene"], "Protein": ["retinoic acid", "RAR - alpha", "retinoic acid receptor alpha", "c - erbA / TR - alpha", "human RAR - alpha", "Thyroid hormone (T3)", "thyroid hormone receptor alpha", "thyroid hormone", "exogenous c - erbA / TR - alpha", "T3", "the proto - oncogene c - erbA", "c - erbA", "retinoic acid receptor", "Retinoic acid (RA)", "RA", "retinoic acid receptors"], "RNA": []}