1. IRF2BP2 modulates the crosstalk between glucocorticoid and TNF signaling
- Author
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Einari A. Niskanen, Marjo Malinen, A.B.M. Kaiser Manjur, Joanna K. Lempiäinen, and Jorma J. Palvimo
- Subjects
0301 basic medicine ,Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,Anti-Inflammatory Agents ,Biochemistry ,03 medical and health sciences ,0302 clinical medicine ,Endocrinology ,Cell Movement ,Interferon ,medicine ,Humans ,Glucocorticoids ,Molecular Biology ,Transcription factor ,Cell Proliferation ,Inflammation ,Tumor Necrosis Factor-alpha ,Chemistry ,Chromatin binding ,HEK 293 cells ,NF-kappa B ,Cell Biology ,Cell biology ,Chromatin ,DNA-Binding Proteins ,Crosstalk (biology) ,HEK293 Cells ,030104 developmental biology ,Gene Expression Regulation ,A549 Cells ,030220 oncology & carcinogenesis ,Molecular Medicine ,Tumor necrosis factor alpha ,Glucocorticoid ,Transcription Factors ,medicine.drug - Abstract
IRF2BP2 (interferon regulatory factor-2 binding protein-2) is an uncharacterized interaction partner of glucocorticoid (GC) receptor (GR), an anti-inflammatory and metabolic transcription factor. Here, we show that GC changes the chromatin binding of IRF2BP2 in natural chromatin milieu. The GC-induced IRF2BP2-binding sites co-occur with GR binding sites and are associated with GC-induced genes. Moreover, the depletion of IRF2BP2 modulates transcription of GC-regulated genes, represses cell proliferation and increases cell movement in HEK293 cells. In A549 cells, the depletion extensively alters the responses to GC and tumor necrosis factor α (TNF), including metabolic and inflammatory pathways. Taken together, our data support the role of IRF2BP2 as a coregulator of both GR and NF-κB, potentially modulating the crosstalk between GC and TNF signaling.
- Published
- 2019
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