Histone deacetylase 3 binds to and regulates the GCMa transcription factor
作者： Hsiao-Ching Chuang , Ching-Wen Chang , Geen-Dong Chang , Tso-Pang Yao , Hungwen Chen
DOI: 10.1093/NAR/GKL048
关键词: Repressor 、 HDAC3 、 Biology 、 HDAC1 、 Transcription factor 、 CREB-binding protein 、 Acetylation 、 Trichostatin A 、 Histone deacetylase 、 Cancer research
摘要: Human GCMa transcription factor regulates expression of syncytin, a placental fusogenic protein mediating trophoblastic fusion. Recently, we have demonstrated that CBP-mediated acetylation underlies the activated cAMP/PKA signaling pathway stimulates Because is reversible modification governed by histone acetyltransferases (HATs) and deacetylase (HDACs), in this study investigated key HDACs responsible for deacetylation thus reduction activity to avoid unwanted fusion events may adverse effects on morphogenesis. We herein demonstrate HDAC inhibitor, trichostatin A (TSA), increases level acetylated HDAC1, 3, 4 5 interact with deacetylate GCMa. Glutathione S-transferase (GST) pull-down assays further verified direct interaction between HDAC3 or CBP HDAC3. counteracts transcriptional coactivator enhancement effect GCMa-mediated activation. Correlatively, found cells associates proximal GCMa-binding site (pGBS) syncytin promoter dissociates from pGBS presence forskolin, which association pGBS. Our studies support morphogenesis depends regulation HAT HDAC.
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