NDLI: Myocyte enhancer factor 2 and microphthalmia-associated transcription factor cooperate with NFATc1 to transactivate the V-ATPase d2 promoter during RANKL-induced osteoclastogenesis.

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Myocyte enhancer factor 2 and microphthalmia-associated transcription factor cooperate with NFATc1 to transactivate the V-ATPase d2 promoter during RANKL-induced osteoclastogenesis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Steer, James H. Leong, Chengloon Zheng, Ming H. Feng, Haotian Liu, Jianzhong Feng, Xu Cheng, Taksum Pavlos, Nathan J. Xu, Jiake Joyce, David A. Kular, Jasreen
Description	Author Affiliation: Feng H ( Centre for Orthopaedic Research, School of Surgery, University of Western Australia, Australia.)
Abstract	The V-ATPase d2 protein constitutes an important subunit of the V-ATPase proton pump, which regulates bone homeostasis; however, currently little is known about its transcriptional regulation. Here, in an attempt to understand regulation of the V-ATPase d2 promoter, we identified the presence of NFATc1, microphthalmia-associated transcription factor (MITF)- and myocyte enhancer factor 2 (MEF2)-binding sites within the V-ATPase d2 promoter using complementary bioinformatic analyses, chromatin immunoprecipitation, and electromobility shift assay. Intriguingly, activation of the V-ATPase d2 promoter by NFATc1 was enhanced by either MEF2 or MITF overexpression. By comparison, coexpression of MITF and MEF2 did not further enhance V-ATPase d2 promoter activity above that of expression of MITF alone. Consistent with a role in transcriptional regulation, both NFATc1 and MITF proteins translocated from the cytosol to the nucleus during RANKL-induced osteoclastogenesis, whereas MEF2 persisted in the nucleus of both osteoclasts and their mononuclear precursors. Targeted mutation of the putative NFATc1-, MITF-, or MEF2-binding sites in the V-ATPase d2 promoter impaired its transcriptional activation. Additionally retroviral overexpression of MITF or MEF2 in RAW264.7 cells potentiated RANKL-induced osteoclastogenesis and V-ATPase d2 gene expression. Based on these data, we propose that MEF2 and MITF function cooperatively with NFATc1 to transactivate the V-ATPase d2 promoter during RANKL-induced osteoclastogenesis.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	21
Volume Number	284
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2009-05-22
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Microphthalmia-Associated Transcription Factor Metabolism Myogenic Regulatory Factors NFATC Transcription Factors Osteoclasts Cytology Promoter Regions, Genetic Genetics Transcriptional Activation Vacuolar Proton-Translocating ATPases Animals Base Pairing Drug Effects Binding Sites COS Cells Cell Differentiation Cell Line Cell Nucleus Cercopithecus Aethiops MEF2 Transcription Factors Mice Molecular Sequence Data Protein Binding Protein Transport RANK Ligand Pharmacology Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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