CR Name:
Species:    Tissue or Cell: 

Chromatin Regulator

Alias

MTA3NA

External Links:

Wiki    GeneCards    NCBI    UniProt

Related histone modifications:

NA

Introduction

Full Name: Metastasis-associated 1 family, member 3 . MTA3 is a cell type-specific component of the NURD (nucleosome remodeling and deacetylase) chromatin remodeling complex, which is highly expressed in normal human placental tissues. Unlike MTA1, which is present in both the nucleus and cytoplasm, NURD is able to regulate cell adhesion proteins and neoangiogenic cytokines, playing a role in primitive hematopoiesis, differentiation, and pathway regulation (1-10).

Function and Interaction

MTA3 interacts with BCL6. The MTA3 Mi2/NuRD complex is capable of deacetylating BCL6 and is therefore involved in B cell fate determination (1). MTA3 directly regulates Wnt4 in a histone deacetylase (HDAC)-dependent fashion, and suppression of MTA3 can enhance the expression of Wnt4 and stimulate the Wnt pathway (2). MTA3 has been shown to be ubiquitously expressed during zebrafish embryogenesis. It is required for primitive hematopoiesis, and its overexpression can lead to increased expression of the earliest hematopoietic markers (3).

Disease Association

MTA3 is involved in the estrogen-dependent pathway responsible for invasive growth and differentiation in breast cancer, and deletion of SP1 or ER-alpha can affect the expression of MTA3 and corepressors such as MTA1 and MTA1s. MTA3 coactivators, such as AIB1 and PELP1/MNAR, act as upstream modulators of this ER regulation, which could directly affect the master modulator of the epithelial-to-mesenchymal transition, Snail, and thereby control the cell adhesion molecule E-cadherin (4-6). MTA3 is thought to be expressed at a high level in chorionic carcinoma cell lines, including BeWo, JEG, and JAR cells (7).

ChIP-Seq data


SpeciesCell lineCell typeTissueDataDownloadSend to CistromeAnalysis FiguresComparisonReference
Homo sapiensGM12878LymphoblastoidBloodGSE32465 ,GSM1010729
Click  DownloadNA24076218

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References

1. Fujita, N., Jaye, D.L., Geigerman, C., Akyildiz, A., Mooney, M.R., Boss, J.M. and Wade, P.A. (2004) MTA3 and the Mi-2/NuRD complex regulate cell fate during B lymphocyte differentiation. Cell, 119, 75-86.
2. Zhang, H., Singh, R.R., Talukder, A.H. and Kumar, R. (2006) Metastatic tumor antigen 3 is a direct corepressor of the Wnt4 pathway. Gene Dev, 20, 2943-2948.
3. Li, X., Jia, S.J., Wang, S.H., Wang, Y.M. and Meng, A.M. (2009) Mta3-NuRD complex is a master regulator for initiation of primitive hematopoiesis in vertebrate embryos. Blood, 114, 5464-5472.
4. Fujita, N., Jaye, D.L., Kajita, M., Geigerman, C., Moreno, C.S. and Wade, P.A. (2003) MTA3, a Mi-2/NuRD complex subunit, regulates an invasive growth pathway in breast cancer. Cell, 113, 207-219.
5. Mishra, S.K., Talukder, A.H., Guraraj, A.E., Yang, Z.B., Singh, R.R., Mahoney, M.G., Franci, C., Vadlamudi, R.K. and Kumar, R. (2004) Upstream determinants of estrogen receptor-alpha regulation of metastatic tumor antigen 3 pathway. J Biol Chem, 279, 32709-32715.
6. Fujita, N., Kajita, M., Taysavang, P. and Wade, P.A. (2004) Hormonal regulation of metastasis-associated protein 3 transcription in breast cancer cells. Mol Endocrinol, 18, 2937-2949.
7. Bruning, A., Makovitzky, J., Gingelmaier, A., Friese, K. and Mylonas, I. (2009) The metastasis-associated genes MTA1 and MTA3 are abundantly expressed in human placenta and chorionic carcinoma cells. Histochem Cell Biol, 132, 33-38.
8. Bowen, N.J., Fujita, N., Kajita, M. and Wade, P.A. (2004) Mi-2/NuRD: multiple complexes for many purposes. Bba-Gene Struct Expr, 1677, 52-57.
9. Denslow, S.A. and Wade, P.A. (2007) The human Mi-2/NuRD complex and gene regulation. Oncogene, 26, 5433-5438.
10. Simpson, A., Uitto, J., Rodeck, U. and Mahoney, M.G. (2001) Differential expression and subcellular distribution of the mouse metastasis-associated proteins Mta1 and Mta3. Gene, 273, 29-39.

Figure Gallery

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About Chromatin Regulator

Chromatin Regulator Cistrome
is a unique database integrating curated information of CRs, CR ChIP-seq datasets, CR related HM ChIP-seq datasets, and analysis of the relationship between CRs and HMs ChIP-seq pairs in human and mouse.