Editorial Special Issues

SMYD proteins in immunity: dawning of a new era

  • Received: 13 October 2016 Accepted: 13 October 2016 Published: 17 October 2016
  • Citation: Maysaa Doughan, Nicholas Spellmon, Chunying Li, Zhe Yang. SMYD proteins in immunity: dawning of a new era[J]. AIMS Biophysics, 2016, 3(4): 450-455. doi: 10.3934/biophy.2016.4.450

    Related Papers:



  • 加载中
    [1] Gottlieb PD, Pierce SA, Sims RJ, et al. (2002) Bop encodes a muscle-restricted protein containing MYND and SET domains and is essential for cardiac differentiation and morphogenesis. Nat Genet 31: 25–32.
    [2] Hamamoto R, Furukawa Y, Morita M, et al. (2004) SMYD3 encodes a histone methyltransferase involved in the proliferation of cancer cells. Nat Cell Biol 6: 731–740. doi: 10.1038/ncb1151
    [3] Donlin LT, Andresen C, Just S, et al. (2012) Smyd2 controls cytoplasmic lysine methylation of Hsp90 and myofilament organization. Genes Dev 26: 114–119. doi: 10.1101/gad.177758.111
    [4] Proserpio V, Fittipaldi R, Ryall JG, et al. (2013) The methyltransferase SMYD3 mediates the recruitment of transcriptional cofactors at the myostatin and c-Met genes and regulates skeletal muscle atrophy. Genes Dev 27: 1299–1312. doi: 10.1101/gad.217240.113
    [5] Fujii T, Tsunesumi S, Yamaguchi K, et al. (2011) Smyd3 is required for the development of cardiac and skeletal muscle in zebrafish. PLoS One 6: e23491. doi: 10.1371/journal.pone.0023491
    [6] Thompson EC, Travers AA (2008) A Drosophila Smyd4 homologue is a muscle-specific transcriptional modulator involved in development. PLoS One 3: e3008. doi: 10.1371/journal.pone.0003008
    [7] Spellmon N, Holcomb J, Trescott L, et al. (2015) Structure and function of SET and MYND domain-containing proteins. Int J Mol Sci 16: 1406–1428. doi: 10.3390/ijms16011406
    [8] Sakamoto LH, Andrade RV, Felipe MS, et al. (2014) SMYD2 is highly expressed in pediatric acute lymphoblastic leukemia and constitutes a bad prognostic factor. Leuk Res 38: 496–502. doi: 10.1016/j.leukres.2014.01.013
    [9] Komatsu S, Imoto I, Tsuda H, et al. (2009) Overexpression of SMYD2 relates to tumor cell proliferation and malignant outcome of esophageal squamous cell carcinoma. Carcinogenesis 30: 1139–1146. doi: 10.1093/carcin/bgp116
    [10] Hu L, Zhu YT, Qi C, et al. (2009) Identification of Smyd4 as a potential tumor suppressor gene involved in breast cancer development. Cancer Res 69: 4067–4072.
    [11] Stender JD, Pascual G, Liu W, et al. (2012) Control of proinflammatory gene programs by regulated trimethylation and demethylation of histone H4K20. Mol cell 48: 28–38. doi: 10.1016/j.molcel.2012.07.020
    [12] Xu G, Liu G, Xiong S, et al. (2015) The histone methyltransferase Smyd2 is a negative regulator of macrophage activation by suppressing interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) production. J Biol chem 290: 5414–5423. doi: 10.1074/jbc.M114.610345
    [13] Nagata DE, Ting HA, Cavassani KA, et al. (2015) Epigenetic control of Foxp3 by SMYD3 H3K4 histone methyltransferase controls iTreg development and regulates pathogenic T-cell responses during pulmonary viral infection. Mucosal immunol8: 1131–1143.
    [14] Hwang I, Gottlieb PD (1995) Bop: a new T-cell-restricted gene located upstream of and opposite to mouse CD8b. Immunogenetics 42: 353–361.
    [15] Hussain SP, Hofseth LJ, Harris CC. (2003) Radical causes of cancer. Nat Rev Cancer 3: 276–285. doi: 10.1038/nrc1046
    [16] Esquivel-Velazquez M, Ostoa-Saloma P, Palacios-Arreola MI, et al. (2015) The role of cytokines in breast cancer development and progression. J Interf Cytok Res 35: 1–16. doi: 10.1089/jir.2014.0026
    [17] Haabeth OA, Lorvik KB, Hammarstrom C, et al. (2011) Inflammation driven by tumour-specific Th1 cells protects against B-cell cancer. Nat Commun 2: 385–396. doi: 10.1038/ncomms1385
    [18] Miyashita M, Sasano H, Tamaki K, et al. (2015) Prognostic significance of tumor-infiltrating CD8+ and FOXP3+ lymphocytes in residual tumors and alterations in these parameters after neoadjuvant chemotherapy in triple-negative breast cancer: a retrospective multicenter study. Breast Cancer Res BCR 17: 11–13. doi: 10.1186/s13058-015-0514-2
    [19] Borlak J, Thum T (2003) Hallmarks of ion channel gene expression in end-stage heart failure. Faseb J 17: 1592–1608. doi: 10.1096/fj.02-0889com
    [20] Platzbecker U, Klingel K, Thiede C, et al. (2001) Acute heart failure after allogeneic blood stem cell transplantation due to massive myocardial infiltration by cytotoxic T cells of donor origin. Bone Marrow Transpl 27: 107–109. doi: 10.1038/sj.bmt.1702744
    [21] Levick SP, Goldspink PH (2014) Could interferon-gamma be a therapeutic target for treating heart failure? Heart Fail Rev 19: 227–236. doi: 10.1007/s10741-013-9393-8
    [22] Streit WJ, Mrak RE, Griffin WS. (2004) Microglia and neuroinflammation: a pathological perspective. J Neuroinflamm 1:1–4. doi: 10.1186/1742-2094-1-1
    [23] Koscielny G, Yaikhom G, Iyer V, et al. (2014) The International Mouse Phenotyping Consortium Web Portal, a unified point of access for knockout mice and related phenotyping data. Nucleic Acids Res 42D: 802–809.
    [24] Mazur PK, Reynoird N, Khatri P, et al. (2014) SMYD3 links lysine methylation of MAP3K2 to Ras-driven cancer. Nature 510: 283–287. doi: 10.1038/nature13320
    [25] Zhao Q, Lee FS (1999) Mitogen-activated protein kinase/ERK kinase kinases 2 and 3 activate nuclear factor-kappaB through IkappaB kinase-alpha and IkappaB kinase-beta. J Biol Chem 274: 8355–8358. doi: 10.1074/jbc.274.13.8355
    [26] Huang J, Perez-Burgos L, Placek BJ, et al. (2006) Repression of p53 activity by Smyd2-mediated methylation. Nature 444: 629–632. doi: 10.1038/nature05287
    [27] Saddic LA, West LE, Aslanian A, et al. (2010) Methylation of the retinoblastoma tumor suppressor by SMYD2. J Biol Chem 285: 37733–37740. doi: 10.1074/jbc.M110.137612
    [28] Santhanam U, Ray A, Sehgal PB. (1991) Repression of the interleukin 6 gene promoter by p53 and the retinoblastoma susceptibility gene product. P Natl Acad Sci USA 88: 7605–7609. doi: 10.1073/pnas.88.17.7605
  • Reader Comments
  • © 2016 the Author(s), licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0)
通讯作者: 陈斌, bchen63@163.com
  • 1. 

    沈阳化工大学材料科学与工程学院 沈阳 110142

  1. 本站搜索
  2. 百度学术搜索
  3. 万方数据库搜索
  4. CNKI搜索

Metrics

Article views(4115) PDF downloads(1092) Cited by(11)

Article outline

/

DownLoad:  Full-Size Img  PowerPoint
Return
Return

Catalog