Establishment and Identification of SETD4gene knockout mice
HUANG Sui, HUANG Meng-yi, ZHONG Yu-yun, LEI Ye-ming, ZHAO Shu-qi, CAI Jun-wei, JIANG Yong, LIU Jing-hua
Chinese Journal of Clinical Anatomy ›› 2016, Vol. 34 ›› Issue (2) : 202-207.
Establishment and Identification of SETD4gene knockout mice
Objective To study the function of SETD4， the SETD4 gene knockout homozygous mice has been established. Methods SETD4flox/+ mice and EIIa-Cre mice were interbred，the offspring of which was genotyping SETD4+/-.EIIa-Cre were crossed with C57BL/6 mice to obtain the mice with the SETD4+/- genotype，SETD4+/- heterozygous mice were inbred and then the SETD4-/- homozygous mice were gained. PCR was used to identify the genotype of the offspring，the expression of SETD4 mRNA was detected by RT-PCR and qPCR，and morphological changes of liver and lung were observed by HE staining. Result PCR results showed genotypes of the offspring of SETD4 gene knockout mice was in accordance with SETD4-/-. Compared with the wild type mice，expression of SETD4 mRNA in SETD4 gene knockout homozygous mice was significantly decreased，and morphological characteristics of liver and lung in SETD4 gene knockout homozygous mice had no significant changes. Conclusion Wehave successfully generated SETD4 gene knockout homozygous mice which can be used for study ofSETD4 function.
[1] Stephen S. Care planning for independence [J]. Provider, 2000, 26(9): 2-3.
[2] Xiao B, Wilson JR, Gamblin SJ. SET domains and histone methylation [J]. Curr Opin Struct Biol, 2003, 13(6): 699-705.
[3] Keating ST, El-Osta A. Transcriptional regulation by Set7 lysine methyltransferse [J]. Epigenetics, 2013, 8(4): 361-372.
[4] Blecher-Gonen R, Amit I. M (odu) LLating the innate response [J]. Immunity, 2012, 36(4): 551-552.
[5] Austenaa L, Barozzi I, Chronowska A, et al. The histone methyltransferase Wbp7 controls macrophage function through GPI glycolipid anchor synthesis [J]. Immunity, 2012, 36(4): 572-585.
[6] Liu Y, Zhang Q, Ding Y, et al. Histone lysine methyltransferase Ezh1 promotes TLR-triggered inflammatory cytokine production by suppressing Tollip [J]. J Immunol, 2015, 194(6): 2838-2846.
[7] Chang Y, Levy D, Horton JR, et al. Structural basis of SETD6-mediated regulation of the NF-κB network via methyl-lysine signaling [J]. Nucleic Acids Res, 2011, 39(15): 6380-6389.
[8] Levy D, Kuo AJ, Chang Y, et al. SETD6 lysine methylation of RelA couples GLP activity at chromatin to tonic repression of NF-κB signaling [J]. Nat Immunol, 2011, 12(1): 29-36.
[9] Chen Z, Yan CT, Dou Y, et al. The role of a newly identified SET domain-containing protein, SETD3, in oncogenesis [J]. Haematologica, 2013, 98(5): 739-743.
[10]Bayarsaihan D. Epigenetic mechanisms in inflammation [J]. J Dent Res, 2011, 90(1): 9-17.
[11]Wilson AG. Epigenetic regulation of gene expression in the inflammatory response and relevance to common diseases [J]. J Periodontol, 2008, 79(8 Suppl): 1514-1519.
[12] Faria JA, Corrêa NC, de Andrade C, et al. SET domain-containing protein 4 (SETD4) is a newly identified cytosolic and nuclear lysine methyltransferase involved in breast cancer cell proliferation [J]. J Cancer Sci Ther, 2014, 5(2): 58-65.
[13] 叶萍, 蔡军伟, 付晓霞, 等. p38信号通路对SETD4在细胞中的表达和定位的影响[J]. 中国病理生理杂志, 2012, 28(5): 878-883.
[14] 雷烨铭, 崔航, 钟玙沄, 等. SETD4蛋白在Bac-to-Bac杆状病毒系统的表达[J]. 中国临床解剖学杂志, 2015, 33(4): 426-429.
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