[1] Anderson ME. Update on Survival in Osteosarcoma. Orthop Clin North Am, 2016; 47, 283-92. doi:  10.1016/j.ocl.2015.08.022
[2] Berner K, Hall KS, Monge OR, et al. Prognostic factors and treatment results of high-grade osteosarcoma in norway:a scope beyond the 'classical' patient. Sarcoma, 2015; 2015, 516843. https://www.hindawi.com/journals/sarcoma/2015/516843/fig3/
[3] Ferrari S, Serra M. An update on chemotherapy for osteosarcoma. Expert Opin Pharmacother, 2015; 16, 2727-36. doi:  10.1517/14656566.2015.1102226
[4] Broadhead ML, Clark JC, Myers DE, et al. The molecular pathogenesis of osteosarcoma:a review. Sarcoma, 2011; 2011, 959248. http://www.oalib.com/paper/3080985
[5] Weissman AM. Regulating protein degradation by ubiquitination. Immunol Today, 1997; 18, 189-98. doi:  10.1016/S0167-5699(97)84666-X
[6] Hatakeyama S. TRIM proteins and cancer. Nat Rev Cancer, 2011; 11, 792-804. doi:  10.1038/nrc3139
[7] Ozato K, Shin DM, Chang TH, et al. TRIM family proteins and their emerging roles in innate immunity. Nat Rev Immunol, 2008; 8, 849-60. doi:  10.1038/nri2413
[8] Zhang Z, Bao M, Lu N, et al. The E3 ubiquitin ligase TRIM21 negatively regulates the innate immune response to intracellular double-stranded DNA. Nat Immunol, 2013; 14, 172-8. https://www.sigmaaldrich.com/catalog/papers/23222971
[9] Reddy BA, van der Knaap JA, Bot AG, et al. Nucleotide biosynthetic enzyme GMP synthase is a TRIM21-controlled relay of p53 stabilization. Mol Cell, 2014; 53, 458-70. doi:  10.1016/j.molcel.2013.12.017
[10] McEwan WA, James LC. TRIM21-dependent intracellular antibody neutralization of virus infection. Prog Mol Biol Transl Sci, 2015; 129, 167-87. doi:  10.1016/bs.pmbts.2014.10.006
[11] Kyriakidis NC, Kapsogeorgou EK, Gourzi VC, et al. Toll-like receptor 3 stimulation promotes Ro52/TRIM21 synthesis and nuclear redistribution in salivary gland epithelial cells, partially via type Ⅰ interferon pathway. Clin Exp Immunol, 2014; 178, 548-60. doi:  10.1111/cei.2014.178.issue-3
[12] Nguyen JQ, Irby RB. TRIM21 is a novel regulator of Par-4 in colon and pancreatic cancer cells. Cancer Biol Ther, 2017; 18, 16-25. doi:  10.1080/15384047.2016.1252880
[13] Muller J, Maurer V, Reimers K, et al. TRIM21, a negative modulator of LFG in breast carcinoma MDA-MB-231 cells in vitro. Int J Oncol, 2015; 47, 1634-46. doi:  10.3892/ijo.2015.3169
[14] Wada K, Niida M, Tanaka M, et al. Ro52-mediated monoubiquitination of IKK{beta} down-regulates NF-{kappa}B signalling. J Biochem, 2009; 146, 821-32. doi:  10.1093/jb/mvp127
[15] Gao X, Xu F, Zhang HT, et al. PKCalpha-GSK3beta-NF-kappaB signaling pathway and the possible involvement of TRIM21 in TRAIL-induced apoptosis. Biochem Cell Biol, 2016; 94, 256-64. doi:  10.1139/bcb-2016-0009
[16] Jauharoh SN, Saegusa J, Sugimoto T, et al. SS-A/Ro52 promotes apoptosis by regulating Bcl-2 production. Biochem Biophys Res Commun, 2012; 417, 582-7. doi:  10.1016/j.bbrc.2011.12.010
[17] Shibata N, Ohoka N, Sugaki Y, et al. Degradation of Stop Codon Read-through Mutant Proteins via the Ubiquitin-Proteasome System Causes Hereditary Disorders. J Biol Chem, 2015; 290, 28428-37. doi:  10.1074/jbc.M115.670901
[18] Espinosa A, Zhou W, Ek M, et al. The Sjogren's syndrome-associated autoantigen Ro52 is an E3 ligase that regulates proliferation and cell death. J Immunol, 2006; 176, 6277-85. doi:  10.4049/jimmunol.176.10.6277
[19] Ding Q, He D, He K, et al. Downregulation of TRIM21 contributes to hepatocellular carcinoma carcinogenesis and indicates poor prognosis of cancers. Tumour Biol, 2015; 36, 8761-72. doi:  10.1007/s13277-015-3572-2
[20] Brauner S, Zhou W, Backlin C, et al. Reduced expression of TRIM21/Ro52 predicts poor prognosis in diffuse large B-cell lymphoma patients with and without rheumatic disease. J Intern Med, 2015; 278, 323-32. doi:  10.1111/joim.2015.278.issue-3
[21] Xue M, Tao W. Upregulation of MUC1 by its novel activator 14-3-3zeta promotes tumor invasion and indicates poor prognosis in lung adenocarcinoma. Oncol Rep, 2017; 38, 2637-46. doi:  10.3892/or.2017.5948
[22] Obsilova V, Kopecka M, Kosek D, et al. Mechanisms of the 14-3-3 protein function:regulation of protein function through conformational modulation. Physiol Res, 2014; 63, S155-64. http://www.academia.edu/12485797/Mechanisms_of_the_14-3-3_protein_function_Regulation_of_protein_function_through_conformational_modulation
[23] Wu YJ, Jan YJ, Ko BS, et al. Involvement of 14-3-3 Proteins in Regulating Tumor Progression of Hepatocellular Carcinoma. Cancers (Basel), 2015; 7, 1022-36. doi:  10.3390/cancers7020822
[24] Watanabe N, Komatsu S, Ichikawa D, et al. Overexpression of YWHAZ as an independent prognostic factor in adenocarcinoma of the esophago-gastric junction. Am J Cancer Res, 2016; 6, 2729-36. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5126287
[25] Ruenauver K, Menon R, Svensson MA, et al. Prognostic significance of YWHAZ expression in localized prostate cancer. Prostate Cancer Prostatic Dis, 2014; 17, 310-4. doi:  10.1038/pcan.2014.32
[26] Nishimura Y, Komatsu S, Ichikawa D, et al. Overexpression of YWHAZ relates to tumor cell proliferation and malignant outcome of gastric carcinoma. Br J Cancer, 2013; 108, 1324-31. doi:  10.1038/bjc.2013.65
[27] Neal CL, Yao J, Yang W, et al. 14-3-3zeta overexpression defines high risk for breast cancer recurrence and promotes cancer cell survival. Cancer Res, 2009; 69, 3425-32. doi:  10.1158/0008-5472.CAN-08-2765
[28] Gao X, Feng J, He Y, et al. hnRNPK inhibits GSK3beta Ser9 phosphorylation, thereby stabilizing c-FLIP and contributes to TRAIL resistance in H1299 lung adenocarcinoma cells. Sci Rep, 2016; 6, 22999. doi:  10.1038/srep22999
[29] Gao X, Wang JY, Gao LM, et al. Identification and analysis of glycogen synthase kinase 3 beta1 interactome. Cell Biol Int, 2013; 37, 768-79. doi:  10.1002/cbin.v37.8
[30] Varjosalo M, Sacco R, Stukalov A, et al. Interlaboratory reproducibility of large-scale human protein-complex analysis by standardized AP-MS. Nat Methods, 2013; 10, 307-14. doi:  10.1038/nmeth.2400
[31] Gao X, Dan S, Xie Y, et al. 14-3-3ζ reduces DNA damage by interacting with and stabilizing proliferating cell nuclear antigen. J Cell Biochem, 2015; 116, 158-69. doi:  10.1002/jcb.v116.1
[32] Huang WS, Xu FM, Zeng QZ, et al. ERK1/2-mediated Cytoplasmic Accumulation of hnRNPK Antagonizes TRAIL-induced Apoptosis through Upregulation of XIAP in H1299 Cells. Biomed Environ Sci, 2017; 30, 473-81. http://www.sciencedirect.com/science/article/pii/S0895398817300818
[33] Pratt EP, Owens JL, Hockerman GH, et al. Bimolecular Fluorescence Complementation (BiFC) Analysis of Protein-Protein Interactions and Assessment of Subcellular Localization in Live Cells. Methods Mol Biol, 2016; 1474, 153-70. doi:  10.1007/978-1-4939-6352-2
[34] Kodama Y, Hu CD. Bimolecular fluorescence complementation (BiFC):a 5-year update and future perspectives. Biotechniques, 2012; 53, 285-98. doi:  10.2144/000113943
[35] Joazeiro CA, Weissman AM. RING finger proteins:mediators of ubiquitin ligase activity. Cell, 2000; 102, 549-52. doi:  10.1016/S0092-8674(00)00077-5
[36] Kubben FJ, Peeters-Haesevoets A, Engels LG, et al. Proliferating cell nuclear antigen (PCNA):a new marker to study human colonic cell proliferation. Gut, 1994; 35, 530-5. doi:  10.1136/gut.35.4.530
[37] Lau JM, Wu C, Muslin AJ. Differential role of 14-3-3 family members in Xenopus development. Dev Dyn, 2006; 235, 1761-76. doi:  10.1002/dvdy.v235:7
[38] Muslin AJ, Lau JM. Differential functions of 14-3-3 isoforms in vertebrate development. Curr Top Dev Biol, 2005; 65, 211-28.
[39] Joshi S, Yang J, Wang Q, et al. 14-3-3zeta loss impedes oncogene-induced mammary tumorigenesis and metastasis by attenuating oncogenic signaling. Am J Cancer Res, 2017; 7, 1654-64. http://www.ajcr.us/files/ajcr0026751.pdf