Cyclin-dependent kinase 1-mediated phosphorylation of SET at serine 7 is essential for its oncogenic activity
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Hong Shen | Yuanhong Chen | Jixin Dong | Yi Xiao | L. Yin | Yongji Zeng
[1] Ana C. Henriques,et al. Mitosis inhibitors in anticancer therapy: When blocking the exit becomes a solution. , 2019, Cancer letters.
[2] S. Lele,et al. Zyxin promotes colon cancer tumorigenesis in a mitotic phosphorylation-dependent manner and through CDK8-mediated YAP activation , 2018, Proceedings of the National Academy of Sciences.
[3] Kuen-Feng Chen,et al. Antagonizing SET Augments the Effects of Radiation Therapy in Hepatocellular Carcinoma through Reactivation of PP2A-Mediated Akt Downregulation , 2018, The Journal of Pharmacology and Experimental Therapeutics.
[4] K. Ye,et al. CK2 Phosphorylating I2PP2A/SET Mediates Tau Pathology and Cognitive Impairment , 2018, Front. Mol. Neurosci..
[5] K. Ye,et al. CK2 Phosphorylating I2PP2A/SET Mediates Tau Pathology and Cognitive Impairment , 2018, Frontiers in Molecular Neuroscience.
[6] Jiuli Zhou,et al. CDK1-mediated mitotic phosphorylation of PBK is involved in cytokinesis and inhibits its oncogenic activity. , 2017, Cellular signalling.
[7] D. Reinberg,et al. Phospho-H1 Decorates the Inter-chromatid Axis and Is Evicted along with Shugoshin by SET during Mitosis. , 2017, Molecular cell.
[8] Xiaoyong Li,et al. Regulation of SET Gene Expression by NFkB , 2016, Molecular Neurobiology.
[9] Shi-Wen Jiang,et al. Oncogenic Role of SET/I2PP2A for Gynecologic Cancers. , 2017, Current drug targets.
[10] H. Mody,et al. SET contributes to the epithelial-mesenchymal transition of pancreatic cancer , 2017, Oncotarget.
[11] Kuen-Feng Chen,et al. Reprogramming the oncogenic response: SET protein as a potential therapeutic target in cancer , 2017, Expert opinion on therapeutic targets.
[12] C. Shiau,et al. Upregulation of the oncoprotein SET determines poor clinical outcomes in hepatocellular carcinoma and shows therapeutic potential , 2016, Oncogene.
[13] Yuanhong Chen,et al. Ajuba Phosphorylation by CDK1 Promotes Cell Proliferation and Tumorigenesis* , 2016, The Journal of Biological Chemistry.
[14] T. Mak,et al. Targeting Mitosis in Cancer: Emerging Strategies. , 2015, Molecular cell.
[15] Kuen-Feng Chen,et al. SET antagonist enhances the chemosensitivity of non-small cell lung cancer cells by reactivating protein phosphatase 2A , 2015, Oncotarget.
[16] M. Gleave,et al. Inhibition of Pten deficient Castration Resistant Prostate Cancer by Targeting of the SET - PP2A Signaling axis , 2015, Scientific Reports.
[17] Nicholas Y. Palermo,et al. The Hippo Pathway Effector YAP Regulates Motility, Invasion, and Castration-Resistant Growth of Prostate Cancer Cells , 2015, Molecular and Cellular Biology.
[18] Bin Zhang,et al. PhosphoSitePlus, 2014: mutations, PTMs and recalibrations , 2014, Nucleic Acids Res..
[19] F. Rojo,et al. Deregulation of the PP2A Inhibitor SET Shows Promising Therapeutic Implications and Determines Poor Clinical Outcome in Patients with Metastatic Colorectal Cancer , 2014, Clinical Cancer Research.
[20] Colin J. Daniel,et al. Targeting c-MYC by antagonizing PP2A inhibitors in breast cancer , 2014, Proceedings of the National Academy of Sciences.
[21] R. Sears,et al. Antagonism of SET Using OP449 Enhances the Efficacy of Tyrosine Kinase Inhibitors and Overcomes Drug Resistance in Myeloid Leukemia , 2014, Clinical Cancer Research.
[22] Miao Liu,et al. CDK1 phosphorylation of YAP promotes mitotic defects and cell motility and is essential for neoplastic transformation. , 2013, Cancer research.
[23] M. Caligiuri,et al. PP2A-activating drugs selectively eradicate TKI-resistant chronic myeloid leukemic stem cells. , 2013, The Journal of clinical investigation.
[24] M. Caligiuri,et al. Antagonistic activities of the immunomodulator and PP2A-activating drug FTY720 (Fingolimod, Gilenya) in Jak2-driven hematologic malignancies. , 2013, Blood.
[25] Jian-Zhi Wang,et al. Ser9 phosphorylation causes cytoplasmic detention of I2 PP2A/SET in Alzheimer disease , 2013, Neurobiology of Aging.
[26] Zhenbo Wang,et al. Overexpression of SET&bgr;, a protein localizing to centromeres, causes precocious separation of chromatids during the first meiosis of mouse oocytes , 2013, Journal of Cell Science.
[27] M. Ji,et al. KIBRA Regulates Aurora Kinase Activity and Is Required for Precise Chromosome Alignment During Mitosis* , 2012, The Journal of Biological Chemistry.
[28] M. Malumbres,et al. Killing cells by targeting mitosis , 2012, Cell Death and Differentiation.
[29] M. Vitek,et al. SET oncoprotein overexpression in B-cell chronic lymphocytic leukemia and non-Hodgkin lymphoma: a predictor of aggressive disease and a new treatment target. , 2011, Blood.
[30] R. Medema,et al. Mitosis as an anti-cancer target , 2011, Oncogene.
[31] D. Hanahan,et al. Hallmarks of Cancer: The Next Generation , 2011, Cell.
[32] M. Ji,et al. KIBRA Regulates Hippo Signaling Activity via Interactions with Large Tumor Suppressor Kinases* , 2011, The Journal of Biological Chemistry.
[33] D. Wink,et al. Targeting SET/I2PP2A Oncoprotein Functions as a Multi-pathway Strategy for Cancer Therapy , 2010, Oncogene.
[34] Z. Szallasi,et al. An online survival analysis tool to rapidly assess the effect of 22,277 genes on breast cancer prognosis using microarray data of 1,809 patients , 2010, Breast Cancer Research and Treatment.
[35] S. Brunak,et al. Quantitative Phosphoproteomics Reveals Widespread Full Phosphorylation Site Occupancy During Mitosis , 2010, Science Signaling.
[36] D. Cleveland,et al. Boveri revisited: chromosomal instability, aneuploidy and tumorigenesis , 2009, Nature Reviews Molecular Cell Biology.
[37] S. Elledge,et al. A quantitative atlas of mitotic phosphorylation , 2008, Proceedings of the National Academy of Sciences.
[38] G. Feldmann,et al. Elucidation of a Universal Size-Control Mechanism in Drosophila and Mammals , 2007, Cell.
[39] M. Mumby. PP2A: Unveiling a Reluctant Tumor Suppressor , 2007, Cell.
[40] O. Bachs,et al. Proteomic analysis of SET‐binding proteins , 2007, Proteomics.
[41] Tohru Natsume,et al. Shugoshin collaborates with protein phosphatase 2A to protect cohesin , 2006, Nature.
[42] Guido Marcucci,et al. The tumor suppressor PP2A is functionally inactivated in blast crisis CML through the inhibitory activity of the BCR/ABL-regulated SET protein. , 2005, Cancer cell.
[43] M. Hollingsworth,et al. Notch2-positive progenitors with the intrinsic ability to give rise to pancreatic ductal cells , 2005, Laboratory Investigation.
[44] G. Grosveld,et al. Effects of SET and SET-CAN on the differentiation of the human promonocytic cell line U937 , 2004, Leukemia.
[45] O. Bachs,et al. The SET Protein Regulates G2/M Transition by Modulating Cyclin B-Cyclin-dependent Kinase 1 Activity* , 2003, The Journal of Biological Chemistry.
[46] P. McNamara,et al. Regulation of Histone Acetylation and Transcription by INHAT, a Human Cellular Complex Containing the Set Oncoprotein , 2001, Cell.
[47] O. Bachs,et al. The Protein SET Regulates the Inhibitory Effect of p21Cip1 on Cyclin E-Cyclin-dependent Kinase 2 Activity* , 1999, The Journal of Biological Chemistry.
[48] K. Nagata,et al. Cellular localization and expression of template-activating factor I in different cell types. , 1998, Experimental cell research.
[49] Z. Damuni,et al. The Myeloid Leukemia-associated Protein SET Is a Potent Inhibitor of Protein Phosphatase 2A (*) , 1996, The Journal of Biological Chemistry.
[50] A. Murray,et al. Members of the NAP/SET family of proteins interact specifically with B- type cyclins , 1995, The Journal of cell biology.
[51] Hong Guo,et al. Purification and characterization of two potent heat-stable protein inhibitors of protein phosphatase 2A from bovine kidney. , 1995, Biochemistry.
[52] T. Copeland,et al. Identification of in vivo phosphorylation sites of SET, a nuclear phosphoprotein encoded by the translocation breakpoint in acute undifferentiated leukemia , 1994, FEBS letters.
[53] Erich A. Nigg,et al. Cellular substrates of p34cdc2 and its companion cyclin-dependent kinases , 1993 .
[54] Marieke,et al. Can, a putative oncogene associated with myeloid leukemogenesis, may be activated by fusion of its 3' half to different genes: characterization of the set gene , 1992, Molecular and cellular biology.
[55] G. Narla,et al. Therapeutic targeting of PP2A. , 2018, The international journal of biochemistry & cell biology.
[56] G. Collins. The next generation. , 2006, Scientific American.
[57] Z. Damuni,et al. I1PP2A and I2PP2A. Two potent protein phosphatase 2A-specific inhibitor proteins. , 1998, Methods in molecular biology.
[58] E. Nigg,et al. Cellular substrates of p34(cdc2) and its companion cyclin-dependent kinases. , 1993, Trends in cell biology.