MiRNA-29c regulates the expression of inflammatory cytokines in diabetic nephropathy by targeting tristetraprolin
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J. Zhao | Jia Guo | Zhangsuo Liu | Jing Xiao | Zhanzheng Zhao | Jing Li | Shuguang Yang | Luyao Wang | Genyang Cheng | Dong Liu
[1] L. Lanting,et al. Anti-Inflammatory Role of MicroRNA-146a in the Pathogenesis of Diabetic Nephropathy. , 2016, Journal of the American Society of Nephrology : JASN.
[2] Wan-Chun Li,et al. Differential microRNA Profiles Predict Diabetic Nephropathy Progression in Taiwan , 2016, International journal of medical sciences.
[3] Fan Yao,et al. 5'-Monophosphate-activated protein kinase (AMPK) improves autophagic activity in diabetes and diabetic complications , 2015, Acta pharmaceutica Sinica. B.
[4] A. Bhatti,et al. Drug Targets for Oxidative Podocyte Injury in Diabetic Nephropathy , 2015, Cureus.
[5] Jia Guo,et al. The Expression of Tristetraprolin and Its Relationship with Urinary Proteins in Patients with Diabetic Nephropathy , 2015, PloS one.
[6] Yang Qu,et al. Circulating miR‐145 is associated with plasma high‐sensitivity C‐reactive protein in acute ischemic stroke patients , 2015, Cell biochemistry and function.
[7] S. Pan,et al. DNA methyltransferase 3, a target of microRNA-29c, contributes to neuronal proliferation by regulating the expression of brain-derived neurotrophic factor. , 2015, Molecular medicine reports.
[8] Hai Lin,et al. Lessons Learned from Whole Exome Sequencing in Multiplex Families Affected by a Complex Genetic Disorder, Intracranial Aneurysm , 2015, PloS one.
[9] Wei Wei,et al. Research progress in signalling pathway in diabetic nephropathy , 2015, Diabetes/metabolism research and reviews.
[10] Yan-ming Sun,et al. Recent advances in understanding the biochemical and molecular mechanism of diabetic retinopathy. , 2012, Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie.
[11] Jinlin Song,et al. Evaluation of miR-29c inhibits endotheliocyte migration and angiogenesis of human endothelial cells by suppressing the insulin like growth factor 1. , 2015, American journal of translational research.
[12] Jingqiu Cheng,et al. Involvement of inflammation-related miR-155 and miR-146a in diabetic nephropathy: implications for glomerular endothelial injury , 2014, BMC Nephrology.
[13] A. Rubio-Guerra,et al. Diabetic nephropathy and inflammation. , 2014, World journal of diabetes.
[14] Jia Guo,et al. The abnormal expressions of tristetraprolin and the VEGF family in uraemic rats with peritoneal dialysis , 2014, Molecular and Cellular Biochemistry.
[15] A. Bhansali,et al. Prevalence and risk factors of development of peripheral diabetic neuropathy in type 2 diabetes mellitus in a tertiary care setting , 2014, Journal of diabetes investigation.
[16] Jun Zhang,et al. Urinary miR-29 Correlates with Albuminuria and Carotid Intima-Media Thickness in Type 2 Diabetes Patients , 2013, PloS one.
[17] L. Tang,et al. miRNA-29c Suppresses Lung Cancer Cell Adhesion to Extracellular Matrix and Metastasis by Targeting Integrin β1 and Matrix Metalloproteinase2 (MMP2) , 2013, PloS one.
[18] Simon Lovell,et al. Phosphorylation of the Leukemic Oncoprotein EVI1 on Serine 196 Modulates DNA Binding, Transcriptional Repression and Transforming Ability , 2013, PloS one.
[19] Ying Sun,et al. MiR-29c suppresses invasion and metastasis by targeting TIAM1 in nasopharyngeal carcinoma. , 2013, Cancer letters.
[20] Yan-ming Sun,et al. Recent advances in understanding the biochemical and molecular mechanism of diabetic nephropathy. , 2013, Biochemical and biophysical research communications.
[21] Peiyong Jiang,et al. Inhibition of miR-29 by TGF-beta-Smad3 Signaling through Dual Mechanisms Promotes Transdifferentiation of Mouse Myoblasts into Myofibroblasts , 2012, PloS one.
[22] Merlin C. Thomas,et al. Suppression of microRNA-29 expression by TGF-β1 promotes collagen expression and renal fibrosis. , 2012, Journal of the American Society of Nephrology : JASN.
[23] Sandhya Sanduja,et al. The role of tristetraprolin in cancer and inflammation. , 2012, Frontiers in bioscience.
[24] M. Okusa,et al. Monocyte/macrophage chemokine receptor CCR2 mediates diabetic renal injury. , 2011, American journal of physiology. Renal physiology.
[25] Youhua Liu. Cellular and molecular mechanisms of renal fibrosis , 2011, Nature Reviews Nephrology.
[26] Chun-mei Wang,et al. miR-29c targets TNFAIP3, inhibits cell proliferation and induces apoptosis in hepatitis B virus-related hepatocellular carcinoma. , 2011, Biochemical and biophysical research communications.
[27] Cheuk-Man Yu,et al. TGF-β/Smad3 signaling promotes renal fibrosis by inhibiting miR-29. , 2011, Journal of the American Society of Nephrology : JASN.
[28] J. Long,et al. MicroRNA-29c Is a Signature MicroRNA under High Glucose Conditions That Targets Sprouty Homolog 1, and Its in Vivo Knockdown Prevents Progression of Diabetic Nephropathy* , 2011, The Journal of Biological Chemistry.
[29] C. Croce,et al. microRNAs: Master regulators as potential therapeutics in cancer. , 2011, Annual review of pharmacology and toxicology.
[30] A. Dick,et al. Mechanisms of TNFα regulation in uveitis: Focus on RNA-binding proteins , 2010, Progress in Retinal and Eye Research.
[31] Subbaya Subramanian,et al. MicroRNAs in Cardiovascular Diseases: Biology and Potential Clinical Applications , 2010, Journal of cardiovascular translational research.
[32] X. Chen,et al. Characterization of microRNAs in serum: a novel class of biomarkers for diagnosis of cancer and other diseases , 2008, Cell Research.
[33] Jeffrey E. Thatcher,et al. Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis , 2008, Proceedings of the National Academy of Sciences.
[34] Stefanie Dimmeler,et al. Role of microRNAs in vascular diseases, inflammation, and angiogenesis. , 2008, Cardiovascular research.
[35] S. Maeda. Do inflammatory cytokine genes confer susceptibility to diabetic nephropathy? , 2008, Kidney international.
[36] C. Burge,et al. The Widespread Impact of Mammalian MicroRNAs on mRNA Repression and Evolution , 2005, Science.
[37] G. Kollias,et al. MK2 Targets AU-rich Elements and Regulates Biosynthesis of Tumor Necrosis Factor and Interleukin-6 Independently at Different Post-transcriptional Levels* , 2002, The Journal of Biological Chemistry.
[38] Thomas D. Schmittgen,et al. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. , 2001, Methods.
[39] P. Blackshear,et al. Evidence that tristetraprolin is a physiological regulator of granulocyte-macrophage colony-stimulating factor messenger RNA deadenylation and stability. , 2000, Blood.
[40] P. Blackshear,et al. Feedback Inhibition of Macrophage Tumor Necrosis Factor-α Production by Tristetraprolin , 1998 .
[41] P. Blackshear,et al. Feedback inhibition of macrophage tumor necrosis factor-alpha production by tristetraprolin. , 1998, Science.
[42] R. Zeller,et al. Rearrangements of the cytoskeleton and cell contacts induce process formation during differentiation of conditionally immortalized mouse podocyte cell lines. , 1997, Experimental cell research.
[43] B. Haynes,et al. A pathogenetic role for TNF alpha in the syndrome of cachexia, arthritis, and autoimmunity resulting from tristetraprolin (TTP) deficiency. , 1996, Immunity.