Advanced glycation endproducts induce podocyte apoptosis by activation of the FOXO4 transcription factor
Open Access
- 1 October 2007
- journal article
- Published by Elsevier BV in Kidney International
- Vol. 72 (8), 965-976
- https://doi.org/10.1038/sj.ki.5002456
Abstract
No abstract availableThis publication has 36 references indexed in Scilit:
- Advanced glycation end products stimulate osteoblast apoptosis via the MAP kinase and cytosolic apoptotic pathwaysBone, 2007
- Advanced glycation end products induce apoptosis in fibroblasts through activation of ROS, MAP kinases, and the FOXO1 transcription factorAmerican Journal of Physiology-Cell Physiology, 2007
- Advanced glycation end product (AGE) receptor 1 suppresses cell oxidant stress and activation signaling via EGF receptorProceedings of the National Academy of Sciences of the United States of America, 2006
- The podocyte's response to injury: Role in proteinuria and glomerulosclerosisKidney International, 2006
- Role of p38 Mitogen-Activated Protein Kinase Activation in Podocyte Injury and Proteinuria in Experimental Nephrotic SyndromeJournal of the American Society of Nephrology, 2005
- Phosphorylation of p66Shc and forkhead proteins mediates Aβ toxicityThe Journal of cell biology, 2005
- Stress-Dependent Regulation of FOXO Transcription Factors by the SIRT1 DeacetylaseScience, 2004
- Prevention of diabetic nephropathy in mice by a diet low in glycoxidation productsDiabetes/Metabolism Research and Reviews, 2002
- FKHR-L1 can act as a critical effector of cell death induced by cytokine withdrawalThe Journal of cell biology, 2002
- Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT MethodMethods, 2001