|
1）Inagi R. Endoplasmic reticulum stress as a progression factor for kidney injury. Curr Opin Pharmacol. 2010; 10: 156-65
|
|
|
|
2）Ostergaard L, Simonsen U, Eskildsen-Helmond Y, et al. Proteomics reveals lowering oxygen alters cytoskeletal and endoplasmatic stress proteins in human endothelial cells. Proteomics. 2009; 9: 4457-67
|
|
|
|
|
|
3）Werno C, Zhou J, Brüne B. A23187, ionomycin and thapsigargin upregulate mRNA of HIF-1alpha via endoplasmic reticulum stress rather than a rise in intracellular calcium. J Cell Physiol. 2008; 215: 708-14
|
|
|
|
|
|
4）Rzymski T, Petry A, Kračun D, et al. The unfolded protein response controls induction and activation of ADAM17/TACE by severe hypoxia and ER stress. Oncogene. 2012; 31: 3621-34
|
|
|
|
|
|
5）Digaleh H, Kiaei M, Khodagholi F. Nrf2 and Nrf1 signaling and ER stress crosstalk: implication for proteasomal degradation and autophagy. Cell Mol Life Sci. 2013; 70: 4681-94
|
|
|
|
|
|
6）Hotamisligil GS. Endoplasmic reticulum stress and the inflammatory basis of metabolic disease. Cell. 2010; 140: 900-17
|
|
|
|
|
|
7）Nakajima S, Kitamura M. Bidirectional regulation of NF-κB by reactive oxygen species: A role of unfolded protein response. Free Radic Biol Med. 2013; 65C: 162-74
|
|
|
|
|
|
8）Shay JE, Celeste Simon M. Hypoxia-inducible factors: crosstalk between inflammation and metabolism. Semin Cell Dev Biol. 2012; 23: 389-94
|
|
|
|
|
|
9）Bruning U, Fitzpatrick SF, Frank T, et al. NF-κB and HIF display synergistic behaviour during hypoxic inflammation. Cell Mol Life Sci. 2012; 69: 1319-29
|
|
|
|
|
|
10）Chiang CK, Nangaku M, Tanaka T, et al. Endoplasmic reticulum stress signal impairs erythropoietin production: a role for ATF4. Am J Physiol Cell Physiol. 2013; 304: C342-53
|
|
|
|
|
|
11）Nitta K, Iimuro S, Imai E, et al. Risk factors for increased left ventricular hypertrophy in patients with chronic kidney disease. Clin Exp Nephrol. 2013; 17: 730-42
|
|
|
|
|
12）Akizawa T, Makino H, Matsuo S, et al. Management of anemia in chronic kidney disease patients: baseline findings from Chronic Kidney Disease Japan Cohort Study. Clin Exp Nephrol. 2011; 15: 248-57
|
|
|
|
|
|
13）Tanaka T, Yamaguchi J, Higashijima Y, et al. Indoxyl sulfate signals for rapid mRNA stabilization of Cbp/p300-interacting transactivator with Glu/Asp-rich carboxy-terminal domain 2 (CITED2) and suppresses the expression of hypoxia-inducible genes in experimental CKD and uremia. FASEB J. 2013; 27: 4059-75
|
|
|
|
|
|
14）Kawakami T, Inagi R, Wada T, et al. Indoxyl sulfate inhibits proliferation of human proximal tubular cells via endoplasmic reticulum stress. Am J Physiol Renal Physiol. 2010; 299: F568-76
|
|
|
|
|
|
15）Mimura I, Nangaku M, Kanki Y, et al. Dynamic change of chromatin conformation in response to hypoxia enhances the expression of GLUT3 (SLC2A3) by cooperative interaction of hypoxia-inducible factor 1 and KDM3A. Mol Cell Biol. 2012; 32: 3018-32
|
|
|
|
|
|
16）Kulshreshtha R, Ferracin M, Wojcik SE, et al. A microRNA signature of hypoxia. Mol Cell Biol. 2007; 27: 1859-67
|
|
|
|
|
|
17）Muratsu-Ikeda S, Nangaku M, Ikeda Y, et al.Downregulation of miR-205 modulates cell susceptibility to oxidative and endoplasmic reticulum stresses in renal tubular cells. PLoS One. 2012; 7: e41462
|
|
|
|
|
|
18）Huber AL, Lebeau J, Guillaumot P, et al. p58(IPK)-mediated attenuation of the proapoptotic PERK-CHOP pathway allows malignant progression upon low glucose. Mol Cell. 2013; 49: 1049-59
|
|
|
|
|
|
19）Young RM, Ackerman D, Quinn ZL, et al. Dysregulated mTORC1 renders cells critically dependent on desaturated lipids for survival under tumor-like stress. Genes Dev. 2013; 27: 1115-31
|
|
|
|
|
|
20）Friedman JR, Lackner LL, West M, et al. ER tubules mark sites of mitochondrial division. Science. 2011; 334: 358-62
|
|
|
|
|
|
21）De Raedt T, Walton Z, Yecies JL, et al. Exploiting cancer cell vulnerabilities to develop a combination therapy for ras-driven tumors. Cancer Cell. 2011; 20: 400-13
|
|
|
|
|