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| 1 | Differential protection with inhibitors of caspase-8 and caspase-3 in murine models of tumor necrosis factor and Fas receptor-mediated hepatocellular apoptosis显示文摘 | Bajt M L Vonderfecht S L Jaeschke H | 2001 | Toxicol Appl Pharmacol2001，175，3： | 1 |
| 2 | Differential protection with inhibitors of caspase-8 and caspase-3 in murine models of tumor necrosis factor and Fas receptor-mediated hepatocellular apoptosis显示文摘 | BAJT ML VONDERFECHT SL JAESCHKE H | 2001 | Toxicol Appl Pharmacol2001，175，3： | 1 |
| 3 | Differential Protection with Inhibitors of Caspase-8 and Caspase-3 in Murine Models of Tumor Necrosis Factor and Fas Receptor-Mediated Hepatocellular Apoptosis显示文摘 | Steven L Vonderfecht | 2001 | Toxicology and Applied Pharmacology2001，175，： | 1 |
| 4 | Virus-specific immunity in neonatal and adult mouse rotavius infect显示文摘 | Sheridan JF Eydelloth RS Vonderfecht SL | 1983 | Infect Immun1983，39，2： | 1 |
| 5 | Transcriptional activation of vascular cell adhesion molecule-1 (VCAM-1) gene in vivo and its role in the pathophyilogy of neutrophil-induced liver injury in murine endotoxin shock 显示文摘 | Essani NA Bait ML Vonderfecht SL | 1997 | J Immunol1997，158，： | 1 |
| 6 | Infectious diarrhea of infant rats produced by a rotavirus-like agent显示文摘 | Vonderfecht S L Huber A C Eiden J | 1984 | J Virol1984，52，： | 1 |
| 7 | Substitution of DNA-contacting amino acids with functional variants in the Gata-1 zinc finger: A structurally and phylogenetically guided mutagenesis显示文摘 | Vonderfecht T R Schroyer D C Schenck B L | 2008 | Biochem Biophys Res Commun2008，369，： | 1 |
| 8 | Protease inhibitors suppress the in vitro and in vivo replication ofrotavirus显示文摘 | Vonderfecht S I Miskuff RI Wee S B | 1988 | Clin Invest1988，82，： | 1 |
| 9 | Protease inhibitors supperss the in vitro and in vivo replication of rotavirus 显示文摘 | Vonderfecht S L Miskuff S B Wee S | 1988 | J Clin Invest1988，82，： | 1 |
| 10 | Protease inhibitots suppress the in vitro and in vivo replication of rotavirus 显示文摘 | Vonderfecht S L Miskuff R L Wee S B | 1988 | J Clin Invest1988，82，： | 1 |
| 11 | Diferential p tection with inh ibitors of caspase-8 and caspase-3 in murine models of tumor necrosis factor an d Fas receptor-mediated hepa-tocelular apoptosis显示文摘 | BAIT ML'VONDERFECHT SL JAESCHKE H | 2001 | Toxicol Appl Pharmacol2001，175，3： | 1 |
| 12 | Transcriptional activation of vascular cell adhesion molecule 21 (VCAM21) gene in vivo and it's role in the pathophysiolgy of neutrophil-induced liver injury in murine endotoxin shock 显示文摘 | Essani NA Bait ML Vonderfecht SL | 1997 | J Immunol1997，158，12： | 1 |
| 13 | Differential protection with inhibitors of caspase-8 and caspase-3 in murine models of tumor necrosis factor and Fas receptor-mediated hepatocellular apoptosis 显示文摘 | Bajt M L Vonderfecht S L Jaeschke H | 2001 | Toxicol Appl Pharmacol2001，175，3： | 1 |
| 14 | The 21-aminosteroid tirilazad mesylate protects against endotoxin shock and acute liver failure in rats显示文摘 | Liu P Vonderfecht SL McGuire GM | 1994 | J Pharmacol Exp Ther1994，271，1： | 1 |
| 15 | Protease inhibitors suppress the invitro and invivo replication of rotavirus显示文摘 | Vonderfecht S L Miskuff S B Wee S | | 0，，： | 1 |
| 16 | Protease inhibitors suppress the invitro and invivo replication of rotavirus显示文摘 | Vonderfecht S L Miskuff S B Wee S | | 0，，： | 1 |
| 17 | Differential protection with inhibitors of caspase-8 and caspase-3 in murine models of tumor necrosis factor and Fas receptor-mediated hepatocellular apoptosis 显示文摘 | Bajt ML Vonderfecht SL Jaeschke H | 2001 | Toxicol Appl Pharmacol2001，175，3： | 1 |
| 18 | Protease inhibitors suppress the in vitro and in vivo replication of rotavirus显示文摘 | Vonderfecht S L Miskuff S B Wee S | 1988 | J Clin Invest1988，82，： | 1 |
| 19 | Protease inhibitors suppress the in vitro and in vivo replication of rotavirus显示文摘 | Vonderfecht S L Miskuff S B Wee S | 1988 | J Clin Invest1988，82，： | 1 |
| 20 | Identification of neuron selective androgen receptor inhibitors显示文摘AIM To identify neuron-selective androgen receptor(AR) signaling inhibitors, which could be useful in the treatment of spinal and bulbar muscular atrophy(SBMA), or Kennedy's disease, a neuromuscular disorder in which deterioration of motor neurons leads to progressive muscle weakness. METHODS Cell lines representing prostate, kidney, neuron, adipose, and muscle tissue were developed that stably expressed the CFP-AR-YFP FRET reporter. We used these cells to screen a library of small molecules for cell typeselective AR inhibitors. Secondary screening in luciferase assays was used to identify the best cell-type specific AR inhibitors. The mechanism of action of a neuronselective AR inhibitor was examined in vitro using luciferase reporter assays, immunofluorescence microscopy, and immunoprecipitations. Rats were treated with the most potent compound and tissue-selective AR inhibition was examined using RT-q PCR of AR-regulated genes and immunohistochemistry.RESULTS We identified the thiazole class of antibiotics as com-pounds able to inhibit AR signaling in a neuronal cell line but not a muscle cell line. One of these antibiotics, thiostrepton is able to inhibit the activity of both wild type and polyglutamine expanded AR in neuronal GT1-7 cells with nanomolar potency. The thiazole antibiotics are known to inhibit FOXM1 activity and accordingly, a novel FOXM1 inhibitor FDI-6 also inhibited AR activity in a neuron-selective fashion. The selective inhibition of AR is likely indirect as the varied structures of these compounds would not suggest that they are competitive antagonists. Indeed, we found that FOXM1 expression correlates with cell-type selectivity, FOXM1 co-localizes with AR in the nucleus, and that sh RNA-mediated knock down of FOXM1 reduces AR activity and thiostrepton sensitivity in a neuronal cell line. Thiostrepton treatment reduces FOXM1 levels and the nuclear localization of beta-catenin, a known co-activator of both FOXM1 and AR, and reduces the association between beta-catenin and AR. Treatment of rats with thiostrepton demonstrated AR signaling inhibition in neurons, but not muscles. CONCLUSION Our results suggest that thiazole antibiotics, or other inhibitors of the AR-FOXM1 axis, can inhibit AR signaling selectively in motor neurons and may be useful in the treatment or prevention of SBMA symptoms. | Maya Otto-Duessel Ben Yi Tew Steven Vonderfecht Roger Moore Jeremy O Jones | 2017 | World Journal of Biological Chemistry2017，8，2： | 0 |
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