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10.1093/hmg/ddw073 http://scihub22266oqcxt.onion/10.1093/hmg/ddw073 C5062587!5062587 !26962150     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26962150 &cmd=llinks): Failed to open stream: HTTP request failed! 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A small-molecule Nrf1 and Nrf2 activator mitigates polyglutamine toxicity in spinal and bulbar muscular atrophy |pdf=|usr=}}{{26962150 }} gab.com Text A small-molecule Nrf1 and Nrf2 activator mitigates polyglutamine toxicity in spinal and bulbar muscular atrophy JO: Hum Mol Genet http://www.kidney.de/pget.php?&tw=1&pmid=26962150 #FOAvip Spinal and bulbar muscular atrophy (SBMA, also known as Kennedy's disease) is one of nine neurodegenerative disorders that are caused by expansion of polyglutamine-encoding CAG repeats. Intracellular accumulation of abnormal proteins in these diseases, a pathological hallmark, is associated with defects in protein homeostasis. Enhancement of the cellular proteostasis capacity with small molecules has therefore emerged as a promising approach to treatment. Here, we characterize a novel curcumin analog, ASC-JM17, as an activator of central pathways controlling protein folding, degradation and oxidative stress resistance. ASC-JM17 acts on Nrf1, Nrf2 and Hsf1 to increase the expression of proteasome subunits, antioxidant enzymes and molecular chaperones. We show that ASC-JM17 ameliorates toxicity of the mutant androgen receptor (AR) responsible for SBMA in cell, fly and mouse models. Knockdown of the Drosophila Nrf1 and Nrf2 ortholog cap 'n' collar isoform-C, but not Hsf1, blocks the protective effect of ASC-JM17 on mutant AR-induced eye degeneration in flies. Our observations indicate that activation of the Nrf1/Nrf2 pathway is a viable option for pharmacological intervention in SBMA and potentially other polyglutamine diseases. Twit Text FOAVip A small-molecule Nrf1 and Nrf2 activator mitigates polyglutamine toxicity in spinal and bulbar muscular atrophy ????Hum Mol Genet http://www.kidney.de/pget.php?&tw=1&pmid=26962150 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26962150 #FOAvip English Wikipedia <ref>{{Cite pmid|26962150 }}</ref> A small-molecule Nrf1 and Nrf2 activator mitigates polyglutamine toxicity in spinal and bulbar muscular atrophy #MMPMID26962150 Bott LC ; Badders NM ; Chen KL ; Harmison GG ; Bautista E ; Shih CC ; Katsuno M ; Sobue G ; Taylor JP ; Dantuma NP ; Fischbeck KH ; Rinaldi C Hum Mol Genet 2016[May]; 25 (10 ): 1979-1989 PMID26962150 show ga Spinal and bulbar muscular atrophy (SBMA, also known as Kennedy's disease) is one of nine neurodegenerative disorders that are caused by expansion of polyglutamine-encoding CAG repeats. Intracellular accumulation of abnormal proteins in these diseases, a pathological hallmark, is associated with defects in protein homeostasis. Enhancement of the cellular proteostasis capacity with small molecules has therefore emerged as a promising approach to treatment. Here, we characterize a novel curcumin analog, ASC-JM17, as an activator of central pathways controlling protein folding, degradation and oxidative stress resistance. ASC-JM17 acts on Nrf1, Nrf2 and Hsf1 to increase the expression of proteasome subunits, antioxidant enzymes and molecular chaperones. We show that ASC-JM17 ameliorates toxicity of the mutant androgen receptor (AR) responsible for SBMA in cell, fly and mouse models. Knockdown of the Drosophila Nrf1 and Nrf2 ortholog cap 'n' collar isoform-C, but not Hsf1, blocks the protective effect of ASC-JM17 on mutant AR-induced eye degeneration in flies. Our observations indicate that activation of the Nrf1/Nrf2 pathway is a viable option for pharmacological intervention in SBMA and potentially other polyglutamine diseases. |Animals [MESH] |Bulbo-Spinal Atrophy, X-Linked/drug therapy/*genetics/pathology [MESH] |Curcumin/administration & dosage/*analogs & derivatives/chemistry [MESH] |DNA-Binding Proteins/*genetics [MESH] |Disease Models, Animal [MESH] |Drosophila Proteins/*genetics [MESH] |Drosophila melanogaster/genetics [MESH] |Gene Knockdown Techniques [MESH] |Heat Shock Transcription Factors [MESH] |Humans [MESH] |Mice [MESH] |Muscular Disorders, Atrophic/drug therapy/*genetics/pathology [MESH] |NF-E2-Related Factor 1/*genetics [MESH] |NF-E2-Related Factor 2/*genetics [MESH] |Oxidative Stress/drug effects [MESH] |Peptides/genetics [MESH] |Proteasome Endopeptidase Complex/drug effects [MESH] |Protein Aggregation, Pathological/genetics [MESH] |Protein Folding/drug effects [MESH] |Receptors, Androgen/*genetics [MESH] |Signal Transduction/drug effects [MESH] |Small Molecule Libraries/administration & dosage [MESH] |Transcription Factors/*genetics [MESH]A small-molecule Nrf1 and Nrf2 activator mitigates polyglutamine toxic(epmc).pdf DeepDyve Pubget Overpricing