有哪些信誉好的足球投注网站fission yeast 26s proteasome mutants are multi-drug resistant due to stabilization of the pap1 transcription factor裂殖酵母26 s蛋白酶体突变体耐多药是由于pap1转录因子的稳定.pdfVIP
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fission yeast 26s proteasome mutants are multi-drug resistant due to stabilization of the pap1 transcription factor裂殖酵母26 s蛋白酶体突变体耐多药是由于pap1转录因子的稳定
Fission Yeast 26S Proteasome Mutants Are Multi-Drug Resistant Due to Stabilization of the Pap1 Transcription Factor 1 1 2 3 5 Mary Penney , Itaru Samejima , Caroline R. Wilkinson , Christopher J. McInerny , Søs G. Mathiassen , 1 4 5 1 Mairi Wallace , Takashi Toda , Rasmus Hartmann-Petersen *, Colin Gordon * 1 Medical Research Council, Human Genetics Unit, Western General Hospital, Edinburgh, United Kingdom, 2 Cell Regulation Group, Paterson Institute for Cancer Research, University of Manchester, Manchester, United Kingdom, 3 Division of Molecular and Cellular Biology, School of Life Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom, 4 Laboratory of Cell Regulation, Cancer Research UK, London Research Institute, Lincoln’s Inn Fields Laboratories, London, United Kingdom, 5 Department of Biology, University of Copenhagen, Copenhagen, Denmark Abstract Here we report the result of a genetic screen for mutants resistant to the microtubule poison methyl benzimidazol-2-yl carbamate (MBC) that were also temperature sensitive for growth. In total the isolated mutants were distributed in ten complementation groups. Cloning experiments revealed that most of the mutants were in essential genes encoding various 26S proteasome subunits. We found that the proteasome mutants are multi-drug resistant due to stabilization of the stress- activated transcription factor Pap1. We show that the ubiquitylation and ultimately the degradation of Pap1 depend on the Rhp6/Ubc2 E2 ubiquitin conjugating enzyme and the Ubr1 E3 ubiquitin-protein ligase. Accordin
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