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| Gene | Phenotype | Experiment Type | Mutant Information | Strain Background | Chemical | Details | Reference |
|---|---|---|---|---|---|---|---|
| HSP104 | prion inheritance: decreased Reporter: [OCT] prion | classical genetics | dominant negative Allele: HSP104-KT K218T, K620T; ATP binding sites mutated | Other | Details: assay loss of lactate utilization, and sucrose fermentation abilities | Patel BK, et al. (2009) PMID:19219034 | |
| SIS1 | prion inheritance: decreased Reporter: [PSI+] prion | classical genetics | reduction of function Allele: sis1-E53A E53A; homologous to DNAJB6-E54A (c.161A>C), a likely pathogenic variant in the J domain of human DNAJB6 that is associated with dominant distal myopathy | Other | Details: decreased propagation of the weak [PSI+] strain, based on lack of nonsense suppression | Pullen MY, et al. (2020) PMID:32497100 | |
| SIS1 | prion inheritance: decreased Reporter: [PSI+] prion | classical genetics | reduction of function Allele: sis1-N56L N56L; homologous to DNAJB6-S57L (c.170C>T), a variant of unknown significance in the J domain of human DNAJB6 that may be associated with dominant distal myopathy | Other | Details: decreased propagation of both weak and strong [PSI+] strains, based on lack of nonsense suppression | Pullen MY, et al. (2020) PMID:32497100 | |
| SIS1 | prion inheritance: decreased Reporter: [RNQ+] prion | classical genetics | reduction of function Allele: sis1-E53A E53A; homologous to DNAJB6-E54A (c.161A>C), a likely pathogenic variant in the J domain of human DNAJB6 that is associated with dominant distal myopathy | Other | Details: slight reduction in propagation of both low and high [RNQ+] strains, based on a loss of SDS-resistant aggregates | Pullen MY, et al. (2020) PMID:32497100 | |
| SIS1 | prion inheritance: decreased Reporter: [RNQ+] prion | classical genetics | reduction of function Allele: sis1-N56L N56L; homologous to DNAJB6-S57L (c.170C>T), a variant of unknown significance in the J domain of human DNAJB6 that may be associated with dominant distal myopathy | Other | Details: reduction in propagation of high [RNQ+] strains, based on a loss of SDS-resistant aggregates | Pullen MY, et al. (2020) PMID:32497100 |