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YGR117C remains poorly characterized. The strongest gene-specific experimental evidence
retrievable links the protein to translation fidelity/termination and overall protein synthesis,
based on reporter assays in a YGR117C deletion strain, and cites prior GFP-tag localization
placing the protein in the cytoplasm.
"The strongest gene-specific experimental evidence located links YGR117C to **translation fidelity/termination** and **overall protein synthesis**, based on reporter assays in a YGR117C deletion strain; the same work cites prior GFP-tag localization placing the protein in the **cytoplasm**."
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In a translation-fidelity follow-up, deletion of YGR117C increased premature stop-codon
readthrough in a beta-galactosidase reporter assay, with qRT-PCR controls indicating the effect
was at the translation level rather than due to altered reporter mRNA abundance. The authors
interpret this as YGR117C being involved in the translation pathway. Evidence is from a 2014 PhD
thesis, not a peer-reviewed gene-specific paper.
"deletion of **YGR117C** was reported to **increase translational stop-codon readthrough** of premature stop codons in β-galactosidase reporter assays, and accompanying qRT-PCR controls supported that the effect was not explained by altered reporter mRNA abundance (i.e., consistent with a translation-level effect)"
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Using a GAL1-driven beta-galactosidase protein-synthesis assay, YGR117C deletion was among
strains showing decreased protein synthesis, again with qRT-PCR indicating mRNA levels did not
account for the effect. This provides convergent but still indirect evidence of an effect on
translation output in vivo.
"YGR117C deletion was reported among strains showing **decreased protein synthesis**, again with qRT-PCR indicating that mRNA levels did not account for the observed effect"
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YGR117C appears as one of 446 candidate genes in a genome-wide nonstop-decay (NSD) screen, but
no gene-specific validation, effect size, or mechanistic interpretation was provided. Falcon
concludes that assignment to NSD/autophagy is not currently supported beyond candidate-list
inclusion and should be treated as speculative.
"Assignment to NSD/autophagy is **not currently supported** beyond candidate-list inclusion and should be treated as speculative pending gene-specific validation"
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The protein product is reported as cytoplasmic based on cited GFP-localization work (Huh et al.
2003), consistent with translation-related roles, though it does not specify association with
ribosomes, stress granules, or other subcompartments.
"Cytoplasmic localization is consistent with translation-related roles (ribosomes and many translation factors are cytoplasmic), but does not specify association with ribosomes, stress granules, or other subcompartments."
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No direct enzymatic activity, substrate specificity, or validated binding partners/complex
membership were identified for YGR117C. The LisH/WD40 scaffold-adaptor hypothesis is explicitly
flagged as an inference not supported by direct evidence in the retrieved corpus and should not
be treated as established function.
"No direct enzymatic activity, substrate specificity, or validated binding partners/complex membership were identified for YGR117C in the retrieved evidence"