Made in error
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB31468 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:NEI Refractive Error Collaboration (KORA)
| PRJNA75817 | ENA
Project description:Assessment of technical error in a dual-channel, two timepoint experiment using White lab Drosophila melanogaster microarrays
2010-06-10 | E-GEOD-2641 | biostudies-arrayexpress
Project description:Assessment of technical error in a dual-channel, two timepoint experiment using White lab Drosophila melanogaster microarrays Keywords: repeat sample
2005-05-12 | GSE2641 | GEO
Project description:Aminoglycoside antibiotics target the ribosome and induce mistranslation, yet which translation errors induce bacterial cell death is unclear. The analysis of cellular proteins by quantitative mass spectrometry shows that bactericidal aminoglycosides induce not only single errors, but also clusters of errors in full-length proteins in vivo with as much as four amino acid substitutions in a row. The downstream errorsin a cluster are up to 10,000-fold more frequent than the first error and independent of the intracellular aminoglycoside concentration. The prevalence, length, and composition of error clusters dependsnot only on the misreading propensity of a given aminoglycoside, but also on its ability to inhibit ribosome translocation along the mRNA. Error clusters constitute a new class of misreading events in vivo that may provide the predominant source of proteotoxic stress at low aminoglycoside concentration, which is particularly important for the autocatalytic uptake of the drugs.
2021-04-06 | PXD022098 | Pride
Project description:DNA replication is sensitive to damage in the template. To bypass lesions and complete replication, cells activate recombination-mediated (error-free) and translesion synthesis-mediated (error-prone) DNA damage tolerance pathways. Crucial for error-free DNA damage tolerance is template switching, which depends on the formation and resolution of damage-bypass intermediates consisting of sister chromatid junctions. Here we show that a chromatin architectural pathway involving the high mobility group box protein Hmo1 channels replication-associated lesions into the error-free DNA damage tolerance pathway mediated by Rad5 and PCNA polyubiquitylation, while preventing mutagenic bypass and toxic recombination. In the process of template switching, Hmo1 also promotes sister chromatid junction formation predominantly during replication. Its C-terminal tail, implicated in chromatin bending, facilitates the formation of catenations/hemicatenations and mediates the roles of Hmo1 in DNA damage tolerance pathway choice and sister chromatid junction formation. Together, the results suggest that replication-associated topological changes involving the molecular DNA bender, Hmo1, set the stage for dedicated repair reactions that limit errors during replication and impact on genome stability. BrdU and proteins ChIP-chip analyses analysis were carried out as described (Bermejo et al., 2009). Labelled probes were hybridized to Affymetrix S.cerevisiae Tiling 1.0 (P/N 900645) arrays and processed with TAS software.
2014-01-28 | E-GEOD-46260 | biostudies-arrayexpress
Project description:Aminoglycoside antibiotics (AGAs) target the ribosome and induce mistranslation, yet which translation errors induce bacterial cell death is unclear. The analysis of cellular proteins by quantitative mass spectrometry shows that bactericidal AGAs induce not only single translation errors, but also clusters of errors in full-length proteins in vivo with as much as four amino acid substitutions in a row. The downstream errors in a cluster are much more frequent than the first error (0.4 vs. 10-3, respectively) and independent of the intracellular AGA concentration. The prevalence, length, and composition of error clusters depends not only on the misreading propensity of a given AGA, but also on its ability to inhibit ribosome translocation along the mRNA. Error clusters constitute a new class of misreading events in vivo that may constitute the predominant source of proteotoxic stress at low AGA concentration, which is particularly important for the autocatalytic uptake of the drugs.
2021-04-06 | PXD019188 | Pride
Project description:DNA replication is sensitive to damage in the template. To bypass lesions and complete replication, cells activate recombination-mediated (error-free) and translesion synthesis-mediated (error-prone) DNA damage tolerance pathways. Crucial for error-free DNA damage tolerance is template switching, which depends on the formation and resolution of damage-bypass intermediates consisting of sister chromatid junctions. Here we show that a chromatin architectural pathway involving the high mobility group box protein Hmo1 channels replication-associated lesions into the error-free DNA damage tolerance pathway mediated by Rad5 and PCNA polyubiquitylation, while preventing mutagenic bypass and toxic recombination. In the process of template switching, Hmo1 also promotes sister chromatid junction formation predominantly during replication. Its C-terminal tail, implicated in chromatin bending, facilitates the formation of catenations/hemicatenations and mediates the roles of Hmo1 in DNA damage tolerance pathway choice and sister chromatid junction formation. Together, the results suggest that replication-associated topological changes involving the molecular DNA bender, Hmo1, set the stage for dedicated repair reactions that limit errors during replication and impact on genome stability.
2014-01-28 | GSE46260 | GEO
Project description:Nuclear chromosome location dictates segregation error frequency
| PRJEB52892 | ENA
Project description:Error profile of the DNA storage channel
| PRJEB32885 | ENA
Project description:Quantifying sequencing error and effective sequencing depth of liquid biopsy NGS with unique molecular identifier error correction
| PRJEB39899 | ENA