Ontology highlight
ABSTRACT:
PROVIDER: PRJNA504536 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8174830.fastq.gz | Fastqsanger.gz | |||
| SRR8174840.fastq.gz | Fastqsanger.gz | |||
| SRR8174831.fastq.gz | Fastqsanger.gz | |||
| SRR8174841.fastq.gz | Fastqsanger.gz | |||
| SRR8174832.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 19 |
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Project description:Evidence for geomycological gold redox transformation under supergene conditions
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Project description:Gold salts has been used in the treatment of rheumatoid arthritis but has been replaced by biologicals such as TNF-alpha inhibitors. The mechanisms behind the anti-inflammatory effect of metallic gold ions are still unknown, however, recent data showed that charged gold atoms are released from pure metallic gold implants by macrophages via a dissolucytosis membrane, and that gold ions are taken up by local macrophages, mast cells and to some extent fibroblasts. These current findings offer new treatment options for metallic gold and deeper understanding of the effect of metallic gold on key inflammatory cells as macrophages are essential. In the present study the impact of phagocytised gold ions on the global gene expression profile of the human monocytic cell line THP-1 was investigated, using microarray analysis comprising approximately 20,000 genes. The gene expression data was confirmed by measurement of three secreted proteins. A unique gene expression signature of dissolucytotic macrophages that had taken up gold ions was demonstrated. A large number of regulated genes were functionally related to immunomodulation/protection. Gold ion uptake into macrophages induced downregulation of central inflammatory cytokines as TNF-alpha, IL-32 and CD28. The data obtained in this study offer new insights into the mode of action of gold ions and suggest a future role of metallic gold as implants or topical applications in treating inflammation.
2012-12-31 | GSE37814 | GEO
Project description:Gold salts has been used in the treatment of rheumatoid arthritis but has been replaced by biologicals such as TNF-alpha inhibitors. The mechanisms behind the anti-inflammatory effect of metallic gold ions are still unknown, however, recent data showed that charged gold atoms are released from pure metallic gold implants by macrophages via a dissolucytosis membrane, and that gold ions are taken up by local macrophages, mast cells and to some extent fibroblasts. These current findings offer new treatment options for metallic gold and deeper understanding of the effect of metallic gold on key inflammatory cells as macrophages are essential. In the present study the impact of phagocytised gold ions on the global gene expression profile of the human monocytic cell line THP-1 was investigated, using microarray analysis comprising approximately 20,000 genes. The gene expression data was confirmed by measurement of three secreted proteins. A unique gene expression signature of dissolucytotic macrophages that had taken up gold ions was demonstrated. A large number of regulated genes were functionally related to immunomodulation/protection. Gold ion uptake into macrophages induced downregulation of central inflammatory cytokines as TNF-alpha, IL-32 and CD28. The data obtained in this study offer new insights into the mode of action of gold ions and suggest a future role of metallic gold as implants or topical applications in treating inflammation. To determine the effect of gold phagocytosis on global gene expression
2012-12-31 | E-GEOD-37814 | biostudies-arrayexpress
Project description:Rubus spectabilis (gold) (salmonberry (gold morph)) genome assembly, drRubSpet2, principal haplotype
| PRJNA1164271 | ENA
Project description:Rubus spectabilis (gold) (salmonberry (gold morph)) genome assembly, drRubSpet2, alternate haplotype
| PRJNA1164272 | ENA
Project description:Transcription factors (TFs) are important regulators of plant growth and development and responses to stresses. TFs themselves are also susceptible to multiple post-translational modifications (PTMs). Relatively, redox-mediated PTM of TFs in plants is not well elucidated. Here, we found that NON-RIPENING (NOR), a master TF regulating tomato fruit ripening, is a target of SlMsrE4 or SlMsrB2, the methionine sulfoxide reductase A and B in tomato, respectively. Methionine oxidation in NOR, i.e. sulfoxidation, or mimicking sulfoxidation by mutating Met138 to glutamine, leads to the decreased DNA-binding capacity and transcriptional regulatory activity in vitro. On the other hand, SlMsrE4 and SlMsrB2 can partially repair oxidized-NOR and restore its DNA-binding capacity. Genetic transformation of the nor mutant with NOR genomic DNA almost completely rescues the ripening phenotype. However, transformation of nor with NOR-M138Q, the mimicked methionine sulfoxidation, inhibits the restore of fruit ripening phenotype, and this is associated with the decreased DNA-binding and transcriptional activation of numerous ripening-related genes. Taken together, these findings uncover a novel mechanism by which Msr-mediated redox modification of NOR regulates the expression of ripening-related genes, thereby influencing tomato fruit ripening. To our knowledge, this is the first report that redox modification of TF regulates fruit ripening. nor is a NOR mutant, the phenotype is obstructed by maturity; NOR-12 is a rotational NOR in NOR mutant, the phenotype is a mature inhibition phenotype that basically restores nor mutant; Nor-18 is a rotation of NOR-M138Q in nor mutant, phenotype with the effect of restoring maturity, but the recovery efficiency is lower than the swing NOR.
2020-05-22 | GSE140853 | GEO