Caenorhabditis elegans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA482604 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7609880.fastq.gz | Fastqsanger.gz | |||
| SRR7609881.fastq.gz | Fastqsanger.gz | |||
| SRR7609882.fastq.gz | Fastqsanger.gz | |||
| SRR7609883.fastq.gz | Fastqsanger.gz | |||
| SRR7609884.fastq.gz | Fastqsanger.gz |
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Project description:Multiple myeloma (MM) evolves from highly prevalent premalignant condition termed Monoclonal Gammopathy of Undetermined Significance (MGUS). We report an MGUS-MM phenotype arising in transgenic mice with Emu-directed expression of the unfolded protein/ER stress response and plasma cell development spliced isoform factor XBP-1s. Emu-XBP-1s elicited elevated serum Ig and IL-6 levels, skin alterations and with advancing age, a significant proportion of Emu-xbp-1s transgenic mice develop features diagnostic of human MM including bone lytic lesions. Transcriptional profiles of Emu-xbp-1s B lymphoid and MM cells show aberrant expression of genes known to be dysregulated in human MM including Cyclin D1, MAF, MAFB, and APRIL. This genetic model coupled with documented frequent XBP-1s overexpression in human MM serve to implicate chronic XBP-1s dysregulation in the development of this common and lethal malignancy. Keywords: XBP-1, MGUS, multiple myeloma, transgenic mouse
2007-04-09 | GSE6980 | GEO
Project description:Multiple myeloma (MM) evolves from highly prevalent premalignant condition termed Monoclonal Gammopathy of Undetermined Significance (MGUS). We report an MGUS-MM phenotype arising in transgenic mice with Emu-directed expression of the unfolded protein/ER stress response and plasma cell development spliced isoform factor XBP-1s. Emu-XBP-1s elicited elevated serum Ig and IL-6 levels, skin alterations and with advancing age, a significant proportion of Emu-xbp-1s transgenic mice develop features diagnostic of human MM including bone lytic lesions. Transcriptional profiles of Emu-xbp-1s B lymphoid and MM cells show aberrant expression of genes known to be dysregulated in human MM including Cyclin D1, MAF, MAFB, and APRIL. This genetic model coupled with documented frequent XBP-1s overexpression in human MM serve to implicate chronic XBP-1s dysregulation in the development of this common and lethal malignancy. Experiment Overall Design: In this study, we have explored the biological impact of sustained XBP-1s expression in the lymphoid system, anticipating that this genetic event would be a necessary component along with other MM-relevant oncogenes and tumor suppressor gene manipulations to generate a MM-prone mouse model. Unexpectedly, XBP-1s overexpression alone yielded an MGUS-MM disease bearing many features classical of the human disease on the clinical, pathological and molecular levels. Experiment Overall Design: We performed expression analysis of B cells derived from the spleen of 20-week old Emu-xbp-1s mice (n=5) and non-transgenic mice (n=5). Additionally, we analyzed the expression profiles from MM tumor cells arising in Emu-xbp-1s mice (n=6).
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Project description:Caenorhabditis elegans Neuronal Cells RNA sequence data
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Project description:RNA-seq quantification of expression changes upon unc-62 knockdown in adult Caenorhabditis elegans.
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Project description:C-type lectin-like domain (CTLD) encoding genes are highly diverse in C. elegans, comprising a clec gene family of 283 members. Since vertebrate CTLD proteins have characterized functions in defense responses against pathogens and since expression of C. elegans clec genes is pathogen-dependent, it is generally assumed that clec genes function in C. elegans immune defenses. In this study we challenged this assumption and focused on the C. elegans clec gene clec-4, whose expression is highly upregulated upon infection with various pathogens. We tested the involvement of clec-4 in the defense response to infection with Pseudomonas aeruginosa PA14, Bacillus thuringiensis BT18247, and the natural pathogen Serratia rubidaea MYb237. Contrary to our expectation clec-4(ok2050) mutant worms were not more susceptible to pathogen infection than wildtype worms. To explore potential redundant function between different C. elegans clec genes, we investigated expression of several clec-4 paralogs, finding that clec-4, clec-41, and clec-42 expression shows similar infection-dependent changes and co-localizes to the intestine. We found that only clec-42 is required for the C. elegans defense response to BT18247 infection and that clec-4 genetically interacts with clec-41 and clec-42. The exact role of clec-4 in pathogen defense responses however remains enigmatic. Our results further indicate that a complex interplay between different clec genes regulates C. elegans defense responses.
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