Project description:Whole Genome Metabolism of "Acidaminococcus fermentans (strain ATCC 25085 / DSM 20731 / VR4)"
This is a whole genome metabolism model of Acidaminococcus fermentans (strain ATCC 25085 / DSM 20731 / VR4).
This model has been automatically generated by the SuBliMinaL Toolbox
and libAnnotationSBML using information coming from from KEGG (release 66, April 2013, accessed via the resource's web services interface) and, where relevant, augmented with metabolic pathway information extracted from MetaCyc (version 17.0, March 2013).
This model has been produced by the path2models
project and is currently hosted on BioModels Database
and identified by: BMID000000141191
Other models with the same genus include BMID000000009879 BMID000000009880 BMID000000009881 BMID000000009882 BMID000000009883 BMID000000009884 BMID000000009885 BMID000000009886 BMID000000009887 BMID000000009888 BMID000000009889 BMID000000009890 BMID000000009891 BMID000000009892 BMID000000068564 BMID000000068565 BMID000000068566 BMID000000068567 BMID000000068568 BMID000000068569 BMID000000068570 BMID000000068571 BMID000000068572 BMID000000068573 BMID000000068574 BMID000000068575 BMID000000068576 BMID000000068577 BMID000000068578 BMID000000068579 BMID000000068580 BMID000000068581 BMID000000068582 BMID000000068583 BMID000000068584 BMID000000068585 BMID000000068586 BMID000000068587 BMID000000068588 BMID000000068589 BMID000000068590 BMID000000068591 BMID000000068592 BMID000000068593 BMID000000068594 BMID000000068595 BMID000000068596 BMID000000068597 BMID000000068598 BMID000000068599 BMID000000068600 BMID000000068601 BMID000000068602 BMID000000068603 BMID000000068604 BMID000000068605 BMID000000068606 BMID000000068607 BMID000000068608 BMID000000068609 BMID000000068610 BMID000000068611 BMID000000068612 BMID000000068613 BMID000000068614 BMID000000068615 BMID000000068616 BMID000000068617 BMID000000068618 BMID000000068619 BMID000000068620 BMID000000068621 BMID000000068622 BMID000000068623 BMID000000068624 BMID000000068625 BMID000000068626 BMID000000068627 BMID000000068628 BMID000000068629 BMID000000068630 BMID000000068631 BMID000000068632 BMID000000068633 BMID000000142045 .
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
Project description:The gene expression levels in murine bone marrow-derived dendritic cells treated with γ-PGA NPs were examined by oligonucleitide microarray and compared with those in the cells treated with other adjuvants. The gene expression of proinflammatory chemokines, cytokines, and costimulatory molecules was upregulated considerably in DCs treated with γ-PGA NPs. The upregulation pattern was similar to that in DCs treated with LPS but not in DCs treated with unparticulate γ-PGA. The activation of DCs by γ-PGA NPs was confirmed by real-time RT-PCR analysis for the genes related to TLR signaling. The effect of γ-PGA NPs on DCs was not annihilated by treating with polymixin B, an inhibitor of LPS. Furthermore, the immunization of mice with γ-PGA NPs carrying OVA significantly induced Ag-specific CD8+ T cells and Ag-specific production of IL-2, TNF-α, and IFN-γ from the cells. Such activities of γ-PGA NPs were more prominent, when compared to the immunization with OVA plus aluminum hydroxide or OVA plus CFA. These results suggest that γ-PGA NPs induce a CD8+ T cell response through activating innate immunity in a fashion different from that of LPS. Thus, γ-PGA NPs may be an attractive adjuvant to be further developed for vaccine therapy. Overall design: The gene expression in murine bone marrow-derived dendritic cell was measured at 6 hours after exposure to γ-PGA NPs (300 µg/ml), LPS(1 µg/ml ), or unparticulate γ-PGA(300 µg/ml). Three independent experiments were performed.
Project description:Clinical isolates of the porcine pathogen Actinobacillus pleuropneumoniae often form adherent colonies on agar plates due to expression of an operon, pgaABCD, encoding a poly-N-acetylglucosamine (PGA) extracellular matrix. The adherent colony phenotype, which correlates with the ability to form a biofilm on the surface of polystyrene plates, is lost following serial passage in broth culture, and repeated passage of the non-adherent variants on solid media does not result in reversion to the adherent colony phenotype. In order to investigate the regulation of PGA expression and biofilm formation in A. pleuropneumoniae, we screened a bank of transposon mutants of the non-adherent serovar 1 strain, S4074T, and identified mutations in two genes, rseA and hns, which resulted in formation of the adherent colony phenotype. In other bacteria, including the Enterobacteriaceae, H-NS acts as a global gene regulator, and RseA is a negative regulator of the extracytoplasmic stress response sigma factor, ?E. Transcription profiling of A. pleuropneumoniae rseA and hns mutants revealed that both ?E and H-NS independently regulate expression of the pga operon. Transcription of the pga operon is initiated from a ?E promoter site in the absence of H-NS, and up-regulation of ?E is sufficient to displace H-NS, allowing transcription to proceed. In A. pleuropneumoniae, H-NS does not act as a global gene regulator, but rather specifically regulates biofilm formation via repression of the pga operon. Positive regulation of the pga operon by ?E indicates that biofilm formation in is part of the extracytoplasmic stress response in A. pleuropneumoniae.
Project description:The gene expression levels in murine bone marrow-derived dendritic cells treated with γ-PGA NPs were examined by oligonucleitide microarray at 6, 12 and 24 hours. The gene expression of proinflammatory chemokines, cytokines, and costimulatory molecules was upregulated considerably in DCs treated with γ-PGA NPs at 6 hours. Overall design: The gene expression in murine bone marrow-derived dendritic cell was measured at 6, 12 and 24 hours after exposure to γ-PGA NPs (300 µg/ml). Three independent experiments were performed.
Project description:We identified the D-galacturonic acid (GA) responsive transcriptional activator GaaR of the saprotrophic fungus Aspergillus niger, which was found to be essential for growth on GA and polygalacturonic acid (PGA). Growth of the ΔgaaR strain was reduced on complex pectins. Genome-wide expression analysis showed that GaaR is required for the expression of genes necessary to release GA from PGA and more complex pectins, to transport GA into the cell and to induce the GA-catabolic pathway. Residual growth of ΔgaaR on complex pectins is likely due to expression of pectinases acting on rhamnogalacturonan and subsequent metabolism of the monosaccharides other than GA. Overall design: The GA-responsive transcriptional activator GaaR of A. niger was identified by in-silico homology search. Deletion analysis and transcriptomic profiling studies performed in this study showed that the A. niger GaaR ortholog is required for growth on GA and PGA and for the induction of the GA-regulon when grown on sugar beet pectin.