Alternaria alternata
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA962067 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24313415_1.fastq.gz | Fastqsanger.gz | |||
| SRR24313415_2.fastq.gz | Fastqsanger.gz | |||
| SRR24316216_1.fastq.gz | Fastqsanger.gz | |||
| SRR24316216_2.fastq.gz | Fastqsanger.gz | |||
| SRR24316136_1.fastq.gz | Fastqsanger.gz |
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Project description:Previous studies have proposed that production of reactive oxygen species (ROS) is an important contributor to renal injury and inflammation following exposure to oxalate or calcium-oxalate crystals. The present study was conducted to determine, utilizing global transcriptome analyses, if the NADPH oxidase system is activated in kidneys of rats fed a diet leading to hyperoxaluria and crystal deposition. HLP was used to induce hyperoxaluria. Hyperoxaluria will lead to crystallization and up regulation of various NADPH oxidase subunits followed by increased expression of different specific genes. It is our hypothesis that crystallization induces inflammation of the kidneys via the activation of renin-angiotensin system (RAS) and production of reactive oxygen species (ROS) through NADPH oxidase complex. Apocynin was used to block hyperoxaluria and production of reactive oxygen species (ROS) with the inhibition of NADPH oxidase system as Apocynin inhibits membrane translocation of p47 subunit of NADPH oxidase.
2012-12-20 | GSE36446 | GEO
Project description:Previous studies have proposed that production of reactive oxygen species (ROS) is an important contributor to renal injury and inflammation following exposure to oxalate or calcium-oxalate crystals. The present study was conducted to determine, utilizing global transcriptome analyses, if the NADPH oxidase system is activated in kidneys of rats fed a diet leading to hyperoxaluria and crystal deposition. HLP was used to induce hyperoxaluria. Hyperoxaluria will lead to crystallization and up regulation of various NADPH oxidase subunits followed by increased expression of different specific genes. It is our hypothesis that crystallization induces inflammation of the kidneys via the activation of renin-angiotensin system (RAS) and production of reactive oxygen species (ROS) through NADPH oxidase complex. Apocynin was used to block hyperoxaluria and production of reactive oxygen species (ROS) with the inhibition of NADPH oxidase system as Apocynin inhibits membrane translocation of p47 subunit of NADPH oxidase. The present study was designed based on NADPH oxidase system and rats were divided into 4 groups (n= 6/group). Group 1 was fed regular rat chow diet, Group 2 received regular rat chow diet supplemented with 5% (Hydroxy-L-Proline) HLP, Group 3 received rat chow diet with 4 mmol Apocynin to drink, and Group 4 received regular rat chow diet with 5% HLP and 4 mmol Apocynin. After 28 days each rat was euthanized, their kidneys freshly explanted and dissected to obtain both cortex and medulla tissues. So the 4 groups were divided into cortex and medulla forming 8 groups. RNA was isolated from all the 8 specimens
2012-12-20 | E-GEOD-36446 | biostudies-arrayexpress
Project description:Genetic defects in neutrophil function or trafficking are highly associated with oral inflammation and periodontitis. The leukocyte NADPH oxidase enzymes complex is a multi-subunit enzyme that has been described to play important immunomodulatory roles in limiting the inflammatory responses of neutrophils and macrophages. Here, we determined the impact of loss of NADPH oxidase dependent reactive oxygen species (ROS) generation in gingival inflammatory responses using a model of ligature induced murine periodontitis.
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Project description:NADPH oxidases are the only know enzyme family that has reactive oxygen species (ROS, e.g. superoxide and hydrogen peroxide) as their main metabolic product. They are therefore a prima candidate gene family to define a molecular source for ROS in physiology and pathophysiology. The type 4 NADPH oxidase (NOX4) is the most abundant isoform with the highest basal expression levels.The Nox4 knockout mouse was designed using a cre/lox recombination technique which allows to create either constitutive (type III recombination) and conditional (type I recombination) knockout alleles.
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Project description:Wild type systemic leaf wound response vs. response in mutants lacking NADPH oxidase (Rboh) Keywords = reactive oxygen species Keywords: other
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Project description:Mycobacterium tuberculosis’success as a pathogen comes from itsability to evade degradation by macrophages. Normally macro-phages clear microorganisms that activate pathogen-recognitionreceptors (PRRs) through a lysosomal-trafficking pathway called“LC3-associated phagocytosis”(LAP). AlthoughM.tuberculosisac-tivates numerous PRRs, for reasons that are poorly understoodLAP does not substantially contribute toM.tuberculosiscontrol.LAP depends upon reactive oxygen species (ROS) generated byNADPH oxidase, butM.tuberculosisfails to generate a robustoxidative response. Here, we show that CpsA, a LytR-CpsA-Psr(LCP) domain-containing protein, is required forM.tuberculosisto evade killing by NADPH oxidase and LAP. Unlike phagosomescontaining wild-type bacilli, phagosomes containing theΔcpsAmutant recruited NADPH oxidase, produced ROS, associated withLC3, and matured into antibacterial lysosomes. Moreover, CpsAwas sufficient to impair NADPH oxidase recruitment to fungal par-ticles that are normally cleared by LAP. Intracellular survival of theΔcpsAmutant was largely restored in macrophages missing LAPcomponents (Nox2,Rubicon,Beclin,Atg5,Atg7,orAtg16L1) butnot in macrophages defective in a related, canonical autophagypathway (Atg14,Ulk1,orcGAS). TheΔcpsAmutant was highlyimpaired in vivo, and its growth was partially restored in micedeficient in NADPH oxidase,Atg5,orAtg7, demonstrating thatCpsA makes a significant contribution to the resistance ofM.tu-berculosisto NADPH oxidase and LC3 trafficking in vivo. Overall,our findings reveal an essential role of CpsA in innate immuneevasion and suggest that LCP proteins have functions beyond theirpreviously known role in cell-wall metabolism.
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Project description:We are testing the ability of spironolactone as a NADPH oxidase inhibitor during an induced dietary oxalate overload by Ethylene Glycol in Sprague Dawley rats at two different time points. We looked into the development of hyperoxaluria and crystal deposition at two different time points and into differences between hyperoxaluria and crystal induced alterations in the kidneys. Eventually, we are expecting to see the role of spironolactone as an inhibitor of NADPH oxidase which is involved in the production of reactive oxygen species (ROS) which leads to oxidative stress in the living organisms leading to a plethora of vascular diseases, hypertension, and kidney diseases.
2017-01-06 | GSE89028 | GEO
Project description:NADPH oxidases are the only know enzyme family that has reactive oxygen species (ROS, e.g. superoxide and hydrogen peroxide) as their main metabolic product. They are therefore a prima candidate gene family to define a molecular source for ROS in physiology and pathophysiology. The type 4 NADPH oxidase (NOX4) is the most abundant isoform with the highest basal expression levels.The Nox4 knockout mouse was designed using a cre/lox recombination technique which allows to create either constitutive (type III recombination) and conditional (type I recombination) knockout alleles. cDNA microarray experiments of brain, kidney, muscle and pancreas of four male mutant mice versus a RNA pool of four male wild type mice. For each animal two technical replicates were performed including a dye swap experiment. All animals with the same age of 17 weeks on a C57BL/6 background.
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Project description:Reactive oxygen species (ROS) production is a conserved immune response, primarily mediated in Arabidopsis by the respiratory burst oxidase homolog D (RBOHD), a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase associated with the plasma membrane. A rapid increase in NADPH is necessary to fuel RBOHD proteins and hence maintain ROS production. However, the molecular mechanism underlying the NADPH generation for fueling RBOHD remains unclear. In this study, we isolated a new mutant allele of flagellin-insensitive 4 (FIN4), encoding the first enzyme in de novo NAD biosynthesis. fin4 mutants show reduced NADPH levels and impaired ROS production. However, FIN4 and other genes involved in the NAD- and NADPH-generating pathways are not highly upregulated upon elicitor treatment. Therefore, we hypothesized that a cytosolic NADP-linked dehydrogenase might be post-transcriptionally activated to keep the NADPH supply close to RBOHD. RPM1-INDUCED PROTEIN KINASE (RIPK), a receptor-like cytoplasmic kinase, regulates broad-spectrum ROS signaling in plant immunity. We then isolated the proteins associated with RIPK and identified NADP-malic enzyme 2 (NADP-ME2), an NADPH-generating enzyme. Compared with wild-type plants, nadp-me2 mutants display decreased NADP-ME activity, lower NADPH levels, as well as reduced ROS production in response to immune elicitors. Furthermore, we found that RIPK can directly phosphorylate NADP-ME2 and enhance its activity in vitro. The phosphorylation of NADP-ME2 S371 residue contributes to ROS production upon immune elicitor treatment and the susceptibility to the necrotrophic bacterium, Pectobacterium carotovorum. Overall, our study suggests that RIPK activates NADP-ME2 to rapidly increase cytosolic NADPH, hence fueling RBOHD to sustain ROS production in plant immunity.
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