MP-LRCC5314_gut_samples
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1055314 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27320800_1.fastq.gz | Fastqsanger.gz | |||
| SRR27320800_2.fastq.gz | Fastqsanger.gz | |||
| SRR27320801_1.fastq.gz | Fastqsanger.gz | |||
| SRR27320801_2.fastq.gz | Fastqsanger.gz | |||
| SRR27320802_1.fastq.gz | Fastqsanger.gz |
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Project description:Understanding the mechanism of action of CSE-Bu on gene level in osteogenic effect. We used microarray to detail the effect of MP and MP+CSE_Bu on gene expression in SD rats and identified various classes of genes that are either upregulated or down-regulated.
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Project description:This study identified gene expression of Side Population (SP) and Main Population (MP) cells, isolated from adult murine skeletal muscle and Bone Marrow. Five different preparations of muscle SP, muscle MP, Bone marrw SP and Bone marrow MP cells were used as replicates.
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Project description:Co-immunoprecipitation assays coupled with mass spectrometry identified a series of host factors that could interact with the OuMV MP and link the MP with various pathways including membrane trafficking, lipid binding, protein phosphorylation and dephosphorylation, RNA binding, cell wall biosynthesis, blue light response, calcium signaling, transport across the plasma membrane, protein folding and homeostasis, proteolysis, and metabolism.
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Project description:Expression data from Vehicle, MP and MP+CSE_Bu treated SD rats
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Project description:Comparison of Zea mays mature silk (MS), mature pollen (MP) and unfertilized ovary (UFO).
2012-06-30 | E-MEXP-3292 | biostudies-arrayexpress
Project description:Background-The endothelial protein C receptor (EPCR) plays an important role within the protein C (PC) pathway in regulating coagulation and inflammation. Recently, we described a novel mechanism of EPCR release from the surface of primary physiological cells. Induced by exogenous activated protein C (APC), EPCR is released in microparticulate form. Its bound APC retains proteolytic anticoagulant activity and we now hypothesise that this microparticulate EPCR-APC complex can also cleave endothelial protease activated receptor 1 (PAR1) to modulate inflammation and cytoprotection. Methods & Results-The gene profiling effect on human endothelial cells by 40nM APC, in free or microparticulate form, was assessed. Transcript profile results showed upregulation of anti-apoptotic and inflammatory genes by APC in either form, which were confirmed by RT-PCR. These translated into increased GM-CSF and interleukin 8 secretion and cytoprotection against staurosporine-induced apoptosis. PC or PAR1 antagonism reversed these results to demonstrate that induced effects by microparticles were APC specific and PAR1-dependent. Further analysis of human plasma from septic patients, by confocal microscopy and ELISA, showed evidence of circulating microparticle-associated EPCR during recombinant APC treatment. Functional coagulation and cellular studies demonstrate that these express APC-specific effects on anticoagulation with PAR1-mediated gene induction and anti-apoptotic function. Conclusions-APC induction of microparticle-associated EPCR release can occur in vivo. These microparticles could potentially disseminate the function of the EPCR-APC complex to PAR1 on different cells and vascular sites. Keywords: pre versus rhAPC-treatment mp in vivo MP were isolated from sepsis patients pre and during-rhAPC treatment. MP were counted by FACS using CD13 positivity and same number of mp was used in pre and during treatment comparisons. HUVEC were incubated with the in vivo mps according to mp number or apc content, and controls for both were done using non-treated patients or free-apc. The role of apc and par1 was analysed by including apc blocking antibody or par1 antaginist peptide respectively.
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Project description:Vascular formation in the leaves of higher plants begins with the selection of cells poised to become preprocambial cells, some of which eventually develop into procambial cells. The initiation of this process is accompanied by auxin-responsive and MONOPTEROS (MP) transcription factor-mediated modulations in gene expression. Here, we show that MP directly activates the expression of Dof5.8, which encodes a transcriptional repressor. Consistently, mutations within Dof5.8 enhanced the phenotype of a weak allele of mp, resulting in abnormal root and cotyledon development. However, although mp mutants showed reduced vascular patterns in cotyledons, the mp dof5.8 double mutants displayed both reduced and more complex vascular patterns in individual cotyledons. Thus, Dof5.8 appears to be associated with both positive and negative regulatory mechanisms for vascular network formation in leaves. Furthermore, both over-expression of Dof5.8 and expression of a Dof5.8 construct engineered to possess enhanced repressor activity in preprocambial cells prevented the formation of procambium for secondary and higher order veins, suggesting a predominantly negative regulatory role for Dof5.8. These results imply that proper vascular patterns in leaves are formed through the modulation of both positive and negative regulation by Dof5.8. MP may direct this fine-tuning mechanism by mediating the expression of Dof5.8.
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Project description:To better understand the molecular mechanisms of SP cells, we screened the miRNAs expression patterns in the SP compared with the MP cells. MiRCURY™ LNA array analysis of sorted SP and MP cells from two relapsed myeloma patients with more than 70% bone marrow plasma cells were performed.
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