H.sapiens - Urine (Integrated)
Ontology highlight
ABSTRACT:
ORGANISM(S): 9606
SUBMITTER: 
Christian von Mering
PROVIDER: 24423709 | PAXDB | 2023
REPOSITORIES: PAXDB
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| bioprojects-abundance-files-v4.0.zip | Other |
Items per page: 5 1 - 1 of 1 |
Similar Datasets
Project description:The species Campylobacter jejuni is naturally competent for DNA uptake; nevertheless, nonnaturally transformable strains do exist. For a subset of strains we previously showed that a periplasmic DNase, encoded by dns, inhibits natural transformation in C. jejuni. In the present study, genetic factors coding for DNase activity in absence of dns were identified. DNA arrays indicated that nonnaturally transformable dns-negative strains contain putative DNA/RNA non-specific endonucleases encoded by CJE0566 and CJE1441 of strain RM1221. These genes are located on C. jejuni integrated element 2 and 4. Expression of CJE0566 and CJE1441 from strain RM1221 and a homologous gene from strain 07479 in DNase-negative Escherichia coli and C. jejuni strains indicated that these genes code for DNases. Genetic transfer of the genes to a naturally transformable C. jejuni strain resulted in a decreased efficiency of natural transformation. Modelling suggests that the C. jejuni DNases belong to the Serratia nuclease family. Overall, the data indicate that the acquisition of prophage encoded DNA/RNA non-specific endonucleases inhibits the natural transformability of C. jejuni through hydrolysis of DNA. The genomic diversity of 15 naturally competent or nonnaturally transformable Campylobacter jejuni strains were examined by microarray-based comparative genomic indexing (CGI) analysis. The CGI analysis allowed the assessment of CDS content for each C. jejuni strain relative to the C. jejuni DNA microarray, which comprises ORFs from strains NCTC 11168, RM1221. ORFs were spotted in duplicate. Genomic DNA from strains NCTC 11168/RM1221 were used as a reference DNA and competitively hybridized with genomic DNA from each of the other C. jejuni strains. Two replicates for each strain were performed. Data normalization was performed as in Parker et al. J Clin Microbiol 2006, 44(11):4125-4135.
2009-11-13 | E-GEOD-18399 | biostudies-arrayexpress
Project description:The impact of dietary Chlorella vulgaris and carbohydrate-active enzymes (CAZymes) on the gut of weaned piglets was investigated using an integrated NMR-metabolomics and LC-MS/MS proteomics approach.
2026-06-05 | PXD070943 | Pride
Project description:The endothelium is the frontline target of multiple metabolic stressors and pharmacological agents. As a consequence, endothelial cells (ECs) display highly dynamic and diverse proteome profiles. We describe here the culture of human aortic ECs from healthy and type 2 diabetic donors, the treatment with a small molecular conformation of trans-resveratrol and hesperetin (tRES+HESP), followed by proteomic analysis of whole-cell lysate. A number of 3666 proteins were presented in all the samples and thus further analyzed. We found that 179 proteins had a significant difference between diabetic ECs vs. healthy ECs, while 81 proteins had a significant change upon the treatment of tRES+HESP in diabetic ECs. Among them, 16 proteins showed a difference between diabetic ECs and healthy ECs and the difference was reversed by the tRES+HESP treatment, with the top 5 drastically altered proteins being ACVRL1, ADAM9, ITGAV, PCCB, and TGFBR2. Follow-up functional assays identified ACVRL1 and TGFBR2 as the most pronounced mediator for tRES+HESP-induced protection of angiogenesis in vitro. Our study has revealed the global changes in proteins and biological pathways in ECs from diabetic donors, which are potentially reversible by the tRES+HESP formula. Furthermore, we have identified the TGFβ signaling axis as a responding mechanism in ECs treated with this formula, shedding light for future studies for deeper molecular characterization
2023-07-20 | PXD036094 | Pride
Project description:We classified samples and deciphered a key genes signature of intratumor heterogeneity by Principal Component Analysis and Weighted Gene Co-expression Network Analysis. At the genome level, we identified common GB copy number alterations and but a strong inter-individual molecular heterogeneity.
2016-09-19 | E-MTAB-5098 | biostudies-arrayexpress
Project description:Alveolar soft part sarcoma (ASPS) is a soft tissue sarcoma with poor prognosis. Apart from the recurrent, non-reciprocal t(X,17)(p11.2;q25) translocation, there is little molecular evidence for the origin, initiation and progression of this cancer. We analysed 16 primary and metastatic ASPS samples to elucidate candidate molecular pathways involved in tumor pathogenesis. FISH analysis identified the ASPL-TFE3 fusion in all cases. High-resolution aCGH revealed a higher number of numerical aberrations in metastatic tumors relative to primaries, but failed to identify any consistent alterations in either group. Gene expression analysis highlighted 1,063 genes which were differentially expressed between primary and metastatic tumors. Gene set enrichment analysis identified 16 enriched genesets (p < 0.1) associated with differentially expressed genes. Notable among these were several stem cell gene expression signatures and pathways related to differentiation. In particular, the paired box transcription factor PAX6 was up-regulated in the primary tumors, along with several genes whose mouse orthologs have previously been implicated in Pax6-DNA binding during neural stem cell differentiation. In addition to suggesting a neural origin for ASPS, these results implicate transcriptional deregulation from fusion genes in the pathogenesis of ASPS, rather than extensive chromosomal instability. 15 different tumor and normal paired samples were analysed
2013-07-30 | E-GEOD-49324 | biostudies-arrayexpress
Project description:Here we examine key regulatory pathways underlying the transition from compensated hypertrophy (HYP) to decompensated heart failure (HF) and sudden cardiac death (SCD) in a guinea pig model by integrated multi-ome analysis. Relative protein abundances from sham-operated, HYP and HF hearts were assessed by iTRAQ shotgun LC-MS/MS. Metabolites were quantified by LC-MS/MS or GC-MS. Transcriptome profiles were obtained using DNA microarrays. The guinea pig HF proteome exhibited classic biosignatures of cardiac HYP, left ventricular dysfunction, fibrosis, inflammation and extravasation. Fatty acid metabolism, mitochondrial transcription/translation factors, antioxidant enzymes, and other mitochondrial processes, were downregulated in HF, but not HYP. Proteins upregulated in HF implicate extracellular matrix remodeling, cytoskeletal remodeling, and acute phase inflammation markers. Among metabolites, downregulation of acyl-carnitines was observed in HYP, while fatty acids accumulated in HF. Correlation of transcript and protein changes in HF is weak (R2=0.23), suggesting transcript/proteome divergence may reveal post-transcriptional gene regulation in HF. Proteome/Metabolome integration suggests metabolic bottlenecks in fatty acyl-CoA processing by carnitine palmitoyl transferase (CPT1B) as well as TCA cycle inhibition. We present a model by which acute signaling in HF, including Ca2+ dysregulation and low cAMP levels, is coupled to mitochondrial metabolic and antioxidant defects, through a CREB/PGC1 transcriptional axis. Animal Model The guinea pig model of heart failure and sudden cardiac death has been described previously. Briefly, the HF and SCD guinea pig model was produced by combining ascending aortic constriction (AC) and daily isoproterenol challenge (ACi model). Specifically, Hartley guinea pigs (~250 g; Hilltop Lab Animals) were anesthetized with 4% isoflurane in a closed box for 4min, and then intubated and ventilated with oxygen and 2% isoflurane. Ascending aortic constriction (AC) was produced by tying a suture around the ascending aorta using an 18‐gauge needle as a spacer, which was then removed. For sham operations the procedure was identical though the suture was not tied. After the procedure, bupronex (0.05 mg/kg) was administered via intramuscular injection for analgesia and animals were observed until full recovery. Isoproterenol was administered daily by intra peritoneal injection at 1 mg/kg for the first week after surgery and at 2 mg/kg for a subsequent 3 weeks. As characterized previously (1), cardiac function of ACi animal is well compensated in the first 2 weeks (HYP) but declined rapidly thereafter (HF). Hypertrophic heart was collected between 1-2 weeks post-surgery (ACi-2w), whereas failing heart was collected at 4 weeks after surgery (ACi-4w). Following retrograde perfusion with 20ml Tyrode’s solution, excised hearts were Snap-frozen in liquid N2 and stored at -80°C Experimental Design The experiment consisted of 3 treatment groups: 1) HYP (ACi-2wk), 2) HF (ACi-4wk) 3) sham-operated animals with daily administration for 4 weeks (Shami-4w). 1 heart from each group was included in an iTRAQ 4-plex experiment wherein peptides from each heart are subjected to reaction with an isobaric label. The experiment was repeated twice, yielding a total of 3 independent experiments quantifying the peptides from 9 hearts. ITRAQ reagents were shuffled among treatment groups for each experiment to minimize labeling bias.
2018-10-26 | PXD003980 | Pride
Project description:To identify substrates of the ubiquitinating E3 enzyme Rsp5 we applied purified Rsp5 to duplicate protein arrays. The Rsp proteins were expressed as fusion proteins to GST. We used as a control Ubr1, a RING domain containing E3 ligase We analyzed Rsp5 from S.cerevisiae on duplicate arrays, with four control chips, two without Rsp5 and two with Ubr1.
2008-12-30 | E-GEOD-14218 | biostudies-arrayexpress
Project description:hgu133a integrated dataset integrated from ArrayExpress and GEO
2007-11-20 | E-TABM-185 | biostudies-arrayexpress
Project description:We performed a systems-level study of disease-associated proteome changes in human frontal cortex of Alzheimer’s disease (AD) patients using an integrated approach that combines mass spectrometry-based quantitative proteomics, differential expression analysis, and co-expression network analysis. Our analyses of 16 human brain tissues from AD patients and age-matched controls showed organization of the cortical proteome into a network of 24 biologically meaningful modules of co-expressed proteins. Of these, 5 modules are positively correlated to AD phenotypes with hub proteins that are up-regulated in AD, and 6 modules are negatively correlated to AD phenotypes with hub proteins that are down-regulated in AD.
2022-10-05 | PXD037133 | Pride
Project description:Background: The cellular reservoir of latent HIV infection remains the main barrier to cure this virus. Elimination of this reservoir would be possible, if molecular identity of latently infected cells were fully elucidated. Biomarkers proposed previously were able to capture only a relatively small fraction of all reservoir cells. In the present study, we set out to conduct comprehensive molecular profiling, at the protein and RNA levels, of CD4+ T cells latently infected with HIV in vitro, using liquid chromatography-mass spectrometry (LC-MS) and RNA sequencing (RNA-Seq), respectively. Protein-based methods such as quantitative proteomic profiling using LC-MS may be more beneficial due to direct transferability of results to antibody-based approaches to capture latently infected cells. Integrated analysis of proteomic and transcriptomic data adds a level of validation and increases confidence in identified biomarkers. Flow cytometry and integrated HIV DNA assay were further used to enrich for latently infected cells with antibodies against selected biomarker proteins. Results: Using quantitative proteomics, we identified a total of 10,886 proteins (peptide level FDR < 0.05), of which 673 were up- and 780 down-regulated in latently infected compared to mock-infected cells in vitro (p < 0.05). Among these proteins, 21 were dysregulated at the RNA level in the same direction. Pathway analysis identified p53, mTOR, Wnt and NOTCH signaling, demonstrating that our in vitro model reflects known mechanisms of latency establishment and maintenance. Comparison of identified proteins with other proteomics studies revealed that identified molecular signatures of latency depend on technology and cell types used; however, a subset of proteins were identified both in the present, and at least one other study. Antibodies against selected protein markers, CEACAM1 and PLXNB2, could enrich for latently infected cells from mixed cell population 3-10 fold (5.8 fold average, p < 0.001). Conclusion: Two new molecules, CEACAM1 and PLXNB2, were identified as biomarkers for HIV latency. However, the level of enrichment for latently infected cells compared to biomarkers proposed previously was not improved. These results are consistent with the idea that each proposed biomarker defines only a subset of latently infected cells, and that a combined biomarker will be required to capture or target the latent HIV reservoir represented by different cell types.
2023-10-24 | PXD024014 | Pride