Influenza serum mIgA and dIgA repertoire on day 29 following seasonal influenza vaccination
Ontology highlight
ABSTRACT:
INSTRUMENT(S):
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Blood Cell, Blood Plasma
DISEASE(S): Influenza
SUBMITTER: 
Juyeon Park
LAB HEAD: George Georgiou
PROVIDER: PXD070307 | Pride | 2026-07-09
REPOSITORIES: Pride
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| 9472_WP_01a.msf | Msf | |||
| 9472_WP_01a.raw | Raw | |||
| 9472_WP_01b.msf | Msf | |||
| 9472_WP_01b.raw | Raw | |||
| 9472_WP_01c.msf | Msf |
Items per page: 5 1 - 5 of 97 |
Similar Datasets
Project description:Dissecting the Clonal Composition and Determinants of Neutralization Potency Enhancement of Circulating Dimeric and Monomeric IgA to Human Norovirus
2026-07-09 | PXD066704 | Pride
Project description:The human genome encodes tens of thousands circular RNAs (circRNAs) whose levels correlate with many disease states. While studies have focused on the non-coding functions of circRNAs, emerging evidence suggests that a handful of circRNAs encode proteins. Translation canonically starts by recognition of mRNA 5’cap and scanning to the start codon; how circRNA translation initiates remains unclear. Here, we developed a high-throughput screen to systematically identify and quantify RNA sequences that can direct circRNA translation. We identify and validate over 17,000 circRNA internal ribosome entry sites (IRES) and reveal that 18S rRNA complementarity and a structured RNA element on the IRES are important for facilitating circRNA cap-independent translation. With genomic and peptidomic analyses of the IRES, we identified nearly 1,000 putative endogenous protein-coding circRNAs and hundreds of translational units encoded by these circRNAs. We further characterized circFGFR1p, a protein encoded by circFGFR1, functions as a negative regulator of FGFR1 to suppress cell growth under stress conditions. The circRNA proteome may be important links among circRNA, biological control, and disease.
2021-08-23 | PXD025235 | Pride
Project description:Here we adapt native elongating transcript sequencing (NET-seq) to develop transcription elongation factor associated nascent elongating transcript sequencing (TEF-seq). In this the RNA polymerase II (Pol2) transcription elongation complex (TEC) is immunoprecipitated via associated transcription elongation factors (TEFs). Sequencing from the 3' end of the Pol2-associated nascent transcript shows the position of the final incorporated nucleotide giving strand-specific, single nucleotide resolution maps of the level of TEF association with Pol2 during transcription.
2021-01-18 | E-MTAB-4568 | biostudies-arrayexpress
Project description:Neurons are almost exclusively cultured in media containing glucose at much higher concentration than found in the brain. To test whether “standard” hyperglycaemic culture conditions affect neuronal respiration compared to near- euglycemic conditions, we grew neuronal cultures with minimal glial contamination from hippocampus and cortex of neonatal C57bl6 mice in standard commercially available media (25 mM Glucose) and in identical media with 5 mM glucose. Neurons grew well in both glucose concentrations until at least 14 days in vitro, with similar morphology and synaptogenesis. Neurons grown in high glucose were more dependent on glycolysis as their primary source of ATP, measured using ATP luminescence and cellular respirometry assays. In contrast, neurons grown in 5 mM glucose showed a more balanced dependence on glycolysis and mitochondrial oxidative phosphorylation (OXPHOS) and greater reserve mitochondrial respiration capacity, relative to standard media. Changes in gene and protein expression levels corroborate these changes in function. Our results suggest that neurons cultured in high glucose media preferentially use glycolysis, opposite to what is known for neurons in vivo as the primary pathway for ATP maintenance. We suggest using neuronal culture systems in 5 mM glucose to better represent physiologically relevant neuronal respiration.
2025-06-30 | PXD059008 | Pride
Project description:Lyme borreliosis (LB) is a tick-borne infection caused by Borrelia burgdorferi. Dogs are at high risk of exposure to ticks and tick-borne pathogens, including B. burgdorferi. Immunodiagnostic assays are usually based on whole-cell preparations of B. burgdorferi as substrate and, consequently, interpretation of results is confounded by antibody cross-reactivity between borrelial antigens and other bacterial species, as well as the anti-LB vaccination status of the dog. For this study, we examined sera from 33 dogs that were experimentally infected with B. burgdorferi through tick bite. These sera were compared with sera from uninfected dogs in their reactivities to 72 different recombinant B. burgdorferi polypeptides on a protein microarray. Amongst antigens frequently recognized by infected dogs were several known to be immunogens for humans, such as Decorin-binding protein A (BBA25), BBA64, fibronectin-binding protein (BBK32), VlsE, Erp and Bdr, CRASP proteins, OspC proteins and some flagellar antigens. Of special interest were the novel antigens BBB14 and BB0844, both hypothetical lipoproteins about which very little is currently known, and that were frequently and strongly recognized by infected dog sera. The antibody response of B. burgdorferi-infected dogs presents both similarities and differences from human counterparts, and both can be important for improvement of canine LB diagnosis and vaccine development. Antibody profiling was performed on sera from dogs experimentally-infected with B. burgdorferi and unexposed controls against antigens of B. burgdorferi. Thirty-three serum samples from experimental infections, and 6 unexposed controls were probed on a protein microarray displaying 72 unique proteins of B. burgdorferi .
2013-08-22 | E-GEOD-50074 | biostudies-arrayexpress
Project description:Behavioral transitions Young infant rats paradoxically prefer odors paired with shock but older pups learn aversions. This transition is amygdala- and corticosterone-dependent. Microarray results showed downregulated dopaminergic presynaptic function in the amygdala with preference learning. Corticosterone injected 8-day-old pups and untreated 12-day-old pups learn aversions and had dopaminergic upregulation in the amygdala. 8 day saline or corticosterone treated- or 12 day old untreated rat pups were trained with odor-shock pairings. Immediately after training pups were sacrificed and the amygdala dissected out. Controls were unpaired shock-odor groups.Paired and unpaired groups were processed together for each experimental condition. Paired and unpaired data were compared by ranked products.
2009-09-27 | E-GEOD-17651 | biostudies-arrayexpress
Project description:Background & Aims: Histone deacetylases (HDACs) are among the most common epigenetic dysregulations found in cancer, and considered as key events in tumour development and progression. Here we explored the therapeutic effects of romidepsin, a class-I HDAC inhibitor (HDACi), alone and in combination with receptor tyrosine kinase inhibitors (RTKi) in hepatocellular carcinoma (HCC). Methods: We bioinformatically evaluated class-I HDACs relevance in HCC patients through available datasets. Effects of romidepsin were assessed in HCC cell and mouse models. Molecular alterations were determined using proteomics, biochemistry, metabolic assays, immunostaining. The proteomic analysis was performed on Huh7 human HCC cell line non-treated or treated with romidepsin, cabozantinib or their combination, for 24h. Results: We report that overexpression of HDAC1 and HDAC2 occurs in HCC patients across five cohorts, and is correlated with decreased overall survival. We found that their targeting by romidepsin in HCC cell lines affects levels of several signals involved in cell cycle/survival and confers RTKi responsiveness. Mechanistically, romidepsin perturbs lipid metabolism, reduces cholesterol levels and upregulates fatty acid modulators. Furthermore, romidepsin affects the mitotic spindle machinery, leading to monopolar spindle formation, altered chromosome segregation, and cell blockage into mitosis illustrated by an accumulation of phospho-histone H3 positive HCC cells. Combined treatment of HCC cells with romidepsin plus cabozantinib (RomiCabo) switches a cytostatic effect, by romidepsin alone, into cell death by apoptosis. In vivo, RomiCabo induces regression of a subset of spontaneous preneoplastic as well as advanced lesions in the Alb-R26Met model faithfully recapitulating HCC resistance and heterogeneity. We characterize the upregulation of HR23B, a biomarker for tumour sensitivity to HDAC inhibition, and downregulation of the HCC marker AFP in RomiCabo treated Alb-R26Met tumours. Conclusions: Our findings provide the rationale of using romidepsin to exacerbate the vulnerability of HCC to RTKi for the treatment of patient subgroups.
2025-08-04 | PXD041166 | Pride
Project description:The main objective of CHARMACOMA is to explore the capacity of the severe asthmatic bronchial smooth muscle to modify bronchial epithelium physiology from a metabolic point of view.
2025-11-26 | PXD055968 | Pride
Project description:Combined therapy with anti-BRAF plus anti-MEK is currently used as first-line treatment of patients with metastatic melanomas harboring the somatic BRAF V600E mutation. However, the main issue with targeted therapy is the acquisition of tumor cell resistance. In 70% of resistant melanoma cells, the resistant process consists in epithelial-to-mesenchymal transition (EMT). This process called phenotype switching makes melanoma cells more invasive. Its signature is characterized by MITF low, AXL high, and actin cytoskeleton reorganization through RhoA activation. In parallel of this phenotype switching phase, the resistant cells exhibit an anarchic cell proliferation due to hyper-activation of the MAP kinase pathway. We show that a majority of human melanoma overexpress discoidin domain receptor 2 (DDR2) after treatment. The same result was found in resistant cell lines presenting phenotype switching compared to the corresponding sensitive cell lines. We demonstrate that DDR2 inhibition induces a decrease in AXL expression and reduces stress fiber formation in resistant melanoma cell lines. In this phenotype switching context, we report that DDR2 control cell and tumor proliferation through the MAP kinase pathway in resistant cells in vitro and in vivo. Therefore, inhibition of DDR2 could be a new and promising strategy for countering this resistance mechanism.
2023-05-02 | PXD028292 | Pride
Project description:ß-catenin is a main oncogene in a large number of cancers (colorectal, liver, melanoma, uterus). Local immunosuppression induced by certain cancers remains a major problem of resistance to immunotherapies and its molecular mechanism remains poorly understood. Recently, ß-catenin mutated tumors (hepatocellular carcinoma (HCC) and melanoma) have been described as promoting immune evasion and resistance to anti-PD1 immunotherapy. Based on preliminary data obtained in HCC, we hypothesize that a defect in intercellular communication could be the cause of this immune evasion. The main objective of this project is to identify proteomic signatures of factors that can induce this immune escape in ß-catenin mutated HCC such as exosomes.
2024-07-08 | PXD043841 | Pride