Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

LC/MS Data for Human CD4+ T cells

ABSTRACT: For metabolic profiling of human CD4+ T cells，stable isotope labeling (SIL) and metabolomics SIL experiments were performed with in vitro-activated T cells using liquid chromatography (LC) coupled to mass spectrometry (MS).

ORGANISM(S): Homo Sapiens

SUBMITTER: Hui Zhang

PROVIDER: PXD055329 | iProX | Sat Aug 24 00:00:00 BST 2024

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Similar Datasets

GC/MS data for mouse spleen CD4+ T cells

Project description:For metabolic profiling of mouse CD4+ T cells, stable isotope labeling (SIL) experiments were performed with in vitro-activated T cells using gas chromatography (GC) coupled to mass spectrometry (MS).

2024-08-24 | PXD055328 |

CD4+ cell transcriptional profiling by RNA sequencing

Project description:<p>We use next generation sequencing to investigate the different transcriptomes of closely related CD4+ T-cells from healthy human donors to elucidate the genetic programs that underlie their specialized immune functions. Six cell types were included: Regulatory T-cells (CD25hiCD127low/neg with >95% FOXP3+ purity), regulatory T-cells activated using PMA/ionomycin, CD25-CD45RA+ ('naive' helper T-cells), CD25-CD45RO+ ('memory' helper T-cells), activated Th17 cells (>98% IL17A+ purity) and activated IL17-CD4+ T-cells (called 'ThPI'). Poly-T capture beads were used to isolate mRNA from total RNA, and fragment sizes of ~200 were sequenced from both ends on Illumina's genome analyzer. We confirm many of the canonical signature genes of T-cell populations, but also discover new genes whose expression is limited to specific CD4 T-cell lineages, including long non-coding RNAs. Additionally, we find that genes encoded at loci linked to multiple human autoimmune diseases are enriched for preferential expression upon T-cell activation, suggesting that an aberrant response to T-cell activation is fundamental to pathogenesis.</p>

| phs000626 | dbGaP

LC-MS to identy the interacting protein with pri-miR-31 in CD4+ T cells

Project description:This project was aimed to identify the proteomic of pri-miR-31 interacting in naïve and activated cd4+ T cells. Immunoprecipitates pulled down by pri-miR-31 were subjected to LC-MS. Our results reveal the interacting protein in different state of CD4+ T cells.

2024-06-24 | PXD038182 | Pride

CD4+T cells activation

Project description:Aanlysis of human resting CD4+T cells and cells activated by two different methods: CD4+ T cells unstimulated (be susceptible but not support to HIV-1) and stimulated either by CD3/CD28 costimulation (reversed susceptibility and resisted to HIV-1) or by PHA/IL-2 for six days (be susceptible and support to HIV-1) to investigate potential mechanism of reversing susceptible to HIV-1. We measured gene expression in resting human CD4+T cells and cells activated by two methods for six days which could induce different effects to HIV-1. Three independent experiments were performed at each treatments using different donors for each experiment.

2013-04-10 | E-GEOD-34252 | biostudies-arrayexpress

GNPS - Nrf2 drives activation-driven expansion of CD4+ T-cells by modulating glucose and glutamine metabolism

Project description:Metabolomics data pertaining to "Nrf2 drives activation-driven expansion of CD4+ T-cells by modulating glucose and glutamine metabolism" manuscript

2025-07-17 | MSV000098549 | GNPS

Multiomic profiling of chronically activated CD4+ T cells identifies drivers of exhaustion and metabolic reprogramming

Project description:T-cell exhaustion occurs when T cells are chronically activated, usually in the context of cancer or chronic infection. Exhausted T cells lose effector functions, upregulate inhibitory receptors, and lose proliferation ability. Understanding the mechanisms of T-cell exhaustion is important as it has critical clinical applications, such as checkpoint blockade therapy. CD4+ T cells are understudied in the context of exhaustion, and no large-scale multiomic datasets containing proteomics, phosphoproteomics, or metabolomics exist. We therefor performed a multiomic experiment to profile this cell state using a time course analysis to also capture progression.

2024-11-28 | PXD057703 | Pride

Immunometabolism in resolving atherosclerosis guides the development of nanometabolite therapy

Project description:A 6-month in vivo study will be carried out at Case Western Reserve University (CWRU) using an ApoE-/- mouse model of atherosclerosis (obtained from The Jackson Laboratory), which will be treated as follows: Control: Mice fed a chow diet (control) (n=12) Progression: Mice fed a high-fat diet with cholesterol (n=12) Regression: Mice fed a high-fat diet with cholesterol followed by a switch to a chow diet (n=12) At the end of the experiment, mice will be euthanized and aorta excised from each animal. They will be immediately incubated in dialyzed serum-containing medium with uniformly C13 labelled glucose for 24 h and then extracted for Stable Isotope Resolved Metabolomics (SIRM) experiments. The incubation media and tissue extracts will be sent to University of Kentucky’s RC-SIRM: Resource Center for Stable Isotope-Resolved Metabolomics for analysis. The samples will undergo the following modes of analysis: nuclear magnetic resonance (NMR), Ion Chromatography Coupled with Mass Spectrometry (ICMS)

2025-05-06 | PXD041137 | Pride

Analysis of BTLA regulated transcripts in human B and CD4+ T cells

Project description:Purified B or CD4+ T cells were analyzed for transcriptional changes induced by the BTLA inhibitory receptor. BTLA receptors were activated using anti-human BTLA coupled to microbeads. Gene expression was analyzed using Nanostring

2022-01-28 | GSE194314 | GEO

Effect of mitochondrial electron transport chain blockade on transcriptomic profile in human H460 cells

Project description:Cancer cells reprogram their metabolism to support cell growth and proliferation in harsh environments. To assess how human cells respond to defective mitochondrial respiration, we analyzed metabolomics profiles in cells with deficient electron transport chain (ETC). We found that ETC deficiency induces an accumulation of purine nucleotides. Additionally, we revealed that ETC blockade suppressed de novo purine nucleotide biosynthesis while enhanced purine salvage. This metabolic rewiring of purine nucleotide biosynthesis is not regulated at the transcriptional level. Instead, stable isotope tracing experiments showed that ETC blockade promoted the oxidative branch of pentose phosphate pathway to elevate phosphoribosyl diphosphate to drive purine salvage. In summary, our findings delineate how cells remodel purine metabolism in response to ETC blockade, and uncover a new metabolic vulnerability in tumors with low respiration.

2024-05-09 | GSE265923 | GEO