Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mouse PSC Q-regulated matrisome

ABSTRACT: The goal of this project was to assess how glutamine availability regulates the matrisome. ECM deposited by pancreatic stellate cells (PSCs) in the presence of TGFb stimulation under 4, 1, or 0.4mM glutamine (Q) was profiled.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture, Fibroblast

DISEASE(S): Pancreatic Carcinoma

SUBMITTER: Simon Schwoerer

LAB HEAD: Simon Schwoerer

PROVIDER: PXD073686 | Pride | 2026-04-19

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	20250819_MSC1971_4_1.raw	Raw
	20250819_MSC1971_4_2.raw	Raw
	20250819_MSC1971_4_3.raw	Raw
	20250820_MSC1971_04_1.raw	Raw
	20250820_MSC1971_04_2.raw	Raw

Items per page:

1 - 5 of 12

Publications

Glutamine-dependent changes in fibroblast-derived extracellular matrix dictate cancer cell behavior.

Guillard Julien J Stradley Jessica J Turan Kristof K Storl-Desmond Marta R MR Lin Shan S Huang Yi-Chia YC Forti Kevin Muñoz KM Weber Christopher R CR Schwӧrer Simon S

Matrix biology : journal of the International Society for Matrix Biology 20260325

The extracellular matrix (ECM) provides key biochemical and biomechanical cues that govern fundamental cellular processes, including growth and migration. ECM dysregulation and altered cell-matrix interactions are drivers of cancer progression, exemplified by pancreatic ductal adenocarcinoma (PDAC), where an abnormally dense, collagen-rich, and stiff ECM correlates with poor patient outcomes. The PDAC microenvironment is poorly perfused, resulting in altered nutrient availability, yet how this m ...[more]

PMID: 41895622

Similar Datasets

2E7 Antigen Identification Using PhAbomics Technology

Project description:Antibody–drug conjugates (ADCs) require antibodies with both high specificity and efficient internalization—features often overlooked by conventional discovery pipelines that rely on preselected antigens and recombinant proteins. Here, we present an integrated phenotypic platform that combines target-unbiased live-cell biopanning with in situ chemical crosslinking and mass spectrometry to concurrently identify internalizing 49 antibodies and their membrane-bound cognate antigens in a physiologic context.

2025-11-20 | PXD065365 | Pride

USP26 overexpressing HEK293T cells LC-MS/MS

Project description:To elucidate the mechanism by which USP26 dictates HCC tumorigenesis, we attempted to identify the protein associated with USP26 using a triple-epitope (S-protein, FLAG tag and streptavidin binding peptide)-tagged version of USP26 (SFB-USP26). Tandem affinity purification followed by mass spectrometric analysis identified several strong interactors of USP26.

2024-09-09 | PXD051958 | Pride

Ribosome dynamics orchestrate mRNA stability and translation across natural and synthetic systems

Project description:The dynamic interplay between ribosomes and mRNAs plays a central role in gene expression regulation, balancing protein synthesis and mRNA stability. However, traditional methods capturing static ribosome occupancy fail to resolve the temporal dynamics governing these processes. Here, we introduce Temporal Ribosome Density Profiling (TRiP), which combines metabolic RNA labeling and polysome sequencing to map ribosome density dynamics across the mRNA lifespan. TRiP reveals a striking temporal symmetry conserved across cell types: gene-specific ribosome loading rates are counterbalanced by coordinated unloading rates, creating a self-regulatory loop that, as demonstrated through biophysical modeling and experimental validation in diverse cellular contexts, directly couples ribosome dynamics to mRNA stability. We further uncover how mRNA structural motifs and m6A methylation fine-tune ribosome dynamics at the isoform level, simultaneously modulating protein output and transcript half-life. In macrophages, this dynamic control enables rapid immune responses by upregulating translation efficiency of pro-inflammatory genes. Remarkably, these principles extend to synthetic mRNAs, where machine learning-guided optimization of ribosome dynamics enhances protein production. Our work establishes ribosome density dynamics as a pervasive and tunable regulatory axis, with broad implications for adaptive immunity, RNA biology, and the design of therapeutic mRNAs.

2025-12-10 | PXD070830 | Pride

THP-1 data for:Ribosome dynamics orchestrate mRNA stability and translation across natural and synthetic systems

2025-12-10 | PXD070845 | Pride

Mapping the Interactome of KRAS and Its G12C/D/V Mutants by Integrating TurboID Proximity Labeling with Quantitative Proteomics

Project description:RAS is one of the most frequently mutated proto-oncogenes in human malignancies, with mutation sites and subtypes exhibiting tumor-type dependent distribution. Oncogenic RAS mutations will maintain continuously GTP-bound activation states that leading to dysregulation of downstream signaling, ultimately disrupting cellular homeostasis to induce malignant transformation of cells. In this study, we employed TurboID proximity-labeling technology integrated with quantitative proteomics LC-MS/MS to systematically characterize the proximal binding proteins of wild-type KRAS and three high-frequency oncogenic mutant subtypes G12C, G12D and G12V. Through comprehensive bioinformatic analysis of mutation-specific interaction networks and distinct metabolic pathways, we identified significant enrichment of mutant KRAS binding proteins in insulin signaling pathway, reactive oxygen species related pathways, glucose and lipid metabolism and so on. Metabolic reprogramming pathways in KRAS G12 mutations collectively fuel tumor proliferation and immune evasion. In addition, we also comparatively analyzed the proximal binding proteins similarity in three G12 mutants. Notably, we observed that the KRAS E3 ubiquitin ligase adaptor LZTR1 diminished binding with mutations, and the mTORC1 important regulatory protein LAMTOR1 was enhanced recruitment by mutations. This multi-dimensional profiling delineates a comprehensive mapping of KRAS WT and G12 mutant interactomes and unveils the metabolic reprogramming pathways associated with KRAS activating mutations. Our analysis result provides potential therapeutic targets for KRAS-driven tumorigenesis while establishing a mechanistic framework for developing KRAS mutation-specific therapeutic strategies.

2025-06-09 | PXD062101 | Pride

Hepa1-6 cell line overexpressing Flag-LTA4H LC-MS/MS

Project description:To explore potential proteins binding with LTA4H, co-immunoprecipitation (co-IP) and LC-MS/MS analysis were performed using Hepa1-6 cells overexpressing Flag-LTA4H. Anti-Flag and anti-IgG antibodies were used for immunoprecipitation to identify the interacting proteins.

2025-05-07 | PXD060326 | Pride

human Embryonic stem cells LC-MSMS

Project description:Genomic instability is the main cause of abnormal embryo development and abortion. NLRP7 dysfunctions affect embryonic development and lead to Hydatidiform Moles, but the underlying mechanisms remain largely elusive. Here, we show that NLRP7 knockout affects the genetic stability, resulting in increased DNA damage in both human embryonic stem cells and blastoids, making embryonic cells in blastoids more susceptible to apoptosis. Mechanistically, NLRP7 can interact with factors related to alternative splicing and DNA damage response, including DDX39B, PRPF8, THRAP3 and PARP1. Moreover, NLRP7 dysfunction leads to abnormal AS of genes involved in Homologous recombination in human embryonic stem cells, Such as Brca1 and Rad51. These results indicate that NLRP7-mediated Alternative splicing is potentially required for the maintenance of genome integrity during early human embryogenesis. Together, this study uncovers that NLRP7 plays an essential role in the maintenance of genetic stability during early human embryonic development by regulating alternative splicing of Homologous Recombination-related genes.

2025-01-17 | PXD059649 | Pride

Proteome-wide identification of cysteine S-sulfenylation in response to low temperature and low-humidity stress in Dendrobium huoshanense

Project description:Objective:Dendrobium huoshanense is a renowned geo-authentic herb, and its excellent quality is closely correlated with the specific combined stress of low temperature and low humidity found in its native habitat.Methods:In this study, we profiled the protein S-sulfenylation landscape of D. huoshanense under simulated low temperature and low humidity stress using Cys-Tag labeling coupled with Data-Independent Acquisition (DIA) mass spectrometry.Results:Physiological analysis revealed a moderate accumulation of H₂O₂ at 12 h of stress, representing an early signaling phase. A total of 9,924 sulfenylation sites mapped to 6,953 proteins were identified. Following stress treatment, 226 sites showed differential modification, 202 of which were upregulated. Motif analysis demonstrated a significant enrichment of lysine and arginine residues flanking the modification sites. Enrichment analysis indicated that S-sulfenylation is primarily involved in vesicle trafficking, carbon metabolism, and amino acid biosynthesis.Conclusion:This study characterizes the response of sulfenylated proteins to low temperature and low humidity stress in D. huoshanense, providing theoretical insights into the molecular mechanisms of plant redox regulation under abiotic stress.

2026-03-02 | PXD074422 | Pride

Mass spectrometry identification of phosphorylation sites of GCN5 in rice

Project description:Firstly, wild type seedlings that had germinated in root tubes for 14 days were taken to prepare protoplasts. The GCN5-FLAG transient expression vector was transformed into wild type protoplasts. The protoplasts were collected and purified by Flag beads. After quality testing of the samples, phosphorylation mass spectrometry sequencing of GCN5 was performed.

2025-10-28 | PXD066361 | Pride

Macrophage SH3GLB1 is required for Rab7-1 mediated mitophagy in inflammation during acute lung injury

Project description:Acute lung injury (ALI) accompanied by an inflammatory response is an important complication after drowning. Macrophage activation and polarization are implicated in the inflammatory process of lipopolysaccharide (LPS)-induced ALI (LPS-ALI), but little is known about drowning-induced ALI (drowning-ALI). SH3GLB1 is a member of the endophilin family and has been shown to be involved in mitochondrial morphological changes and autophagy. However, its role in ALI remains unclear. Here,we performed single-cell profiling of lung immune cells isolated from the lungs of drowning-ALI mouse models. We found that the regulation of macrophages in drowning-ALI was similar to that in LPS-ALI. Specifically, SH3GLB1 was highly expressed in macrophages of drowning-ALI mouse models and was related to inflammation. Furthermore, SH3GLB1 deletion ameliorated LPS-ALI or drowning-ALI. In contrast, the restoration of SH3GLB1 expression provoked LPS-ALI and drowning-ALI. Mechanistically, SH3GLB1 was shown to interact with Rab7 to contribute to mitophagy, which resulted in mitochondrial dysfunction. Overall, these findings indicated that SH3GLB1 is required for Rab7-mediated mitophagy in inflammation during ALI and could be a novel target for lung protection.

2026-02-10 | PXD073650 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data