Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Label free quantification approach comparing hepatic tissue from SCD and healthy mice

ABSTRACT: Sickle cell disease (SCD) is characterized by the expression of an abnormal hemoglobin variant (HbS) that promotes distortion and early destruction of red blood cells, resulting in hemolytic anemia, vaso-occlusive crisis, ischemia and, ultimately, tissue damage. Hepatic function is specially compromised in SCD patients; however, the underlying pathological mechanisms remain largely unknown. In the current study, through a label free quantitative proteomic approach, we identified significant alterations in protein expression compared to healthy controls. These changes unveiled distinct proteome expression profiles between groups.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Liver

DISEASE(S): Sickle Cell Disease

SUBMITTER: Lucía Beltrán-Camacho

LAB HEAD: Lucía Beltrán Camacho

PROVIDER: PXD069285 | Pride | 2026-03-10

REPOSITORIES: pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	checksum.txt	Txt
	sol2022031_experimentohigadocompleto.zip	Other
	sol2022031_muestra10_S1-C1_1_3244.d.zip	Other
	sol2022031_muestra1_S1-B1_1_3241.d.zip	Other
	sol2022031_muestra2_S1-B2_1_3245.d.zip	Other

Items per page:

1 - 5 of 12

Similar Datasets

Muscle Cathepsin B benefits Alzheimer's Disease mice

Project description:Muscle secretes factors during exercise that enhance cognition. Myokine Cathepsin B (Ctsb) is linked to memory, but its role in neurodegeneration is unclear. Here we show that AAV-vector-mediated Ctsb overexpression in skeletal muscle, in an Alzheimer’s Disease (AD) mouse model (APP/PS1), improved motor coordination, memory and adult hippocampal neurogenesis, while plaque density was unchanged. Conversely, in wildtype (WT) mice Ctsb impaired memory. To understand underlying mechanisms, hippocampus, muscle and plasma proteomic analyses were performed. In AD mice, Ctsb treatment increased abundance of hippocampal proteins involved in mRNA metabolism and protein synthesis. In muscle, Ctsb treatment increased protein translation in AD mice, whereas in WT mitochondrial proteins decreased. Additionally, in AD mice Ctsb enhanced plasma metabolic and mitochondrial processes, and reduced inflammatory responses. The differing protein abundance profiles in the AD and WT treatment groups correspond to effects on memory function. Overall, skeletal muscle Ctsb expression is a potential AD therapeutic.

2025-11-17 | PXD057069 | Pride

The protein composition of 10A EV and 231 EV samples

Project description:Proteins in the EVs of MCF-10A and MDA-MB-231 cells were determined by mass spectrometry using a timsTOF Pro mass spectrometer (Bruker) coupled to an Aurora Ultimate reverse-phase column (IonOpticks)

2025-10-05 | PXD069130 | Pride

Loss of Cullin 5 in myeloid cells protects against autoimmune neuroinflammation

Project description:Autoimmune neuroinflammation occurs when an individual’s immune cells attack the brain, spinal cord or peripheral nerves. Several Suppressor of Cytokine Signaling (SOCS) proteins have been shown to limit pro-inflammatory signaling pathways in myeloid cells and prevent neuroinflammation. They rely on several mechanisms to accomplish this. Their SH2 domain allows them to bind phosphorylated tyrosine residues on surface receptors to prevent downstream signaling while their C-terminal SOCS domain can promote their assembly with Cullin5 (CUL5) to degrade signaling proteins. To date, the role of CUL5 in myeloid-cell-mediated function is poorly understood. Here we show that loss of Cul5 in myeloid cells resulted in reduced neuroinflammation and attenuated progression of Experimental Autoimmune Encephalomyelitis (EAE). Although peripheral CD4+ T cell activation was not overtly affected, Cul5-deficient macrophages in the Central Nervous System (CNS) demonstrated a significant shift towards an anti-inflammatory phenotype, characterized by increased expression of Arginase 1. This correlated with an enhanced frequency of FoxP3+ regulatory T cells. In contrast to what would be predicted if CUL5 and SOCS proteins work together to degrade pro-inflammatory cytokine signaling, Cul5 deletion in myeloid cells selectively enhanced IL-4-mediated Arginase 1 expression. These findings identify CUL5 as an unanticipated pro-inflammatory mediator during neuroinflammation and reveal its potential as a therapeutic target for autoimmune diseases.

2025-08-04 | PXD066533 | Pride

Personalized Molecular Signatures of Insulin Resistance and Type 2 diabetes

Project description:Insulin resistance is a hallmark of type 2 diabetes, a highly heterogeneous condition with diverse pathological characteristics. Understanding the molecular adaptation to insulin resistance and its association with individual phenotypic traits is crucial for advancing precision medicine in diabetes. By utilizing cutting-edge proteomics technology, we mapped the proteome and phosphoproteome of basal and insulin-stimulated skeletal muscle from >120 individuals with varying degrees of insulin sensitivity, both with and without type 2 diabetes. Leveraging deep in vivo phenotyping data, we reveal that the basal proteome and phosphoproteome are strong predictors of insulin sensitivity. The insulin-stimulated phosphoproteome identified preserved and dysregulated signaling even in individuals with the most severe insulin resistance. Our study elucidates substantial differences in the male and female (phospho)proteome; however, the molecular signature associated with insulin resistance remains largely similar between sexes. These findings emphasize the importance of recognizing disease heterogeneity and advocate for the precision medicine approach for effective care in type 2 diabetes.

2025-05-27 | PXD049129 | Pride

MYC deregulation sensitizes cancer cells to N-myristoyltransferase inhibition - Th-MycN tumour proteomics

Project description:Human N-myristoyltransferases (NMTs) catalyze N-terminal protein N-myristoylation and are promising targets in cancer, with an emerging mechanistic rationale for targeted therapy. Here, we screened 245 cancer cell lines against IMP-1320, a potent NMT inhibitor (NMTi), and conducted pathway-level analyses to identify that deregulated MYC increases cancer cell sensitivity to NMTi. Proteomics on detergent-enriched membrane fractions in MYC or MYCN-deregulated cancer cell models revealed that cell death is associated at least in part with loss of membrane association of mitochondrial respiratory complex I. This is concurrent with loss of myristoylation and degradation of the complex I assembly factor NDUFAF4, and induction of mitochondrial dysfunction, driven by MYC or MYCN-deregulation. NMTi eliminated or suppressed MYC and MYCN-driven tumors in vivo without overt toxicity, suggesting that this constitutive co-translational protein modification can be targeted in MYC-driven cancers. This dataset comprises the proteomic data obtained from Th-MycN tumours, excised from 129SvJ mice treated intraperitoneally with vehicle or IMP1320 (25 mg/kg/day), on a three days on/four days off dosing schedule.

2025-07-30 | PXD063661 | Pride

MYC deregulation sensitizes cancer cells to N-myristoyltransferase inhibition - DoHH2 proteomics

Project description:Human N-myristoyltransferases (NMTs) catalyze N-terminal protein N-myristoylation and are promising targets in cancer, with an emerging mechanistic rationale for targeted therapy. Here, we screened 245 cancer cell lines against IMP-1320, a potent NMT inhibitor (NMTi), and conducted pathway-level analyses to identify that deregulated MYC increases cancer cell sensitivity to NMTi. Proteomics on detergent-enriched membrane fractions in MYC or MYCN-deregulated cancer cell models revealed that cell death is associated at least in part with loss of membrane association of mitochondrial respiratory complex I. This is concurrent with loss of myristoylation and degradation of the complex I assembly factor NDUFAF4, and induction of mitochondrial dysfunction, driven by MYC or MYCN-deregulation. NMTi eliminated or suppressed MYC and MYCN-driven tumors in vivo without overt toxicity, suggesting that this constitutive co-translational protein modification can be targeted in MYC-driven cancers. This dataset comprises the proteomic data obtained from DoHH2 tumours, excised from CB17/SCID mice treated intraperitoneally with vehicle or IMP1320 (25 mg/kg/day), on a three days on/three days off dosing schedule.

2025-07-30 | PXD063851 | Pride

Proteomic changes to immune and inflammatory processes underlie lung preservation using ex vivo cytokine adsorption

Project description:The field of graft preservation has made considerable strides in recent years improving outcomes related to solid organ restoration and regeneration. In lungs, the use of ex vivo lung perfusion (EVLP) in line with devices and treatments has shown promising results within preclinical and clinical studies with the potential to improve graft quality. The benefit of the therapy would be to render marginal and declined donor lungs suitable for transplantation, ultimately increasing the donor pool available for transplantation. Additionally, such therapies used in machine perfusion could also increase preservation time, facilitating logistical planning. Cytokine adsorption has been demonstrated as a potentially safe and effective therapy when applied to the EVLP circuit and post transplantation. The mechanism by which this treatment improves the donor lung on a molecular basis is not yet fully elucidated. We hypothesized that there were characteristic inflammatory and immunomodulatory differences between lungs treated with and without cytokine adsorption, reflecting in proteomic changes in gene ontology pathways and across inflammation-related proteins. In the current study we investigate the molecular mechanisms and signaling pathways of how cytokine adsorption impacts the lung function when used during EVLP and when used post transplantation as hemoperfusion in a porcine model. Lung tissue from EVLP and post lung transplantation were analyzed for their proteomic profile using mass spectrometry. The inflammatory and immune processes were compared between the treated and the non-treated groups to show the differences occurring between the forms of graft preservation.

2023-10-24 | PXD044413 | Pride

Deep Proteome profiling reveals signatures of age and sex differences in paw skin and sciatic nerve of naïve mice

Project description:The age and sex of studied animals profoundly impacts experimental outcomes in animal-based biomedical research. However, most preclinical studies in mice use a wide-spanning age range from 4 to 14 weeks and do not assess study parameters in male and female mice in parallel. This raises concerns regarding reproducibility and neglect of potentially relevant age and sex differences. Furthermore, the molecular setup of tissues in dependence of age and sex is unknown in naïve mice precluding efficient translational research. Here, we first compared two different mass spectrometric acquisition methods – DDA- and DIA-PASEF – in order to maximize the depth of proteome quantitation. We then employed an optimized workflow of quantitative proteomics based on DIA-PASEF followed by DIA-NN data analysis, and revealed significant differences in mouse paw skin and sciatic nerve (SCN) when comparing (i) male and female mice, and, in parallel, (ii) adolescent mice (4 weeks) with adult mice (14 weeks).

2022-11-29 | PXD034476 | Pride

Full proteome analysis of Chlorotonil treated S. aureus

Project description:Part of manuscript for the identifiaction of the cellular targets of Chlorotonil and its derivatives,

2025-03-08 | PXD051735 | Pride

Time-resolved profiling of linear Ub chain interactors

Project description:Synergizing photocaged linear diubiquitin-Dha with biotinylated linear-Fab for time-resolved profiling of interactors in living cells.

2026-02-06 | PXD070194 | Pride