Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomic Profiling of Microsporum canis Unveils the Fungicidal Mechanisms of Methylene Blue-Mediated Photodynamic Therapy

ABSTRACT: This study applied an integrated DIA proteomics and untargeted metabolomics approach to investigate the molecular responses of Microsporum canis following methylene blue-mediated photodynamic therapy (MB-PDT). The combined datasets revealed widespread and coordinated changes across protein expression and metabolite pools. MB-PDT induced a systemic, multi-targeted disturbance of fungal physiology that converges on cellular energetics, proteostasis, membrane integrity, virulence determinants, and stress-response networks. Key mechanisms included disruption of membrane integrity, downregulation of virulence factors like secreted proteases, and impairment of the antioxidant defense system. The findings suggest that MB-PDT exerts its fungicidal effect through a multi-pronged mechanism, providing novel insights and supporting its development as an effective therapy for dermatophytosis.

ORGANISM(S): Microsporum Canis

SUBMITTER: Xinyu Zhang

PROVIDER: PXD069640 | iProX | Mon Oct 20 00:00:00 BST 2025

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Similar Datasets

RIPK3 activation leads to cytokine synthesis that continues after loss of cell membrane integrity

Project description:Necroptosis is a form of programmed cell death that is defined by activation of the kinase RIPK3, and subsequent cell membrane permeabilization by the effector MLKL. In addition to triggering cell death, RIPK3 activation can promote immune responses through the production of cytokines and chemokines. How active cytokine production is coordinated with the terminal process of necroptosis is unclear. Here, we report that cytokine production continues within necroptotic cells after cells have lost plasma membrane integrity and irreversibly commited to death. The continued production of inflammatory mediators was dependent on mRNA translation, and required maintanence of endoplasmic reticulum integrity, which remained in tact after plasma membrane integrity was lost. The continued translation of cytokines by cellular corpses contributed to necroptotic cell uptake by innate immune cells, as well as priming of adaptive immune responses to antigens associated with necroptotic corpses. These findings imply that necroptosis may represent a program in which cell death and production of inflammatory mediators are coordinated to optimize the immunogenicity of necroptotic cells.

2019-07-13 | GSE134234 | GEO

Genomic comparison in Enteroheamorragic E. coli O157 and non-O157 serotypes by comparative genomic hybridization.

Project description:Background: Enterohemorrhagic Escherichia coli (EHEC) O157 causes severe food-bone illness in humans. The chromosome of O157 consists of 4.1-Mb backbone sequences shared by benign E. coli K-12, and 1.4-Mb O157-specific sequences encoding many virulence determinants such as Shiga toxin genes (stxs) and the locus of enterocyte effacement (LEE). Non-O157 EHECs belonging to clonal lineages distinct from O157 also cause similar illness in humans. According to the parallel evolution model, they have independently acquired the major virulence determinants, stxs and LEE. However, the genomic differences between O157 and non-O157 EHECs have not yet systematically been analyzed. Results: By using the microarray and Whole Genome PCR scanning analyses, we performed a whole genome comparison of 20 EHEC strains of O26, O111, and O103 serotypes with O157. In non-O157 EHEC strains, although genome sizes were similar with or rather larger than O157 and the backbone regions were well conserved, O157-specific regions were very poorly conserved. Only around 20% of the O157-specific genes were fully conserved in each non-O157 serotype. However, the non-O157 EHECs contained a significant number of virulence genes found on prophages and plasmids in O157, and also multiple prophages similar but significantly divergent from those in O157. Conclusion: Although O157 and non-O157 EHECs have independently acquired a huge amount of serotype- or strain-specific genes by lateral gene transfer, they share an unexpectedly large number of virulence genes. Independent infections of similar but distinct bacteriophages carrying these virulence determinants appear to be involved in the parallel evolution of EHEC. Keywords: comparative genomic hybridization, CGH

2007-08-23 | GSE7931 | GEO

Plasma Membrane Integrity Signaling

Project description:Plasma Membrane Integrity Signaling

| PRJNA701242 | ENA

Expression profiling by array of Salmonella enterica serovar Typhimurium (SL1344) qseC mutant x wild type

Project description:“Stress, survival and virulence: the multi-faceted host/microbial interactions.” Bacteria employ epinephrine and norepinephrine, which converge to distinct bacterial crucial processes, like survival and pathogenicity. A novel stress periplasmic membrane protein belonging to previously described BOF family, protein renamed here SrpP, and together with membrane sensor kinase QseC has an essential role in stress response and virulence of S. Typhimurium. SrpP employs its predicted binding pocket, specifically the SrpPE110 residue, and interacts with lipid A modification enzyme, LpxO dioxygenase. Upon this interaction SrpP in S. Typhimurium finely manages multiple membrane functions to culminate in survival upon stress and pathogenesis in vivo, connecting host-stress chemical signaling to cell stress in bacteria. Comparison of sensor histidine kinase qseC mutant expression levels versus wild type strain.

2012-05-31 | E-GEOD-38353 | biostudies-arrayexpress

Expression profiling by array of Salmonella enterica serovar Typhimurium (SL1344) qseC mutant x wild type

2012-06-01 | GSE38353 | GEO

A forward genetic screen identifies potassium channel essentiality in SHH medulloblastoma maintenance [RNA-seq]

Project description:Sequencing cancer genomes is predicted to uncover therapeutic tumor vulnerabilities. This has been complicated by the abundance of genetic alterations which are either non-functional, or only important in tumor initiation or progression. Distinguishing tumor maintenance genes from initiation, progression, and passenger genes is critical for developing effective cancer therapy. We employed a functional genomic approach using the Lazy Piggy transposon to identify tumor maintenance genes in vivo, and apply this to SHH medulloblastoma (MB). Combining Lazy Piggy screening in mice and transcriptomic profiling of human MB, we discovered candidate maintenance genes including the voltage-gated potassium channel Kcnb2. Genetic knockout of Kcnb2 impairs MB growth. Kcnb2 mediates potassium efflux in MB-propagating cells to govern cell volume. Loss of Kcnb2 leads to chronic osmotic swelling and decreased plasma membrane tension, which elevates endocytosis to dampen Egfr signaling, thereby mitigating proliferation of MB-propagating cells. Kcnb2 is largely dispensable for mouse development and synergizes with anti-SHH therapy in treating MB. These results demonstrate the utility of the Lazy Piggy functional genomic approach in identifying cancer maintenance genes, and elucidate a mechanism by which a potassium channel integrates biomechanical and biochemical signaling to promote MB aggression.

2024-09-16 | GSE277171 | GEO

A forward genetic screen identifies potassium channel essentiality in SHH medulloblastoma maintenance [DNA-seq]

2024-09-16 | GSE277172 | GEO

Transcriptional profile of Mycobacterium tuberculosis mycP1-eccE1 deletion mutant

Project description:Mycobacterium tuberculosis is a slow-growing intracellular bacterium with the ability to induce host cell death and persist indefinitely in the human body. This pathogen uses the specialised ESX-1 secretion system to secrete virulence factors and potent immunogenic effectors required for disease progression. ESX-1 is a multi-subunit apparatus with a membrane complex that is predicted to form a pore in the cytoplasmic membrane. In M. tuberculosis this complex is made of five membrane proteins: EccB1, EccCa1, EccCb1, EccD1, EccE1. In this study, we have characterised the membrane component EccE1, and we found that deletion of eccE1 leads to disruption of ESX-1 secretion and attenuation of M. tuberculosis ex vivo.

2019-09-01 | GSE119582 | GEO

Multi-omics-based phenotyping of AFG3L2-mutant lymphoblasts determines key factors of a pathophysiological interplay between mitochondrial vulnerability and neurodegeneration in spastic ataxia type 5

Project description:This study employs a multi-omics approach to investigate the biochemical impact of AFG3L2 mutations in immortalized lymphoblastoid cell lines derived from a SPAX5 patient. Our proteomic analysis revealed significant dysregulation in proteins involved in mitochondrial function, cytoskeletal integrity, and cellular metabolism. Specifically, we observed disruptions in mitochondrial dynamics and calcium homeostasis, characterized by the downregulation of critical mitochondrial proteins such as COX11 and NFU1, and upregulation of key regulatory proteins like PRKCB and KCTD12. Consistent with this, metabolomic profiling identified a marked reduction in acetyl-CoA levels, indicating impaired TCA cycle activity and potential energy deficits. Lipidomic analysis highlighted substantial alterations in lipid composition, with significant decreases in sphingomyelins, phosphatidylethanolamine, and phosphatidylcholine, reflecting disruptions in lipid metabolism and membrane integrity. Our comprehensive investigation into AFG3L2 deficiency elucidates a pathophysiology extending beyond mitochondrial proteostasis, implicating a wide array of cellular processes. The findings reveal substantial cellular disturbances at multiple levels, contributing to neurodegeneration through disrupted mitochondrial calcium homeostasis, cytoskeletal integrity, and altered metabolic and lipid homeostasis. This study underscores the complexity of SPAX5 pathophysiology and the importance of multi-omics approaches in developing effective strategies to address the impact of AFG3L2 deficiency. Our data also highlight the value of immortalized lymphoblastoid cells as a tool for pre-clinical testing and research, offering a detailed biochemical fingerprint that enhances our understanding of SPAX5 and identifies potential areas for further investigation.

2025-05-07 | PXD056395 | Pride

Transcriptomes of 35000HP, ΔcpxA, ΔcpxR mutant strains of Haemophilus ducreyi in mid-log, transition, and stationary phase

Project description:To better understand the role of H. ducreyi CpxRA in controlling virulence determinants, here we defined genes potentially regulated by CpxRA by using RNA-Seq. Activation of CpxR by deletion of cpxA repressed nearly 70% of its targets, including seven established virulence determinants. Inactivation of CpxR by deletion of cpxR differentially regulated few genes and increased the expression of one virulence determinant. We identified a CpxR binding motif that was enriched in downregulated but not upregulated targets. These data reinforce the hypothesis that CpxA phosphatase activity plays a critical role in controlling H. ducreyi virulence in vivo. Characterization of the downregulated genes may offer new insights into pathogenesis.

2015-11-21 | GSE75237 | GEO

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