Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mouse inguinal white adipose tissue (iWAT) LC-MS

ABSTRACT: Proteomic analysis of whole tissue and isolated mitochondria from iWAT in a mouse model of diet induced obesity with or without SANA.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Subcutaneous Adipose Tissue

DISEASE(S): Obesity

SUBMITTER: Alejandro Leyva

LAB HEAD: Rosario Durán

PROVIDER: PXD030485 | Pride | 2025-03-24

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	190314_HFD_iWAT_0.raw	Raw
	190314_HFD_iWAT_0.txt	Txt
	190314_HFD_iWAT_0_1.raw	Raw
	190314_HFD_iWAT_1.raw	Raw
	190314_HFD_iWAT_1.txt	Txt

Items per page:

1 - 5 of 39

Similar Datasets

Evaluation of the secretome of senescent melanoma cells and the impact of silencing Mfn1 on the senescence-associated secretory phenotype (SASP) by shotgun proteomics analysis.

Project description:Cellular senescence is a therapy endpoint in melanoma, and the senescence-associated secretory phenotype (SASP) can affect tumor growth and microenvironment, influencing treatment outcomes. Metabolic interventions can modulate the SASP, and an enhanced mitochondrial energy metabolism supports resistance to therapy in melanoma. In a previous report we showed that in melanoma, senescence induced by the DNA methylating agent temozolomide, increases fusion proteins mitofusins 1 and 2. Silencing Mfn1 or Mfn2 expression reduced interleukin-6 secretion by senescent cells. Here we expanded these observations evaluating the secretome of senescent melanoma cells using shotgun proteomics, and explored the impact of silencing Mfn1 on the SASP. A significant increase in proteins reported to reduce the immune response towards the tumor was found in the media of senescent cells. The secretion of several of these immunomodulatory proteins was affected by Mfn1 silencing, among them was galectin-9. In agreement, tumors lacking mitofusin 1 responded better to treatment with the methylating agent dacarbazine, tumor size was reduced and a higher immune cell infiltration was detected in the tumor. Our results highlight mitochondrial dynamic proteins as potential pharmacological targets to modulate the SASP in the context of melanoma treatment.

2024-01-26 | PXD043779 | Pride

LC-MS/MS proteomic analysis of pharyngeal swabs and plasma from MHV-infected and uninfected mice

Project description:Recent developments have broadened our perception of SARS-CoV-2, indicating its capability to affect the body systemically beyond its initial recognition as a mere respiratory pathogen. However, the pathways of its widespread are not well-understood. Employing a dual-modality approach, we integrated findings from a Murine Hepatitis Virus (MHV) infection model with corroborative clinical data to investigate the pervasive reach of Coronaviruses. The novel presence of viral particles within red blood cells (RBCs) was demonstrated via High Resolution Transmission Electron Microscopy, with computational modeling elucidating a potential heme-mediated viral entry mechanism via Spike protein affinity. Our data affirm viral localization in RBCs, suggesting heme moieties as facilitators for cellular invasion. Exacerbation of MHV pathology upon hemin administration, contrasted with chloroquine-mediated amelioration, underscoring a heme-centric pathway in disease progression. These observations extend the paradigm of Coronavirus pathogenicity to include hemoprotein interactions. This study casts new light on the systemic invasion capabilities of Coronaviruses, linking RBC hemoproteins with viral virulence. The modulation of disease severity through heme-interacting agents heralds a promising avenue for COVID-19 therapeutics. Our findings propose a paradigm shift in the treatment approach, leveraging the virus-heme interplay as a strategic hinge for intervention.

2024-12-11 | PXD054355 | Pride

SopB and SifA modify the proteome of the Salmonella-containing vacuole in the social amoeba Dictyostelium discoideum

Project description:Salmonella enterica serovar Typhimurium is a rod-shaped Gram-negative bacterium. It is a leading cause of gastroenteritis and public health problem. In the environment, it interacts with protozoa, particular amoeba, however the interactions between Salmonella and these eukaryotic microbes have not been addressed in detail. We and others recently described that S. Typhimurium is able to survive in the model amoeba Dictyostelium discoideum requiring the Salmonella pathogenicity islands 1 and 2 (SPI-1 and SPI-2, respectively)-encoded type three secretion systems (T3SSs). In this work, we investigated the role of two particular effector proteins, SopB and SifA that are secreted by either one of the T3SSs. SopB and SifA are involved in the remodelling of the intracellular compartment that contains Salmonella (Salmonella-containing vacuole, SCV) in other cellular models. We combined genetic and proteomics analysis to investigate the roles of SopB and SifA during infections of D. discoideum. We identified over 1,000 proteins per sample performing proteomics on fractions enriched in SCVs from amoeba cells infected with wild-type, sopB or sifA S. Typhimurium. Among them, we observed several Rho GTPases, guanine nucleotide exchange factors and motor proteins. Finally, we decided to evaluate if the changes observed in the proteome from the SCV of wild-type and mutants affect the intracellular survival of S. Typhimurium. These finding suggest that Salmonella exploits this route to survive intracellularly, a process that requires SopB and/or SifA effectors. To our knowledge this is the first proteomic description of the Salmonella intracellular compartment in D. discoideum.

2020-09-23 | PXD014955 | Pride

Proteomic comparison between two Salmonella serovars with differential pathogenicity in humans.

Project description:Salmonella infections are among the most common foodborne diseases worldwide. The Enteritidis and Dublin serovars of Salmonella enterica are closely related yet they differ significantly in pathogenicity and epidemiology. Enteritidis is a broad-host-range serovar that commonly causes gastroenteritis and infrequently causes invasive disease in humans. Dublin mainly colonizes cattle but upon infecting humans often results in invasive disease. The aim of this work was to elucidate the molecular factors responsible for the differential pathogenic behavior between both serovars. We performed a quantitative proteomic comparative analysis between one clinical isolate of each serovar grown in vitro under gut mimicking conditions (GMC). Compared to S. Enteritidis, the S. Dublin proteome was enriched in proteins linked to response to several stress conditions, such as those encountered during host infection, as well as to virulence. The S. Enteritidis proteome contained proteins related to central anaerobic metabolism pathways that were undetected in S. Dublin. Similar differences were also found at the transcriptional level, as mRNA levels correlated with proteomic results for 17 of the 20 genes tested in 4 natural isolates of each serovar grown in GMC. This work reveals proteomic differences between two Salmonella serovars with markedly different invasive and host-range characteristics, grown in an infection relevant condition, which were not evident in previous comparative genomic analyses.

2021-09-09 | PXD021353 | Pride

Quantitative proteomic dataset from oro- and naso-pharyngeal swabs used for COVID-19 diagnosis: detection of viral proteins and host’s biological processes altered by the infection

Project description:We recovered proteins from SARS-CoV-2 positive and negative oro/naso-pharyngeal swabs, obtained from diagnostic center localized at Institut Pasteur de Montevideo, and performed comparative quantitative proteomic analysis.

2020-07-28 | PXD020394 | Pride

Proteome remodeling in the Mycobacterium tuberculosis PknG knockout: molecular hints for the role of this kinase in cell envelope biogenesis and hypoxia.

Project description:Tuberculosis, a pulmonary disease caused by the etiological agent Mycobacterium tuberculosis, is the leading cause of death by a single infectious agent among human beings. One of M. tuberculosis's pathogenic hallmarks is its ability to persist in a dormant state in the host for long periods, reinitiating the infectious cycle when favorable environmental conditions are found. Thus, it is not surprising that this pathogen has developed different mechanisms to withstand the stressful conditions found in the host. In particular, the Ser/Thr protein kinase PknG has gained special relevance since it regulates nitrogen metabolism and facilitates bacterial survival inside macrophages. Nevertheless, the molecular mechanisms underlying these effects are far from being elucidated. To further investigate these issues, we performed quantitative proteomics analyses of protein extracts from M. tuberculosis H37Rv and a mutant derivative lacking PknG. Our results show that in the absence of PknG the mycobacterial proteome was remodeled since 6.5% of the proteins encoded by M. tuberculosis presented significant changes in its relative abundance when compared to the wild-type strain. The main biological processes affected by PknG deletion were the biosynthesis of cell envelope components and the response to hypoxic conditions. Altogether, the results presented here allow us to postulate that PknG regulation of bacterial fitness to stress conditions in host macrophages might be an essential mechanism underlying its reported effect on intracellular bacterial survival.

2021-06-02 | PXD023975 | Pride

Quantitative proteomic analysis reveals altered enzyme expression profile in Zea mays roots during the early stage of colonization by Herbaspirillum seropedicae

Project description:It was investigated the changes in protein expression in maize roots in response to treatment with Herbaspirillum seropedicae. To identify maize proteins whose expression levels were altered in the presence of bacteria, a label-free quantitative proteomic approach was used.

2024-07-02 | PXD019200 | Pride

Physicochemical and proteomic characterization reveals a remodeling of Escherichia coli and Proteus mirabilis outer membrane vesicles obtained under culture conditions mimicking urine growth

Project description:Uropathogenic bacteria present a variety of mechanisms that allow them to colonize the urinary tract. These mechanisms include biofilm formation, urothelial cell invasion, and the production of adhesins, toxins, and siderophores. Uropathogenic Escherichia coli and Proteus mirabilis are two of the most common etiological agents causing urinary tract infections (UTI). In addition to virulence factors, Gram-negative bacteria can produce outer membrane vesicles (OMVs). The OMVs may have several functions in the context of UTI. In the present work, we isolated and characterized OMVs from two clinical strains: E. coli U144 and P. mirabilis 2921 cultured in Luria-Bertani broth and artificial urine. The OMVs were examined using DLS, NTA and TEM and found to be between 85 and 260 nm in size, the largest being those obtained in artificial urine. All OMVs had a low polydispersity factor and negative charge in their surface. Through proteomic analysis (nanoLC-MS/MS), 282 and 353 proteins were identified in OMVs obtained from E. coli and P. mirabilis LB cultures respectively, and 215 and 103 proteins when they were grown in AU. The majority of proteins were from the bacterial envelope. Also, several proteins related to motility and adhesion were found. The composition of OMVs proteins was different according to the culture medium. Among the identified proteins, those related with zinc and iron uptake systems could have an important role in AU. These results bring us closer to understanding the possible role of OMVs in the pathogenesis of UTIs.

2024-10-25 | PXD052681 | Pride

Aberrant astrocyte protein secretion contributes to altered neuronal development in diverse disorders

Project description:Astrocytes negatively impact neuronal development in a range of neurodevelopmental disorders (NDs), however how they do this, and if mechanisms are shared across multiple disorders, is not known. We developed an in vitro system to ask how astrocyte protein secretion and gene expression change in 3 genetic NDs. This identified disorder specific changes, as well as core proteins that are increased in release in all 3 NDs. ND astrocytes increase release of Igfbp2, and blocking Igfbp2 partially rescues the neurite outgrowth inhibitory effects of Rett Syndrome astrocytes. We identified that ND astrocytes upregulate release of Bmp6, which acts on astrocytes themselves and is upstream of astrocyte secretion changes in NDs. Blocking Bmp signaling in Fragile X Syndrome astrocytes reverses the inhibitory effects of FXS astrocytes on neuronal development. We provide a resource of astrocyte secreted proteins in health and NDs, as well as novel targets for intervention in diverse NDs.

2022-07-11 | PXD015996 | Pride

Secretome analysis of basidiomycetous yeast Tausonia pullulans growing on glucose and starch

Project description:We performed the genomic sequencing, assembly and annotation of T. pullulans strain CRUB 1754 (Perito Moreno glacier, Argentina), a gene survey of Carbohydrate-active enzymes (CAZymes); and analyzed its secretome by Liquid-Chromatography coupled to tandem Mass Spectrometry (LC-MS/MS) after growth in glucose (GLU) or starch (STA) as main carbon sources.

2022-12-02 | PXD031068 | 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