Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

BACE2 and lipid metabolism (spatial proteomics)

ABSTRACT: spatial proteomic analysis of malanoma IGR37 cell lines

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Malignant Cell

SUBMITTER: vittoria matafora

LAB HEAD: Angela Bachi

PROVIDER: PXD058731 | Pride | 2026-02-09

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	FF_37D1S.raw	Raw
	FF_37D1Srepl.raw	Raw
	FF_37D2S.raw	Raw
	FF_37D2S_20200919092825.raw	Raw
	FF_37D3S.raw	Raw

Items per page:

1 - 5 of 27

Publications

BACE2 tunes lipid uptake through lipid transporters shedding supporting cancer cell proliferation.

Matafora Vittoria V Elhagh Alice A Morelli Alessandra A Tronci Laura L Cattaneo Angela A Conti Camilla C Casagrande Francesca F Farris Francesco F Bachi Angela A

Journal of experimental & clinical cancer research : CR 20260108 1

PMID: 41507981

Similar Datasets

BACE2 and lipid metabolism (global proteomic analysis)

Project description:global proteomic analysis of melanoma cell lines expressing different bace2 levels

2026-02-09 | PXD058702 | Pride

BACE2 and lipid metabolism (DMSO versus BACE2i 3I proteomic analysis)

Project description:proteomic analysis of melanoma, PDAC cells and fibroblast treated with DMSO vs 3I

2026-02-09 | PXD058789 | Pride

BACE2 and lipid metabolism (SSO treatment plus BACE2i time couse proteomic analysis)

Project description:SSO treatment and BACe2i time couse proteomic analysis in melanoma IGR37 cell lines

2026-02-09 | PXD058751 | Pride

Chemoproteomic Approach for Identifying Nuclear Arsenite-binding Proteins

Project description:Trivalent arsenic [As(III)], the predominant environmental form, poses significant health risks, including cancer, diabetes, and cardiovascular and neurodegenerative diseases, through contaminated food and water ingestion. Studies have explored As(III) toxicity mechanisms, particularly its displacement of Zn(II) in zinc-binding proteins, but identifying direct As(III)-binding proteins remains crucial. Given the nucleic acid binding capacity of many zinc-binding proteins, we hypothesized that nuclear As(III)-binding proteins could reveal key toxicity targets. Using a quantitative proteomics approach, we performed affinity pull-down with a biotin-As(III) probe on nuclear protein lysate. We identified splicing factor 1 (SF1) as a direct As(III)-binding protein and demonstrated that this interaction modulates mRNA splicing in human cells.

2025-05-03 | PXD061537 | Pride

Quantitative RNA interactome capture (qRIC) identifies phosphorylation sites with regulatory potential - RBM20 BioID

Project description:RNA binding proteins (RBPs) are major regulators of gene expression at the post-transcriptional level. While many posttranslational modification sites in RBPs have been identified, less is known about how these modifications regulate RBP function. Here, we develop quantitative RNA-interactome capture (qRIC) to quantify the fraction of cellular RBPs pulled down with polyadenylated mRNAs. Applying qRIC to HEK293T cells quantified pulldown efficiencies of over 300 mRBPs. Combining qRIC with phosphoproteomics allowed us to systematically compare pulldown efficiencies of phosphorylated and non-phosphorylated forms of mRBPs. Over hundred phosphorylation sites show increased or decreased pull-down efficiency compared to their host RBPs and thus have regulatory potential. Our data captures known regulatory phosphorylation sites in ELAVL1, SF3B1 and UPF1 and identifies new potentially regulatory sites. Follow-up experiments on the cardiac splicing regulator RBM20 revealed that multiple phosphorylation sites in the C-terminal disordered region affect nucleo-cytoplasmic shuttling, association with cytosolic RNA granules and alternative splicing. Together, we show that qRIC is a scalable method to identify the function of posttranslational modifications in RBPs.

2022-09-05 | PXD027138 | Pride

Paradiplonema papillatum CENPA-V5 IP

Project description:Transmission of genetic material from one generation to the next is a fundamental feature of all living cells. In eukaryotes, a macromolecular complex called the kinetochore plays crucial roles in this process by providing linkage between chromosomes and spindle microtubules. Little is known about this process in evolutionarily diverse protists. Within the supergroup Discoba, Eeuglenozoans forms a highly diversespeciose group of unicellular flagellates -including kinetoplastids, euglenids, and diplonemids. Kinetoplastids have an unconventional kinetochore system, while euglenids have a canonical onekinetochore system. It remains unclear what kind of kinetochores are present in diplonemids, a group of extremely diverse and abundant marine flagellatesplankton. Here, we employed deep homology detection protocols using profile-versus-profile Hidden Markov Model searches and AlphaFold-based structural comparisons to detect homologies that might have been previously missed. Interestingly, we still could not detect orthologs for most of the kinetoplastid nor canonical kinetochore subunits with few exceptions including a putative centromere-specific histone H3 variant (cenH3/CENP-A), the spindle checkpoint protein Mad2, the chromosomal passenger complex members Aurora and INCENP, and broadly conserved proteins like the CLK kinase and the meiotic synaptonemal complex proteins SYCP2 that function at kinetoplastid kinetochores. We examined the localization of five candidate kinetochore-associated proteins in the model diplonemid, Paradiplonema papillatum. PpCENP-A shows discrete dots in the nucleus, implying that it is likely a kinetochore component. PpMad2, PpCLK, PpSYCP2L1 and INCENP reside in the nucleus, but no clear kinetochore localization was observed. Altogether, these results raise a possibility that diplonemids evolved a hitherto unknown type of kinetochore system.

2024-10-21 | PXD054535 | Pride

Hypolipidemic effects of beetroot juice in SHR-CRP and HHTg rat models of metabolic syndrome: Analysis of hepatic proteome.

Project description:Recently, red beetroot has attracted attention as a health promoting functional food. Studies showed that beetroot administration can reduce blood pressure and ameliorate parameters of glucose and lipid metabolism, however, mechanisms underlying these beneficial effects of beetroot are not fully understood. In the current study, we analyzed effects of beetroot on parameters of glucose and lipid metabolism in two models of metabolic syndrome, (i) transgenic spontaneously hypertensive rats expressing human C-reactive protein (SHR-CRP rats), and (ii) hereditary hypertriglyceridemic (HHTg) rats. Treatment with beetroot juice for 4 weeks was in both models associated with amelioration of oxidative stress, reduced circulating lipids, smaller visceral fat depots, and lower ectopic fat accumulation in the liver, compared to their respective untreated controls. On the other hand, beetroot treatment had no significant effects on sensitivity of muscle and adipose tissue to insulin action in both models. Analyses of hepatic proteome revealed significantly deregulated proteins involved in glycerophospholipid metabolism, mTOR signalling, inflammation, and cytoskeleton rearrangement.

2023-03-11 | PXD039605 | Pride

Identification of tissue-specific SPD-5 and PLK-1 proximity interactors by direct and indirect TurboID

Project description:In this set of proof of principle experiments we compare the proximity interactomes obtained for two C. elegans centrosomal proteins, SPD-5 and PLK-1, by direct TurboID and indirect, GFP nanobody-targeted, TurboID in a range of different tissues, embryos, germ cell precursors and ciliated neurons.

2022-04-01 | PXD031970 | Pride

Spontaneous nonsense mutation in Tuft1 (tuftelin 1) gene is associated with abnormal hair appearance and amelioration of glucose and lipid metabolism in the rat

Project description:A new spontaneous mutation, abnormal hair appearance in the rat, has been identified as a non-functional Tuft1 (tuftelin 1) gene. The pleiotropic effects of this mutation regulate glucose and lipid metabolism. Analysis of the liver proteome revealed possible molecular mechanisms for the metabolic effects of the Tuft1 gene. Recently, we identified a recessive mutation, an abnormal coat appearance, in BXH6 strain, a member of the HXB/BXH set of recombinant inbred strains derived from the SHR (spontaneously hypertensive rat) and BN-Lx (Brown Norway rat) progenitors. Whole genome sequencing of the mutant rats identified the 195875980 G/A mutation in the Tuft1 (tuftelin 1) gene on chromosome 2, which resulted in a premature stop codon. Compared to wild-type BXH6 rats, BXH6-Tuft1 mutant rats exhibited lower body weight due to reduced visceral fat and ectopic fat accumulation in the liver and heart. Reduced adiposity was associated with decreased serum glucose and insulin, and increased insulin-stimulated glycogenesis in skeletal muscle. In addition, mutant rats had lower serum MCP-1 and leptin levels, indicative of reduced inflammation. Analysis of the liver proteome identified differentially expressed proteins from fatty acid metabolism and beta oxidation, peroxisomes, carbohydrate metabolism, inflammation, and proteasome pathways. These results provide evidence for an important role of Tuft1 gene in the regulation of lipid and glucose metabolism and suggest underlying molecular mechanisms.

2024-03-12 | PXD045880 | Pride

Detection of putative PKA target phosphorylation sites in Atg5flox:CamKII-Cre wildtype and knockout mice brain tissue

Project description:The experiment was performed to identify PKA phosphorylation substrates in wildtype and autophagy-deficient brains. Therefore, hippocampus and cortex of wildtype and conditional knockout mice were isolated and sliced. The brain slices were incubated with DMSO or Forskolin, a cAMP elevating agent, to induce PKA activity. Samples were measured by LC-MS/MS and were used to quantify proteomic and phosphoproteomic changes.

2022-11-15 | PXD031106 | 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