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

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

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Malignant Cell

SUBMITTER: vittoria matafora

LAB HEAD: Angela Bachi

PROVIDER: PXD058751 | Pride | 2026-02-09

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	DirectDIA.txt	Txt
	VM_230518_3I1.raw	Raw
	VM_230518_3I2_r.raw	Raw
	VM_230518_3I3.raw	Raw
	VM_230518_3I_SSO1.raw	Raw

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1 - 5 of 29

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

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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.

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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.

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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.

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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.

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