The effect of carbon starvation on the Escherichia coli SLE1 proteome.
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: MODEL1109130000MODEL1311110000MODEL1909260003MODEL1311110001MODEL1909260004MODEL1703310000MODEL1909260005MODEL1909260006
INSTRUMENT(S): Q Exactive
ORGANISM(S): Escherichia Coli Escherichia Coli Ht115
SUBMITTER: 
Rakhan Aimbetov
LAB HEAD: Vasily Ogryzko
PROVIDER: PXD003255 | Pride | 2019-11-08
REPOSITORIES: Pride
Dataset's files
Items per page: 5 1 - 5 of 34 |
Similar Datasets
Project description:Monounsaturated fatty acid (MUFA) oleic acid (OA) has been reported to reverse saturated fatty acid palmitic acid (PA)-induced hepatic insulin resistance (IR). However, the detailed molecular mechanism remains elusive. In addition, previous research also showed that -3 polyunsaturated fatty acid (PUFA) eicosapentaenoic acid (EPA), exerted opposite effects to PA in muscle IR, but whether it plays the same role in hepatic IR and the possible mechanism involved needs to be further explored. Here, we confirmed that EPA reversed PA-induced IR in HepG2 cells and compared the proteome change after different free fatty acids (FFAs) treatments. For MUFA, 234 proteins were identified as differentially expressed proteins, and their functions were mainly related to response to stress and endogenous stimuli, lipid metabolic process and protein binding. For PUFA, the PA-induced expression change of 1326 proteins could be reversed by EPA and 415 of them were mitochondrial proteins, which covered most of the functional proteins in oxidative phosphorylation (OXPHOS) and tricarboxylic acid cycle (TCA). Mechanism study revealed that c-Jun and ROS played a role in OA- and EPA-reversed PA-induced IR, respectively. EPA or OA alleviated PA-induced abnormal ATP production, ROS generation, and calcium content. Importantly, H2O2-activated production of ROS increased the expression of c-Jun, further resulting in IR of HepG2 cells. Besides, we provided more feasible candidates as potential c-Jun-targeted “responders” for FFAs treatments. Taken together, we demonstrated that ROS/c-Jun is a common pathway to different FFAs-regulated IR in HepG2 cells.
2019-07-11 | PXD012066 | Pride
Project description:HHV-6A is a human herpesvirus that integrates into human sub telomeric regions to acquire latency. This latent virus frequently reactivates causing numerous diseases. The project was aimed to understand changes in host cell prteomics upon virus reactivation, which might helpin understanding the pathophysiology of virus reactivation.
2020-04-07 | PXD016211 | Pride
Project description:Cancer metastasis is a complex mechanism involving multiple processes. In an earlier study, we reported that the levels of serine/threonine phosphatase POPX2 were positively correlated with cancer cell motility through modulating MAPK signaling. Surprisingly, here we found that POPX2 knockdown cells induced more numerous and larger tumor nodules in lungs in longer term animal studies, suggesting that lower levels of POPX2 may favor tumor progression in later stages of metastasis. We hypothesize that POPX2 may do so by modulation of angiogenesis. Secretome analysis of POPX2-knockdown MDA-MB-231 cells using SILAC-mass spectrometry and cytokine array showed that silencing of POPX2 leads to increased secretion of exosomes, which may in turn induce multiple pro-angiogenic cytokines. This study, combined with our earlier findings, suggests that a single ubiquitously expressed phosphatase POPX2 influences cancer metastasis via modulating multiple biological processes including MAPK signaling and exosome-cytokine secretion.
2019-10-21 | PXD001618 | Pride
Project description:High-resolution MS/MS spectra of peptides can be deisotoped to identify monoisotopic masses of peptide fragments. The use of such masses should improve protein identification rates. However, deisotoping is not universally used and its benefits have not been fully explored. Here, we developed MS2-Deisotoper, a tool for use prior to database search, to identify monoisotopic peaks in centroided MS/MS spectra. MS2-Deisotoper works by comparing the mass and relative intensity of each peptide fragment peak to every other peak of greater mass, and by applying a set of rules concerning mass and intensity differences. After comprehensive parameter optimisation, we show that MS2-Deisotoper could improve the number of peptide spectrum matches (PSMs) identified by up to 8.2% and proteins by up to 2.8%. It was effective with SILAC and non-SILAC MS/MS data. The identification of unique peptide sequences was also improved, increasing the number of human proteoforms by 3.7%. Detailed investigation of results showed that deisotoping increases Mascot ion scores, improves FDR estimation for PSMs and leads to greater protein sequence coverage. At a peptide level, we found that the efficacy of deisotoping was affected by peptide mass and charge. MS2-Deisotoper can be used via a user interface or as a command-line tool.
2019-08-05 | PXD010587 | Pride
Project description:Altered metabolism is a hallmark of cancer, but little is still known about its regulation. Here we measure transcriptomic, proteomic, phospho-proteomic and fluxomics data in a breast cancer cell-line across three different conditions. Integrating these multiomics data within a genome scale human metabolic model in combination with machine learning we systematically chart the different layers of metabolic regulation in breast cancer, predicting which enzymes and pathways are regulated at which level. We distinguish between two types of reactions, directly or indirectly regulated. Directly-regulated reactions include those whose flux is regulated by transcriptomic alterations (~890) or via proteomic or phospho-proteomics alterations (~140) in the enzymes catalyzing them. Indirectly regulated reactions are those that currently lack evidence for direct regulation in our measurements or predictions (~930). Remarkably, we find that the flux of indirectly regulated reactions is strongly coupled to the flux of the directly regulated ones, uncovering a hierarchical organization of breast cancer metabolism. Furthermore, the predicted indirectly regulated reactions are predominantly bi-directional. Taken together, this architecture may facilitate the formation of stochiometrically consistent flux distributions in response to the varying environmental conditions incurred by the tumor cells. The approach presented lays a conceptual and computational basis for a more complete mapping of metabolic regulation in different cancers with incoming additional data.
2020-05-26 | PXD006449 | Pride
Project description:Human PAK4 is an ubiquitously expressed p21-activated kinase which acts downstream of Cdc42. Since PAK4 is demonstrably enriched in cell-cell junctions, we probed the local protein environment around the kinase with a view to understanding its location and substrates. In U2OS cells expressing PAK4-BirA-GFP the resultant SILAC proximity analyses revealed a subset of 28 proteins that are primarily cell-cell junction components. The protein with highest relative biotin labelling was Afadin/AF6, which associates with the nectin family of homophilic junctional proteins. Reciprocally >50% of the PAK4-proximal proteins were identified by Afadin BioID. Pull-down experiments failed to identify junctional proteins, emphasizing the advantage of the BioID method. Mechanistically PAK4 depended on Afadin for its junctional localization, which is similar to the situation in Drosophila. A highly ranked PAK4-proximal protein LZTS2 was immuno-localized with Afadin at cell-cell junctions. Though PAK4 and Cdc42 are junctional, BioID analysis did not yield conventional cadherins, indicating their spatial segregation. To identify cellular PAK4 substrates we then assessed changes in phospho-proteome after 12 min PF-3758309 treatment. Among the PAK4-proximal junctional proteins 17 PAK4 sites were identified. Thus we show PAK4 is selective for the mammalian Afadin/nectin sub-compartment, with a demonstrably distinct localization from tight and cadherin junctions.
2021-11-30 | PXD024464 | Pride
Project description:Skeletal muscle is known to adapt dynamically to changes in workload by regulatory processes of the phosphatidylinositide 3-kinase (PI3K)/Akt pathway. We performed a global quantitative phosphoproteomics analysis of contracting mouse C2 myotubes treated with insulin growth factor 1 (IGF-1) or LY294002 to activate or inhibit PI3K/Akt signaling, respectively.
2020-05-25 | PXD009117 | Pride
Project description:The classification of histologically similar yet molecularly distinct tumors into specific subtypes remains a clinically challenging task. Classification of such tumors into distinct entities based on their cell surface protein expression profiles has been hindered by the lack of an unbiased global approach. Here we use N-glyco FASP, a recently developed mass spectrometric approach based on lectin-enrichment of N-linked glycoproteins, in conjunction with a super-SILAC based quantitative strategy, on patient derived diffuse large B-cell lymphoma cell lines. We mapped 2383 glycosites on more than 1300 proteins, which were highly enriched for cell membrane proteins. The resulting sub-proteome was highly enriched for cell membrane proteins. This N-glyco sub-proteome alone allowed the segregation of the ABC from the GCB subtypes of diffuse large B-cell lymphoma, which before gene expression studies had been considered one disease entity. Encouragingly, many of the glycopeptides driving the segregation belong to proteins previously characterized as segregators in a deep proteome study of these subtypes (S. J. Deeb et al MCP 2012 PMID 22442255). This conforms to the high correlation that we observed between the expression level of the glycosites and their corresponding proteins. Detailed examination of glycosites and glycoprotein expression levels uncovered, amongst other interesting findings, enrichment of transcription factor binding motifs, including known NF-kappa-B related ones. Thus, enrichment of a class of post-translationally modified peptides can classify cancer types as well as reveal cancer specific mechanistic changes.
2016-08-25 | PXD000332 | Pride
Project description:VAPB (Vesicle-Associated-membrane Protein-associated proteins B) is a tail-anchored mem-brane protein of the endoplasmic reticulum that can also be detected at the inner nuclear mem-brane. As a component of many contact sites between the endoplasmic reticulum and other or-ganelles, VAPB is engaged in multiple protein interactions with a plethora of binding partners. A mutant version of VAPB, P56S-VAPB, that results from a single point mutation is involved in a familial form of amyotrophic lateral sclerosis (ALS8). We performed RAPIDS (rapamycin- and APEX-dependent identification of proteins by SILAC) to identify proteins that interact with or are in close proximity to P56S-VAPB. The mutation abrogates the interaction of VAPB with many known binding partners. Instead, Sequestosome 1 (SQSTM1) was identified as a major in-teraction/proximity partner, a protein that is known as an autophagic adapter. Remarkably, not only the mutant P56S-VAPB, but also the wild type protein interacts with SQSTM1, as shown by proximity ligation assays and co-immunoprecipiation experiments.
2022-02-15 | PXD029113 | Pride
Project description:The relevance of mitochondrial proteostasis for the differentiation and function of hematopoietic and immune cells is unknown. Dissecting the HCLS1-associated protein X-1 (HAX1) –related protein network, we define a functional CLPB-HAX1-PRKD2-HSP27 axis with critical importance for the differentiation of neutrophil granulocytes and thus elucidate molecular mechanisms underlying congenital neutropenia in patients with mutations in HAX1 and CLPB. As shown by SILAC proteomics, CLPB and HAX1 control the balance of protein synthesis and persistence in mitochondria, leading to dysfunction of the respiratory complex 1. Impaired mitochondrial proteostasis is associated with decreased abundance of the serine-threonine kinase PRKD2 and Ser82-phosphorylated HSP27. Cellular defects in HAX1-/- cells can be functionally reconstituted by HSP27. Thus, mitochondrial proteostasis emerges as a critical mechanism governing the differentiation and function of neutrophil granulocytes.
2022-05-19 | PXD023790 | Pride