Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hs_Stomach

ABSTRACT: Hs_Stomach

REANALYSIS of: PXD000865

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Digestive System

SUBMITTER: Wilhelm et al.

PROVIDER: PAe004931 | PeptideAtlas | 2014-12-31

REPOSITORIES: PeptideAtlas

ACCESS DATA

Json Xml

Publications

Mass-spectrometry-based draft of the human proteome.

Wilhelm Mathias M Schlegl Judith J Hahne Hannes H Gholami Amin Moghaddas AM Lieberenz Marcus M Savitski Mikhail M MM Ziegler Emanuel E Butzmann Lars L Gessulat Siegfried S Marx Harald H Mathieson Toby T Lemeer Simone S Schnatbaum Karsten K Reimer Ulf U Wenschuh Holger H Mollenhauer Martin M Slotta-Huspenina Julia J Boese Joos-Hendrik JH Bantscheff Marcus M Gerstmair Anja A Faerber Franz F Kuster Bernhard B

Nature 20140501 7502

Proteomes are characterized by large protein-abundance differences, cell-type- and time-dependent expression patterns and post-translational modifications, all of which carry biological information that is not accessible by genomics or transcriptomics. Here we present a mass-spectrometry-based draft of the human proteome and a public, high-performance, in-memory database for real-time analysis of terabytes of big data, called ProteomicsDB. The information assembled from human tissues, cell lines ...[more]

PMID: 24870543

Similar Datasets

ER alpha coregulator peptide screening profiling by MARCoNI (Microarray Assay for Real-time Coregulator-Nuclear receptor Interaction) assay from human embryonic kidney HEK293 cells after tranfected with ER alpha or Q375 mutations

Project description:Estrogen insensitivity syndrome (EIS) arises from rare mutations in ERα resulting in the inability of estrogen to exert its biological effects. Due to the rarity, mutations in ESR1 gene and the underlying molecular mechanisms of EIS have not been thoroughly studied. We used PamChip array with 154 coregulator motifs (PamGene #88101) array to compare the peptide profiles between the WT and 5 of Q375 mutants in HEK293 cells after transferred with ER alpha or Q375 mutatnts. 93 ligand-modulated peptides were reported here.

2020-09-28 | GSE155085 | GEO

Serological autoantibody profiling of type 1 diabetes by protein arrays.

Project description:The study was aimed to identify novel autoantibody(AAB) biomarkers for Type 1 diabetes.

2019-03-05 | GSE45515 | GEO

Buparlisib-treated Patient Derived Xenograft (PDX) Reversed Phase Protein Array (RPPA) Data

Project description:Phosphoinositide 3-kinase (PI3K) signaling activation is frequently observed in triple negative breast cancer, however, PI3K inhibitors have shown limited clinical activity. To investigate resistance mechanisms, we performed global transcriptome, proteome, phosphoproteome and kinome analysis of a panel of triple negative breast cancer patient derived xenograft models with varying responsiveness to buparlisib, a pan-PI3K inhibitor, for differentially expressed baseline and post-treatment biomarkers. Resistance was associated with incomplete inhibition of PI3K and upregulated MAPK/MEK signaling in response to buparlisib. Outlier phosphoproteome and kinome analyses identified additional candidates in association with buparlisib resistance, including NEK9 and MAP2K4. Knockdown of NEK9 or MAPK2K4 reduced both baseline and feedback MAPK/MEK signaling and enhanced buparlisib efficacy in vitro. Interestingly, we show that a complex ins/del in PIK3CA led to a change in buparlisib response in a NEK9/MAP2K4 dependent manner. In summary, our study indicates a role for NEK9 and MAP2K4 in mediating buparlisib resistance and demonstrates the value of unbiased global analyses in uncovering resistance mechanisms to targeted therapy.

2018-05-29 | GSE100567 | GEO

AKT Inhibition Promotes Non-autonomous Cancer Cell Survival [Antibody Arrays (L-507)]

Project description:Small-molecule inhibitors of AKT signaling are being in evaluated in patients with various cancer types, but have so far proven therapeutically disappointing for reasons that remain unclear. Here, we treat cancer cells with sub-therapeutic doses of Akti-1/2, an allosteric small molecule AKT inhibitor, in order to experimentally model pharmacologic inhibition of AKT signaling in vitro. We then apply a combined RNA, protein, and metabolite profiling approach to develop an integrated, multi-scale, molecular snapshot of this “AKTlow” cancer cell state. We find that AKT-inhibited cancer cells suppress thousands of mRNA transcripts, and proteins related to the cell cycle, ribosome, and protein translation. Surprisingly, however, these AKT-inhibited cells simultaneously up-regulate a host of other proteins and metabolites post-transcriptionally, reflecting activation of their endo-vesiculo-membrane system, secretion of inflammatory proteins, and elaboration of extracellular microvesicles. Importantly, these microvesicles enable rapidly proliferating cancer cells of various types to better withstand different stress conditions, including serum deprivation, hypoxia, or cytotoxic chemotherapy in vitro and xenografting in vivo. These findings suggest a model whereby cancer cells experiencing a partial inhibition of AKT signaling may actually promote the survival of neighbors through non-cell autonomous communication.

2015-12-09 | GSE71892 | GEO

AKT Inhibition Promotes Non-autonomous Cancer Cell Survival [Antibody Arrays (L-493)]

2015-12-09 | GSE71891 | GEO

Targeting β-catenin overcomes resistance to MEK inhibitor in PIK3CA mutant colon cancer

Project description:Mitogen-activated protein kinases (MEK 1/2) are central components of the RAS signaling pathway and attractive targets for cancer therapy. However, PIK3CA mutation, which commonly co-occurs with KRAS mutation, offered resistance to MEK inhibitor through activation of PI3K-AKT signaling. We identified a gene that cooperates with MEK inhibitors to forcefully treat PIK3CA mutant colon cancer cells. -catenin, a key molecule of the WNT pathway, emerged as a candidate by protein/Ab Chip array. MEK inhibitor treatment led to a decrease in -catenin in PIK3CA wild-type colon cancer cells but not in PIK3CA mutant colon cancer cells. Tumor regression was promoted by a combination of MEK inhibitor and NVP-TNS656, which targets the WNT pathway. Furthermore, combined inhibition of MEK and -catenin by NVP-TNS656 promoted tumor regression in colon cancer patient-derived xenograft (PDX) models expressing mutant PIK3CA. Taken together, we propose that inhibition of the WNT pathway, particularly -catenin, may bypass resistance to MEK inhibitor in human PIK3CA mutant colon cancer. Additionally, -catenin is a potential PD marker of MEK inhibitor resistance.

2015-08-13 | GSE71981 | GEO

Anti-glycan humoral responses after vaccination with PROSTVAC-VF

Project description:This SuperSeries is composed of the SubSeries listed below.

2015-08-26 | GSE50410 | GEO

Post-vaccination serum anti-glycan total Ig antibodies of 113 subjects in a clinical trial of PROSTVAC-VF, a therapeutic cancer vaccine. (Dilution = 1:200)

Project description:Purpose: There is evidence that therapeutic cancer vaccines can lengthen survival for some cancer patients, but responses vary widely from one person to another. Methods to predict clinical outcomes will advance the field and provide new insights into critical determinants of in vivo efficacy. This study uses a high-throughput glycan microarray to assess correlations between a subject's overall survival after receiving PROSTVAC-VF and his anti-glycan humoral responses occuring in the first months after treatment with PROSTVAC-VF. Results: Humoral responses to the terminal Forssman disaccharide (Fsdi) were found to have a statistically significant correlation with survival. Long-term survival was approximately doubled in subjects with four-fold or larger anti-Fsdi responses relative to subjects with little or no anti-Fsdi response. This survival correlation was specific to vaccine treatment, as no correlation was observed in control patients immunized with wild-type poxviruses lacking the key tumor antigen, prostate specific antigen (PSA). Moreover, anti-Fsdi humoral responses were not correlated with general measures of disease severity, such as PSA levels, Gleason score, or Halabi predicted survival. Conclusion: In addition to reporting a new biomarker for monitoring benefical responses to PROSTVAC-VF, this study highlights the potential of glycan microarray technology for personalized medicine.

2015-08-26 | GSE50239 | GEO

Nucleos(t)ide analogs for hepatitis B virus infection differentially regulate the growth factor signaling in hepatocytes

Project description:Recent clinical studies have suggested that the risk of developing hepatocellular carcinoma might be lower in chronic hepatitis B (CHB) patients receiving tenofovir disoproxil fumarate (TDF) than in patients receiving entecavir (ETV), although there is no difference in biochemical and virological remission between two drugs. The effects of nucleoside analogs (NsAs; lamivudine and ETV) or nucleotide analogs (NtAs; adefovir disoproxil [ADV], TDF, and tenofovir alafenamide [TAF]) on cell growth and the expression of growth signaling molecules were investigated. The tumor inhibitory effects of NsAs or NtAs were evaluated using a mouse xenograft model, and protein phosphorylation profiles were investigated.

2024-01-17 | GSE249861 | GEO

Alterations to the Hidradenitis Suppurativa Serum Proteome with Spleen Tyrosine Kinase Antagonism: Proteomic Results from a Phase 2 Clinical Trial.

Project description:Serum Proteomic Analysis of patients with Hidradenitis Suppurativa treated with Fostamatinib

2023-08-10 | GSE240607 | GEO