Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Leukemia_RPMI_8226

ABSTRACT: Leukemia_RPMI_8226

INSTRUMENT(S): LTQ Orbitrap XL

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Others

SUBMITTER: Moghaddas Gholami A, Hahne H, Wu Z, Auer FJ, Meng C, Wilhelm M, Kuster B

PROVIDER: PAe005396 | PeptideAtlas | 2013-12-31

REPOSITORIES: PeptideAtlas

ACCESS DATA

Json Xml

Publications

Global proteome analysis of the NCI-60 cell line panel.

Gholami Amin Moghaddas AM Hahne Hannes H Wu Zhixiang Z Auer Florian Johann FJ Meng Chen C Wilhelm Mathias M Kuster Bernhard B

Cell reports 20130808 3

The NCI-60 cell line collection is a very widely used panel for the study of cellular mechanisms of cancer in general and in vitro drug action in particular. It is a model system for the tissue types and genetic diversity of human cancers and has been extensively molecularly characterized. Here, we present a quantitative proteome and kinome profile of the NCI-60 panel covering, in total, 10,350 proteins (including 375 protein kinases) and including a core cancer proteome of 5,578 proteins that w ...[more]

PMID: 23933261

Similar Datasets

YBX1 integration of oncogenic PI3K/mTOR signalling regulates the fitness of malignant epithelial cells [RPPA]

Project description:In heterogeneous head and neck cancer (HNC), subtype-specific treatment regimens are currently missing. An integrated analysis of patient HNC subtypes using single-cell sequencing and proteome profiles revealed an epithelial-mesenchymal transition (EMT) signature within the epithelial cancer-cell population. The EMT signature coincided with PI3K/mTOR inactivation in the mesenchymal subtype. Conversely, the signature was suppressed in epithelial cells of the basal subtype which exhibits hyperactive PI3K/mTOR signalling. We further identified YBX1 phosphorylation, downstream of the PI3K/mTOR pathway, restrains basal-like cancer cell proliferation. In contrast, YBX1 acts as a safeguard against the proliferation-to-invasion switch in mesenchymal-like epithelial cancer cells, and its loss accentuates partial-EMT and in vivo invasion. Interestingly, phospho-YBX1 that is mutually exclusive to partial-EMT, emerged as a prognostic marker for overall patient outcomes. Expression profiling by reverse-phase protein array were performed to explore the underlying molecular mechanisms.

2023-03-03 | GSE226356 | GEO

Effect of human beta defensin-2 (hBD-2) on T cells

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

2022-12-20 | GSE198405 | GEO

Effect of human beta defensin-2 (hBD-2) on T cells [mouse]

Project description:In this experiment, we studied how human beta defensin-2 (hBD-2) affects kinase activity of T cells.

2022-12-20 | GSE198404 | GEO

Effect of human beta defensin-2 (hBD-2) on T cells [human]

Project description:In this experiment, we studied how human beta defensin-2 (hBD-2) affects kinase activity of T cells.

2022-12-20 | GSE198402 | GEO

Autoantibodies are highly prevalent in non-SARS-CoV-2 respiratory infections and critical illness [ACA]

Project description:We used protein arrays to measure IgG autoantibodies associated with Connective Tissue Diseases (CTDs) and Anti-Cytokine Antibodies (ACA) in patients with non-COVID-19 infections such as influenza

2023-01-12 | GSE222760 | GEO

TLR7 agonism accelerates disease in a mouse model of primary Sjögren’s syndrome and drives expansion of age-associated B cells

Project description:Primary Sjögren’s syndrome (pSS) is a systemic autoimmune disease characterized by chronic inflammation of exocrine tissue, resulting in loss of tears and saliva. Patients also experience many extra-glandular disease manifestations. Treatment for pSS is palliative, and there are currently no treatments available that target disease etiology. Previous studies in our lab demonstrated that Myd88 is crucial for pSS pathogenesis in the NOD.B10Sn-H2b (NOD.B10) pSS mouse model, although the way in which Myd88-dependent pathways become activated in disease remains unknown. Based on its importance in other autoimmune diseases, we hypothesized that TLR7 activation accelerates pSS pathogenesis. We administered the TLR7 agonist Imiquimod (Imq) or sham treatment to pre-disease NOD.B10 females for 6 weeks. Parallel experiments were performed in age and sex-matched C57BL/10 controls. Imq-treated pSS animals exhibited cervical lymphadenopathy, splenomegaly, and expansion of TLR7-expressing B cells. Robust lymphocytic infiltration of exocrine tissues, kidney and lung was observed in pSS mice following treatment with Imq. TLR7 agonism also induced salivary hypofunction in pSS mice, which is a hallmark of disease. Anti-nuclear autoantibodies, including Ro (SSA) and La (SSB) were increased in pSS mice following Imq administration. Cervical lymph nodes from Imq-treated NOD.B10 animals demonstrated an increase in the percentage of activated/memory CD4+ T cells. Finally, aged-associated B cells (ABCs) were expanded in the spleens of Imq-treated pSS mice. Thus, activation of TLR7 accelerates local and systemic disease and promotes expansion of the ABC subset in pSS.

2022-09-01 | GSE212467 | GEO

High-throughput mediation analysis of human proteome and metabolome identifies mediators of post-bariatric surgical diabetes control

Project description:To improve the power of mediation in high-throughput studies, here we introduce High-throughput mediation analysis (Hitman), which accounts for direction of mediation and applies empirical Bayesian linear modeling. We apply Hitman in a retrospective, exploratory analysis of the SLIMM-T2D clinical trial in which participants with type 2 diabetes were randomized to Roux-en-Y gastric bypass (RYGB) or nonsurgical diabetes/weight management, and fasting plasma proteome and metabolome were assayed up to 3 years. RYGB caused greater improvement in HbA1c, which was mediated by growth hormone receptor (GHR). GHR’s mediation is more significant than clinical mediators, including BMI. GHR decreases at 3 months postoperatively alongside increased insulin-like growth factor binding proteins IGFBP1/BP2; plasma GH increased at 1 year. Experimental validation indicates (1) hepatic GHR expression decreases in post-bariatric rats; (2) GHR knockdown in primary hepatocytes decreases gluconeogenic gene expression and glucose production. Thus, RYGB may induce resistance to diabetogenic effects of GH signaling.

2021-08-24 | GSE122279 | GEO

DNA methylation shapes transcription factor binding beyond canonical CpG contexts - array 1

Project description:Here, we systematically profile the methylation sensitivity of 18 human TFs spanning 11 structural families using chemically synthesized DNA libraries containing position-specific 5-methylcytosines (5mC) in CpG, non-CpG, and hemi-methylated contexts, measured via high-throughput protein-binding microarrays. Our results reveal extensive TF sensitivity to methylation state, position, and strand orientation—including strong binding of several TFs to non-CpG and hemi-methylated sites. The presence of 5mC can dramatically alter TF-DNA interactions: transforming low-affinity sites into high-affinity ones by enabling new contacts, or silencing otherwise favorable motifs through steric hindrance. Genomic analyses further show that the methylation-sensitive sequences identified in vitro are represented within enhancers and regulatory elements, exhibiting distinct methylation patterns across cell types. Together, our findings uncover a previously hidden layer of methylation-dependent TF-DNA recognition, broadening the understanding of epigenetics in transcriptional regulation.

2026-04-01 | GSE324570 | GEO

DNA mismatches reveal conformational penalties in protein-DNA recognition II

Project description:Transcription factors (TF) recognize specific genomic sequences to regulate complex gene expression programs. Although it is well established that TFs bind specific DNA sequences using a combination of base readout and shape recognition, some fundamental aspects of protein-DNA binding remain poorly understood. Many DNA-binding proteins induce changes in the DNA structure outside the intrinsic B-DNA envelope. However, how the energetic cost associated with distorting DNA contributes to recognition has proven difficult to study because the distorted DNA exists in low-abundance in the unbound ensemble. Here, we use a novel high-throughput assay called SaMBA (Saturation Mismatch-Binding Assay) to investigate the role of DNA conformational penalties in TF-DNA recognition. In SaMBA, mismatches are introduced to pre-induce DNA structural distortions much larger than those induced by changes in Watson-Crick sequence. Strikingly, approximately 10% of mismatches increased TF binding, and at least one mismatch was found that increased the binding affinity for each of 22 examined TFs. Mismatches also converted non-specific sites into high-affinity sites, and high-affinity sites into super-sites stronger than any known canonical binding site. Determination of high-resolution X-ray structures, combined with NMR measurements and structural analyses revealed that many of the mismatches that increase binding induce distortions similar to those induced by protein binding, thus pre-paying some of the energetic cost to deform the DNA. Our work indicates that conformational penalties are a major determinant of protein-DNA recognition, and reveals mechanisms by which mismatches can recruit TFs and thus modulate replication and repair activities in the cell.

2020-08-18 | GSE156373 | GEO

Reverse Phase Protein Array (RPPA) profiling of cell signaling events in 468 cells induced by PTEN overexpression or PTEN-Long overexpression

Project description:To investigate the novel functions of PTEN-L, we performed a Reverse Phase of Protein Array (RPPA) profiling on 468.Ctrl, 468.PTEN, and 468.PTEN-L sublines to compare cell signaling events between PTEN expression

2019-05-25 | GSE131746 | GEO

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