Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TMT analysis of phosphorylated proteomics of human osteosarcoma cell 143B treated with BEA

ABSTRACT: Phosphorylated proteomics was used to detect the changes of phosphotalin after administration.

INSTRUMENT(S): 6220 Time-of-Flight LC/MS

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

DISEASE(S): Acute Leukemia

SUBMITTER: Ye Geni

LAB HEAD: Geni Ye

PROVIDER: PXD044225 | Pride | 2023-10-24

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Publications

Beauvericin suppresses the proliferation and pulmonary metastasis of osteosarcoma by selectively inhibiting TGFBR2 pathway.

Ye Geni G Jiao Yubo Y Deng Lijuan L Cheng Minjing M Wang Sheng S Zhang Junqiu J Ouyang Jie J Li Yong Y He Yuxin Y Tu Zhengchao Z Wang Zhen Z Song Xiaojuan X Wang Chenran C Qi Qi Q Zhang Dongmei D Wang Lei L Huang Maohua M Ye Wencai W Chen Minfeng M

International journal of biological sciences 20230821 14

Osteosarcoma (OS) patients, particularly those with distant metastasis, experience rapid progression and derive poor survival benefits from traditional therapies. Currently, effective drugs for treating patients with metastatic OS remain scarce. Here, we found that the cyclic hexadepsipeptide beauvericin (BEA) functioned as a new selective TGFBR2 inhibitor with potent antiproliferative and antimetastatic activities against OS cells<i>.</i> Functionally, BEA inhibited TGF-β signaling-mediated pro ...[more]

PMID: 37781043

Similar Datasets

Using CRISPR-Cas9/Phosphoproteomics to Identify Kinase Substrates: Calmodulin Kinase 2 Delta

Project description:The Ca2+/CaM-dependent protein kinase 2 (CAMK2) family of protein kinases are key protein kinases involved in regulation of cellular processes in a variety of tissues including brain, smooth muscle and kidney. One member, CAMK2-delta (CAMK2D), has been proposed to be involved in vasopressin signaling in the renal collecting duct, which controls water and salt excretion by the kidney. To identify CAMK2D target proteins in renal collecting duct cells (mpkCCD), we deleted Camk2d in mpkCCD cells and carried out LC-MS/MS-based quantitative phoshoproteomics analysis. Using CRISPR/Cas9 with two different gRNAs targeting the CAMK2D catalytic domain, we created multiple CAMK2D knock-out cell lines. Using these cells and control cell lines, we carried out large-scale quantitative phosphoproteomic analysis (TMT-labeling) in the presence of the vasopressin analog dDAVP (0.1 nM, 30 min). Of the 11,570 phosphopeptides quantified, 206 were significantly increased and 169 were decreased. These data are available for browsing or download at https://esbl.nhlbi.nih.gov/Databases/CAMK2D-proteome/. Motif analysis of the decreased phosphorylation sites revealed a target preference of –(R/K)-X-X-p(S/T)-X-(D/E), matching the motif identified in previous in vitro studies using recombinant CAMK2D. Thirty-five of the significantly down-regulated phosphorylation sites in CAMK2D knock-out cells had exactly this motif and are judged to be sites that are most likely direct CAMK2D targets. These targets include Ser256 of aquaporin-2 (AQP2), a site known to regulate AQP2 trafficking to the plasma membrane, controlling water excretion by the kidney. The other changes, including phosphorylation sites that increased in response to CAMK2D deletion, are likely phosphorylated by other protein kinases that are regulated by CAMK2D in kinase cascades.

2023-11-06 | PXD040159 | Pride

phosphoproteomic profile of chicken embryos LC-MS/MS

Project description:we evaluated the phosphoproteomic profiles of chicken embryos in pre-diapause, diapause, and reactivated states.

2021-12-16 | PXD029941 | Pride

MBOAT7-Driven Lysophosphatidylinositol Acylation in Adipocytes Contributes to Systemic Glucose Homeostasis

Project description:We previously demonstrated that antisense oligonucleotide (ASO)-mediated knockdown of Mboat7, the gene encoding Membrane Bound O-Acyltransferase 7, in the liver and adipose tissue of mice promoted high fat diet-induced hepatic steatosis, hyperinsulinemia, and systemic insulin resistance. Thereafter, other groups showed that hepatocyte-specific genetic deletion of Mboat7 promoted striking fatty liver and NAFLD progression in mice but does not alter insulin sensitivity, suggesting the potential for cell autonomous roles. Here, we show that MBOAT7 function in adipocytes contributes to diet-induced metabolic disturbances including hyperinsulinemia and systemic insulin resistance. We generated floxed Mboat7 mice and created hepatocyte- and adipocyte-specific knockout mice using Cre-recombinase mice under the control of the albumin and adiponectin promoter, respectively. After chow and high fat diet feeding (60% kCal fat), mice were subjected to metabolic phenotyping and tissues to molecular workup and analysis. Here, we show that MBOAT7 function in adipocytes contributes to diet-induced metabolic disturbances including hyperinsulinemia and systemic insulin resistance. The expression of Mboat7 in white adipose tissue closely correlates with diet-induced obesity across a panel of ~100 inbred strains of mice fed a high fat/high sucrose diet. Moreover, we found that adipocyte-specific genetic deletion of Mboat7 is sufficient to promote hyperinsulinemia, systemic insulin resistance, and mild fatty liver. Unlike in the liver, where Mboat7 plays a relatively minor role in maintaining arachidonic acid (AA)-containing PI pools, Mboat7 is the major source of AA-containing PI pools in adipose tissue. Our data demonstrate that MBOAT7 is a critical regulator of adipose tissue PI homeostasis, and adipocyte MBOAT7-driven PI biosynthesis is closely linked to hyperinsulinemia and insulin resistance in mice.

2023-05-10 | PXD039894 | Pride

Proteome and Phosphoproteome of AhR-dependent non-genomic signaling in endotoxin-activated macrophages

Project description:Emerging studies revealed an immunomodulatory role of the Aryl hydrocarbon receptor (AhR), a receptor sensing environmental contaminants, and involved in their detoxification. Besides its function as a transcription factor, AhR can participate in non-genomic signaling through ubiquitination and phosphorylation-dependent processes. In this study, a multi-PTM-omics approach, including proteome, ubiquitome, and phosphoproteome, was utilized to examine mechanisms of non-genomic AhR-signaling in endotoxin-activated monocyte-derived macrophages. This dataset entails proteome and phosphoproteome data.

2021-03-30 | PXD020770 | Pride

TBK1 interacts with tau and enhances neurodegeneration in tauopathy

Project description:One of the defining pathological features of Alzheimer’s Disease (AD) is the deposition of neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau in the brain. Aberrant activation of kinases in AD has been suggested to enhance phosphorylation and toxicity of tau, making the responsible tau kinases attractive therapeutic targets. The full complement of tau interacting kinases in AD brain and their activity in disease remains incompletely defined. Here, immunoaffinity enrichment coupled with mass spectrometry (MS) identified TANK-binding kinase 1 (TBK1) as a tau-interacting partner in human AD cortical brain tissues. We validated this interaction in human AD, familial frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) caused by mutations in MAPT (R406W & P301L) and corticobasal degeneration (CBD) postmortem brain tissues as well as human cell lines. Further, we document increased TBK1 activation in both AD and FTDP-17 and map TBK1 phosphorylation sites on tau based on in vitro kinase assays coupled to MS. Lastly, in a Drosophila tauopathy model, activating expression of a conserved TBK1 ortholog triggers tau hyperphosphorylation and enhanced neurodegeneration, whereas knockdown had the reciprocal effect, suppressing tau toxicity. Collectively, our findings suggest that increased TBK1 activation may promote tau hyperphosphorylation and neuronal loss in AD and related tauopathies.

2022-03-01 | PXD025301 | Pride

FAM111A regulates replication origin activation and cell fitness

Project description:FAM111A is a replisome associated protein and dominant mutations within its trypsin-like peptidase domain are linked to severe human developmental syndrome, the Kenny-Caffey syndrome. However, FAM111A functions remain unclear. Here, we show that FAM111A facilitates efficient activation of DNA replication origins. Upon replication fork stalling, FAM111A promotes dormant origin activation and ssDNA exposure. Furthermore, unrestrained expression of FAM111A wild-type as well as patient mutants causes accumulation of DNA damage and cell death, only when the peptidase domain remains intact. The peptidase domain is responsible for ssDNA exposure during S phase, which is not caused by caspase dependent apoptosis. Altogether, these data unveil how FAM111A promotes DNA replication in normal conditions and becomes harmful in a disease context.

2023-10-03 | PXD044180 | Pride

Comparative phosphoproteomic profiling in prefrontal cortex of prenatal stressed offspring rats

Project description:We used MS-based TMT quantitative proteomics in combination with phosphopeptide enrichment method to compare phosphoproteomic profiling in prefrontal cortex of of PS-S and CON offspring rats.

2022-08-12 | PXD026563 | Pride

Phosphoproteomic Datasets for Mec1/ATR Signaling Upon Hyper-Resection (TMT Supplement)

Project description:The Mec1/ATR kinase is crucial for genome maintenance, although the mechanisms by which it controls DNA repair pathways remain elusive. Here we uncovered a role for Mec1/ATR in controlling homologous recombination (HR) factors in response to hyper-resection of DNA ends. Cells lacking RAD9, a checkpoint activator and an inhibitor of resection, exhibit Mec1-dependent hyper-phosphorylation of proteins associated with single strand DNA transactions, including the ssDNA binding protein Rfa2, the translocase/ubiquitin ligase Uls1 and the HR-regulatory Sgs1-Top3-Rmi1 (STR) complex. Extensive Mec1-dependent phosphorylation of the STR complex, mostly on the Sgs1 helicase subunit, promotes an interaction between STR and the DNA repair scaffolding protein Dpb11.

2021-03-10 | PXD023438 | Pride

Snf1/AMPK fine-tunes TORC1 signaling in response to glucose starvation

Project description:Three sets of DDA-based proteomics studies were performed to characterize Snf1-dependent phosphorylation kinetics in the yeast Saccharomyces cerevisiae. In vivo assays as well as in vitro kinase assays were performed. For each set, five biological replicates were analyzed.

2023-02-17 | PXD037381 | Pride

Phosphoproteomic Datasets for Mec1/ATR Signaling Upon Hyper-Resection

2021-03-10 | PXD017286 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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