Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Impact of STAU1 depletion on the protein expression profile of rhabdomyosarcoma cell lines

ABSTRACT: Two human rhabdomyosarcoma cell lines (RD, RH36, RH30, and RH18) and one none-transformed skeletal muscle cell line (HSMM-C3) cell line were studied for the impact of Staufen1 depletion on their protein expression profile. Proteomics was performed for control and Staufen1 knockdown cells (n=3). For this, we generated STAU1 knockdown cell lines using a mixture of three independent STAU1-targeting lentiviral-shRNA constructs. cells were cultured for 72 hours and then protein extraction was performed as follow: Cells were lysed in 1X RIPA buffer (20 mM Tris-HCl (pH 7.5), 150mM NaCl, 1mM Na2- EDTA, 1mM EGTA, 1% NP-40, 1% sodium deoxycholate, 2.5 mM sodium pyrophosphate, 1mM β-glycerophosphate, 1mM Na3 VO4, 1µg/ml leupeptin). Protein concentration was tested according to the BCA assay protocol (Thermofisher Scientific) and samples were used in proteomics experiment.

INSTRUMENT(S): Orbitrap Exploris 480

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Skeletal Muscle Cell Proliferation, Skeletal Muscle Cell Line

DISEASE(S): Embryonal Rhabdomyosarcoma

SUBMITTER: Shekoufeh Almasi

LAB HEAD: Bernard J. Jasmin

PROVIDER: PXD042156 | Pride | 2023-10-22

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	HSMM-C3-and-RH36.zip	Other
	HSMM-C3.zip	Other
	RD-cells.zip	Other
	RD.zip	Other
	RH36.zip	Other

Items per page:

1 - 5 of 6

Similar Datasets

Transcription profiling by array of ESC derived hepatocytes treated with either vehicle or high energy substrates to model non alcoholic fatty liver disease

Project description:Female H9 ESCs were maintained on matrigel and differentiated into hepatocyte like cells as previously described (Szkolnicka D, Farnworth SL, Lucendo-Villarin B, Hay DC. Curr Protoc Stem Cell Biol. 2014 Aug 1;30:1G.5.1-12. doi: 10.1002/9780470151808.sc01g05s30) . Sodium L-Lactate (L7022, Sigma, Gillingham, UK) 10mM, Sodium Pyruvate 1mM (Sigma, Dorset, UK) and Octanoic Acid (C2875, Sigma, Gillingham, UK) 2mM for 48 hours before harvesting.

2018-01-30 | E-MTAB-6227 | biostudies-arrayexpress

Cellular States Dictate Adaptive Signaling Responses to KRASG12C Inhibition: H358 Drug Response Phosphoproteomics

Project description:Covalent inhibitors of KRASG12C (KRASi) hold considerable progress for tumors driven by this oncogene yet early studies suggest rapid mechanisms of adaptive resistance that appear cell type dependent. To address these challenges, we performed mass spsectrometry baesd phosphoproteomics analysis in KRASG12C cell lines after short term treatment with ARS-1620 and compared phosphoproteomes of KRASG12C cells to understand signaling diversity. Our analysis suggests individual KRASG12C cells responds uniquely to perturbation of KRASG12C. Cell line models can be categorized in epithelial or mesenchymal subtypes and a similar pattern was observed in KRASG12C human lung cancer tumor tissues. ERBB2/3 signaling compensate for repressed ERK signaling following ARS-1620 treatment in epithelial cell type, and this subtype was also more responsive to inhibition of SHP2, IGFR, and SOS1. Conversely, FGFR signaling drives resistance to KRASi in mesenchymal cells in part via mTOR signaling. These studies suggest transcriptional subtypes of KRASG12C dictate responsiveness to specific combinations.

2021-02-15 | PXD021611 | Pride

Cellular States Dictate Adaptive Signaling Responses to KRASG12C Inhibition: Drug Response pY Profiling

2021-02-15 | PXD021607 | Pride

Cellular States Dictate Adaptive Signaling Responses to KRASG12C Inhibition: Calu-1 Drug Response Phosphoproteomics

Project description:therapy, drug resistance, signal transduction Covalent inhibitors of KRASG12C (KRASi) hold considerable progress for tumors driven by this oncogene yet early studies suggest rapid mechanisms of adaptive resistance that appear cell type dependent. To address these challenges, we performed mass spsectrometry baesd phosphoproteomics analysis in KRASG12C cell lines after short term treatment with ARS-1620 and compared phosphoproteomes of KRASG12C cells to understand signaling diversity. Our analysis suggests individual KRASG12C cells responds uniquely to perturbation of KRASG12C. Cell line models can be categorized in epithelial or mesenchymal subtypes and a similar pattern was observed in KRASG12C human lung cancer tumor tissues. ERBB2/3 signaling compensate for repressed ERK signaling following ARS-1620 treatment in epithelial cell type, and this subtype was also more responsive to inhibition of SHP2, IGFR, and SOS1. Conversely, FGFR signaling drives resistance to KRASi in mesenchymal cells in part via mTOR signaling. These studies suggest transcriptional subtypes of KRASG12C dictate responsiveness to specific combinations.

2021-02-15 | PXD021608 | Pride

Cellular States Dictate Adaptive Signaling Responses to KRASG12C Inhibition: Tyrosine Phosphorylation

2021-02-15 | PXD021604 | Pride

Cellular States Dictate Adaptive Signaling Responses to KRASG12C Inhibition: H1792 Drug Response Phosphoproteomics

2021-02-15 | PXD021609 | Pride

Cellular States Dictate Adaptive Signaling Responses to KRASG12C Inhibition: Protein Expression

2021-02-15 | PXD021603 | Pride

Determination of Gag stoichiometry for different production platforms by PRM analysis

Project description:In this work we established an analytical method of characterization for the Gag protein core and clarify the current variability of Gag stoichiometry in HIV-1 VLPs depending on the cell-based production platform, directly determining the number of Gag molecules per VLP in each case. Three Gag peptides have been validated to quantify the number of monomers using parallel reaction monitoring (PRM)

2022-12-07 | PXD021278 | Pride

Lysine benzoylation - Here we report the identification and characterization of a histone mark, lysine benzoylation (Kbz). Our study identifies 22 Kbz sites on histones from HepG2 and RAW cells. This type of histone mark can be stimulated by sodium benzoate (SB), a FDA-approved drug and a widely used chemical food preservative, via generation of benzoyl CoA.

Project description:Here we report the identification and characterization of a histone mark, lysine benzoylation (Kbz). Our study identifies 22 Kbz sites on histones from HepG2 and RAW cells. This type of histone mark can be stimulated by sodium benzoate (SB), a FDA-approved drug and a widely used chemical food preservative, via generation of benzoyl CoA.

2018-07-11 | PXD010332 | Pride

3'READS+RIP defines differential Staufen1 binding to alternative 3'UTR isoforms and reveals structures and sequence motifs influencing binding and polysome association

Project description:Using 3ʹ region extraction and deep sequencing coupled to ribonucleoprotein immunoprecipitation (3’READS+RIP), together with reanalyzing previous STAU1 binding and RNA structure data, we delineate STAU1 interactions transcriptome-wide, including binding differences between alternative polyadenylation (APA) isoforms. Consistent with previous reports, RNA structures are dominant features for STAU1 binding to CDSs and 3ʹUTRs. Overall, relative to short 3ʹUTR counterparts, longer 3ʹUTR isoforms of genes have stronger STAU1 binding, most likely due to a higher frequency of RNA structures, including specialized IRAlus. However, a sizable fraction of genes express transcripts showing the opposite trend, attributable to AU-rich sequences in their alternative 3'UTRs, possibly recruiting antagonistic RBPs and/or destabilizing STAU1-binding RNA structures. Using STAU1-knockout cells, we show that strong STAU1 binding to mRNA 3'UTRs generally enhances polysome association. However, IRAlus have little impact on STAU1-mediated polysome association despite having strong interactions with the protein.

2020-11-05 | GSE148771 | GEO