Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PDGF induction of immediate early genes in NIH3T3 cells

ABSTRACT: This experiment was performed to identify immediate early genes that were induced by PDGF specifically through Src family kinases (SFKs), MEK1/2, or PI 3-K. Keywords: repeat sample

ORGANISM(S): Mus musculus

PROVIDER: GSE2196 | GEO | 2005/02/23

SECONDARY ACCESSION(S): PRJNA91261

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcription profiling of NIH3T3 cells treated with platelet-derived growth factor and Src kinase inhibitors to identify immediate early genes that are induced by PDGF through Src family kinases and other kinases.

Project description:This experiment was performed to identify immediate early genes that were induced by PDGF specifically through Src family kinases (SFKs), MEK1/2, or PI 3-K.

2007-09-22 | E-GEOD-2196 | biostudies-arrayexpress

Src heterodimerically activates Lyn or Fyn to serve as targets for esophageal squamous cell carcinoma (ESCC) diagnosis and treatment

Project description:we combined phosphoproteomics and several cellular and molecular biologic strategies to identify that Src specifically interacted with the members of Src-family kinases (SFKs), such as Fyn or Lyn to form heterodimers, and subsequently phosphorylate the tyrosine sites in SH2 and kinase domains, which critically contributed to the ESCC malignancy.

2022-03-15 | PXD032306 |

PDGF-induced genes regulated by the PI3K and MEK/ERK signaling pathways

Project description:Human T98G glioblastoma cells were stimulated with platelet-derived growth factor (PDGF) and analyzed by DNA microarrays, which identified 74 immediate-early gene transcripts. Cells were then treated with inhibitors to identify subsets of genes that are targets of the phosphatidylinositol 3-kinase (PI3K) and MEK/ERK signaling pathways. Four groups of PDGF-induced genes were defined: independent of PI3K and MEK/ERK signaling, dependent on PI3K signaling, dependent on MEK/ERK signaling, and dependent on both pathways. Cells were grown in Minimal Essential Medium (Invitrogen) supplemented with fetal calf serum (10%). For growth factor/inhibitor treatments, cells were incubated in serum-free medium for 72 h, and either left unstimulated, or stimulated for 30 min with human PDGF-BB (50 ng/ml) (Sigma). U0126 (Cell Signaling Technology) and LY294002 (BioMol) were added 60 min prior to PDGF addition. Keywords: other

2004-03-13 | GSE1128 | GEO

Src Family Kinases as potential therapeutic targets for chemotherapy-resistant triple negative breast cancer

Project description:Here we quantified tyrosine phosphorylation (pTyr) mediated signaling networks in chemotherapy sensitive (CS) and resistant (CR) TNBC patient derived xenografts (PDX) to gain novel therapeutic insights. We identified Src Family Kinases (SFKs) as potential therapeutic targets in CR TNBC PDXs. Additionally, we performed pTyr analysis on tumor specimens derived from TNBC patients and observed lower prevalence of SFK driven tumors.

2022-10-13 | PXD034154 | Pride

PDGF-hSyn Synaptosomes (vGlut FASS) nanoLC-MS/MS

Project description:This project studies the differential abundance of proteins at excitatory synapses of PDGF-hSyn mice (Masliah et al., 2000, Science), which are a model for Parkinson’s disease/dementia with Lewy bodies. The mice overexpress human alpha synuclein under the human PDGF promoter. Synapses were purified from animals expressing fluorescently tagged vGlut1 (vGlut1-Venus) using fluorescence activated synapse sorting (FASS; cf. Biesemann et al., 2014, EMBO J).

2019-09-02 | PXD006812 | Pride

PDGF and FGF treatment in E13.5 MEPMs II

2015-05-07 | GSE66484 | GEO

PDGF and FGF treatment in E13.5 MEPMs II

Project description:PDGF and FGF treatment in E13.5 MEPMs. 4 hr PDGF treated MEPMs (3 replicates), 4 hr FGF treated MEPMs (3 replicates), 1 hr PDGF + PD325901 treated MEPMs (2 replicates), 4 hr PDGF + PD325901 treated MEPMs (2 replicates), 1 hr FGF + PD325901 treated MEPMs (2 replicates), 4 hr FGF + PD325901 treated MEPMs (2 replicates), 1 hr PDGF + LY294002 treated MEPMs (2 replicates), 4 hr PDGF + LY294002 treated MEPMs (2 replicates), 1 hr FGF + LY294002 treated MEPMs (2 replicates), 4 hr FGF + LY294002 treated MEPMs (2 replicates) 4 hr PDGF treated MEPMs (3 replicates), 4 hr FGF treated MEPMs (3 replicates), 1 hr PDGF + PD325901 treated MEPMs (2 replicates), 4 hr PDGF + PD325901 treated MEPMs (2 replicates), 1 hr FGF + PD325901 treated MEPMs (2 replicates), 4 hr FGF + PD325901 treated MEPMs (2 replicates), 1 hr PDGF + LY294002 treated MEPMs (2 replicates), 4 hr PDGF + LY294002 treated MEPMs (2 replicates), 1 hr FGF + LY294002 treated MEPMs (2 replicates), 4 hr FGF + LY294002 treated MEPMs (2 replicates)

2015-05-07 | E-GEOD-66484 | biostudies-arrayexpress

Gene expression profiling regulated by PDGF in pBSMCs

Project description:To explore global molecular changes in smooth muscle in response to PDGFR activation, primary human bladder smooth muscle cells were treated with 1 nM PDGF-BB (hereafter PDGF) for 0, 4 or 24 h. Total RNA were prepared, and analyzed using expression profiling, and subjected to bioinformatic and functional interrogation. To identify molecular signatures of bladder smooth muscle peturbed by PDGF, primary human bladder smooth muscle cells were treated with 1 nM PDGF-BB (hereafter PDGF) for 0, 4 or 24 h.

2014-10-06 | E-GEOD-52488 | biostudies-arrayexpress

A gene expression signature of PDGF-stimulated fibroblasts

Project description:Analysis of platelet-derived growth factor (PDGF)-stimulated fibroblasts. Results provide insight into novel pro-tumorigenic factors induced by PDGF-activation of fibroblasts.

2012-09-10 | GSE40720 | GEO

Dose-dependent dual roles of PDGF-BB–PDGFR-? in vascular remodeling and opposing effects of anti-PDGF drug-induced metastasis

Project description:Anti-PDGF agents are routinely used as a key component in front-line therapy for the treatment of various cancers. However, molecular mechanisms underlying their impact on vascular remodeling in relation to the dose issue remain poorly understood. Here we show that in high PDGF-BB-producing tumors, anti-PDGF drugs significantly inhibited tumor growth and metastasis by preventing pericyte (PC) loss and vascular permeability. Surprisingly, the same anti-PDGF-BB drugs promoted tumor cell dissemination and metastasis in PDGF-BB-low-producing or negative tumors by ablating PCs from tumor vessels. At the molecular level, we show that the PDGFR-? signaling pathway in PCs mediated the opposing effects and persistent exposure of PCs to PDGF-BB led to marked downregulation of PDGFR-?. Inactivation of the PDGFR-? signaling system led to decreased levels of integrin ?1?1, resulted in impaired adhesion of PCs to collagen I, IV and laminin, two principal extracellular matrix components in blood vessels for interaction with these integrins. Our data suggest that tumor PDGF-BB levels may serve as an important biomarker for selection of tumor-bearing hosts for beneficial therapy and unsupervised practice of this group of drugs could potentially promote tumor invasion and metastasis. Pericytes were isolated and treated with PDGF-BB or control for 5 days.

2013-07-22 | E-GEOD-46564 | biostudies-arrayexpress

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