Browse
Submit Data
Databases
API
Help

Dataset Information

246 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Human Glioblastoma Cell Line Secretome LC-MS/MS

ABSTRACT: To investigate the effect of glioblastoma secretome in activating tau pathology, Glioblastoma cell line secretome were prefractionated with gel filtration chromatography. Secretome analyzed by LC-MS/MS and identified targets using PSM count quantitation.

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Permanent Cell Line Cell, Cell Culture

DISEASE(S): Glioblastoma

SUBMITTER: Shinyeong Ju

LAB HEAD: Cheolju Lee

PROVIDER: PXD007969 | Pride | 2018-07-16

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Publications

Glioblastoma-secreted soluble CD44 activates tau pathology in the brain.

Lim Sungsu S Kim Dohee D Ju Shinyeong S Shin Seulgi S Cho Il-Joo IJ Park Sung-Hye SH Grailhe Regis R Lee Cheolju C Kim Yun Kyung YK

Experimental & molecular medicine 20180406 4

During aggressive tumor growth and migration, glioblastoma cells secrete diverse molecules and adhesion proteins to the extracellular matrix. Yet, the biochemical effects of the glioblastoma secretome in the brain remain largely unknown. Here we show that soluble CD44 secreted from glioblastoma cells induces neuronal degeneration through the activation of tau pathology in the brain. Glioblastoma-xenograft tissues showed a number of degenerating neurons bearing highly phosphorylated tau. Through ...[more]

PMID: 29622771

Similar Datasets

Expression data of mESCs differentiated into Paraxial mesoderm

Project description:Stem cell-derived tissues have wide potential for modelling developmental and pathological processes as well as cell-based therapy. However, it has proven difficult to generate several key cell types in vitro, including skeletal muscle. In vertebrates, skeletal muscles derive during embryogenesis from the presomitic mesoderm (PSM). Using PSM development as a guide, we establish conditions for the differentiation of monolayer cultures of mouse embryonic stem (ES) cells into PSM-like cells without the introduction of transgenes or cell sorting. We differentiated mouse ESCs in serum-free medium supplemented with Rspo3 ( or as an alternative with Chir 9902) and the Bmp inhibitor LDN193189. In vivo, the PSM cells are first expressing Msgn1 (posterior PSM marker) and then mature to express Pax3 (anterior PSM marker). After 4 days of differentiation of mESCs, Msgn1-positive cells were FACS-sorted and their transcriptome analyzed. After 6 days of differentiation, Pax3-positive cells were sorted and their transcriptome analyzed. Mouse ESCs differentiated for 0, 4 and 6 days in serum-free medium containing a Wnt activator, a BMP inhibitor and DMSO, to study paraxial mesoderm in vitro

2015-08-03 | E-GEOD-71348 | biostudies-arrayexpress

Transcriptome of human glioblastoma stem cells isolated from four patients

Project description:The transcriptome of human glioblastoma stem cells (GSCs) isolated from brain tumours of four patients (#5, #7, #8, #9) was comparatively analysed among them and in respect to common established human glioblastoma cell lines (U87MG, U373MG) and non-transformed human neural stem cells (NSCs). Cells were grown under optimal culture conditions, total RNA carefully isolated form the seven cell samples, and then subjected to global transcriptomic analysis in Array

2021-07-12 | E-MTAB-9346 | biostudies-arrayexpress

Mitochondrial proteome analysis from LC-MS/MS glioblastoma cell lines

Project description:Proteomic Analysis of metabolic change in T98G and U87MG glioblastoma cell lines

2022-03-02 | PXD011151 | Pride

Abernathy2016 - glioblastoma treatment

Project description:The paper describes a model of glioblastoma. Created by COPASI 4.25 (Build 207) This model is described in the article: Modeling the Treatment of Glioblastoma Multiforme and Cancer Stem Cells with Ordinary Differential Equations Kristen Abernathy and Jeremy Burke BMC Computational and Mathematical Methods in Medicine Volume 2016, Article ID 1239861, 11 pages Abstract: Despite improvements in cancer therapy and treatments, tumor recurrence is a common event in cancer patients. One explanation of recurrence is that cancer therapy focuses on treatment of tumor cells and does not eradicate cancer stem cells (CSCs). CSCs are postulated to behave similar to normal stem cells in that their role is to maintain homeostasis. That is, when the population of tumor cells is reduced or depleted by treatment, CSCs will repopulate the tumor, causing recurrence. In this paper, we study the application of the CSC Hypothesis to the treatment of glioblastoma multiforme by immunotherapy. We extend the work of Kogan et al. (2008) to incorporate the dynamics of CSCs, prove the existence of a recurrence state, and provide an analysis of possible cancerous states and their dependence on treatment levels. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

2019-07-24 | BIOMD0000000757 | BioModels

Glioblastoma Orthotopic Xenograft Transcriptome and Glioblastoma Xenograft Comparative Genomic Hybridization Arrays

Project description:This SuperSeries is composed of the following subset Series: GSE38814: Glioblastoma Orthotopic Xenograft Transcriptome GSE38815: Glioblastoma Xenograft Comparative Genomic Hybridization Arrays Refer to individual Series

2012-07-10 | E-GEOD-39242 | biostudies-arrayexpress

Glioblastoma Orthotopic Xenograft Transcriptome

Project description:Transcriptional profiling of glioblastoma orthotopic xenografts Descriptive experiment, comparison of 39 glioblastoma tumors as orthotopic xenografts

2012-07-10 | E-GEOD-38814 | biostudies-arrayexpress

INC280 Combined With Bevacizumab in Patients With Glioblastoma Multiforme

Project description:The purpose of this study is to determine whether the combination of two agents, INC280 and bevacizumab, is safe and effective when administered to patients with Glioblastoma Multiforme (GBM) who have progressed after receiving prior therapy or who have unresectable GBM.

| 2185625 | ecrin-mdr-crc

PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis [Tau with inhibitors]

Project description:Microtubule-binding protein tau is a misfolding-prone protein associated with tauopathies. As tau undergoes cell-to-cell transmission, extracellular tau aggregates convert astrocytes into a pro- inflammatory state via integrin activation, causing them to release unknown neurotoxic factors. Here we combine transcriptomics with isotope labeling-based quantitative mass spectrometry analysis of mouse primary astrocyte secretome to establish PI3K-AKT as a critical differentiator between pathogenic and physiological integrin activation; simultaneous activation of PI3K-AKT and focal adhesion kinase (FAK) in tau fibril-treated astrocytes changes the output of integrin signaling, causing pro-inflammatory gene upregulation, trans-Golgi network restructuring, and altered secretory flow. Furthermore, NCAM1, as a proximal signaling component in tau-stimulated integrin and PI3K-AKT activation, facilitates the secretion of complement C3 as a main neurotoxic factor. Significantly, tau fibrils-associated astrogliosis and C3 secretion can be mitigated by FAK or PI3K inhibitors. These findings reveal an unexpected function for PI3K-AKT in tauopathy-associated astrogliosis and a target for anti-inflammation-based Alzheimer’s therapy.

2023-10-04 | GSE236866 | GEO

PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis [Tau vs OPN]

2023-10-04 | GSE236024 | GEO

Metabolic heterogeneity in Glioblastoma

Project description:2 cell populations [slow and fast-cycling cells] were isolated from 3 different patient-derived glioblastoma stem cell lines [L0, L1, L2].

2015-03-24 | ST000248 | MetabolomicsWorkbench

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