Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Compare transcriptional profile of AXL knockdown cell and AXL wild type cell

ABSTRACT: Compare transcriptional profile of AXL knockdown cell and AXL wild type cell

PROVIDER: PRJNA518770 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8518586_1.fastq.gz	Fastqsanger.gz
	SRR8518586_2.fastq.gz	Fastqsanger.gz
	SRR8518587_1.fastq.gz	Fastqsanger.gz
	SRR8518587_2.fastq.gz	Fastqsanger.gz
	SRR8518588_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Compare transcriptional profile of AXL knockdown cell and AXL wild type cell

Project description:We report the comparative investigation of gene expression profiles between genetic inactivation AXL cell and AXL wild type cells in two independent We found a list of AXL signaling target genes that are important for tumor invasion and angiogenesis.

2020-04-03 | GSE125994 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and AXL-/- astrocytes Transcriptomes

Project description:Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare Wild Type astrocytes transcriptome profiling (RNA-seq) to AXL-/- astrocytes transcriptome profiling and to explore the mechanism by which AXL interferes with type I IFN signaling in WT astrocytes. We performed an RNA-Seq analysis of WT and AXL-/- U-251MG cells in the absence of ZIKV. Surprisingly, the intrinsic level of type I IFN signaling was lower in AXL-/- cells than in WT cells. This result was further confirmed by RT-qPCR

2017-11-06 | GSE106545 | GEO

AXL targeting overcomes human lung cancer cell resistance to NK and CTL-mediated cytotoxicity

Project description:To investigate the effect of AXL inhibition on gene expression in carcinoma cell clones derived from NSCLC IGR-Heu cells, we profiled gene expression in cells treated with the AXL inhibitor bemcentinib (1 µmol/L) or with vehicle (dmso) for 72 hours

2019-10-25 | E-MTAB-8294 | biostudies-arrayexpress

compare the difference of gene expression between wild type ESCs and Mll2 Knockdown ESCs

2014-01-25 | GSE54382 | GEO

RNA-seq of MMTV-Neu AXL KO tumors

Project description:AXL is activated by its ligand GAS6 and is expressed in triple-negative breast cancer cells. We report that AXL is also detected in HER2+ breast cancer specimens where its expression correlates with poor patients’ survival. Using murine models of HER2+ breast cancer, AXL, but not Gas6, was found essential for metastasis. We determined that AXL is required for intravasation, extravasation and growth at the metastatic site. AXL is expressed in HER2+ cancers displaying EMT signatures and contributes to sustain EMT in murine tumors. Interfering with AXL in patient-derived xenograft impaired TGF-β-induced cell invasion. Lastly, pharmacological inhibition of AXL decreased the metastatic burden of mice developing HER2+ breast cancer. Our data identify AXL as a potential co-therapeutic target during the treatment of HER2+ breast cancers to limit metastasis.

2018-05-01 | GSE102368 | GEO

Effect of Gas6/Axl on HCC cell line gene expression

Project description:We adressed the impact of the receptor tyrosine kinase Axl and ist ligand Gas6 on gene expression in cellular HCC models, including cells harbouring Axl KO and exogenous reexpression.

2023-04-20 | GSE229731 | GEO

RNA-seq of MMTV-Neu AXL KO tumor grafts in FVB

2018-05-01 | GSE102369 | GEO

compare the difference of gene expression between wild type ESCs and Mll2 Knockdown ESCs

Project description:Mll2 (ALR) is a histone 3 lysine 4 trimethyltransferase to function as gene activation.In our study, we found that Mll2 is vital for proper control of proliferation and lineage differentiation of mouse ESCs, particularly towards the cardiac-specific lineages. We used microarrays to detail the global programme of gene expression to compare the difference after Mll2 knockdown in E14 cell lines. E14 cells were infected with lentiviruses expressing short hairpin RNA (shRNA) for Mll2 for 24 hours, and then puromycin was added at 2mg/ml to select for 5 days. Then collet samples of control and Mll2 knockdown E14 cells for RNA extraction and hybridization on Affymetrix microarrays.

2014-01-25 | E-GEOD-54382 | biostudies-arrayexpress

Low MITF/AXL ratio predicts early resistance to multiple targeted drugs in melanoma

Project description:Increased MITF expression contributes to melanoma progression and resistance to BRAF pathway inhibition. We show that, unexpectedly, lack of MITF is associated with more severe resistance to a range of inhibitors. Indeed, the presence of endogenous MITF was essential for robust drug responses. Both in primary and acquired resistance, MITF levels inversely correlated with expression of several activated receptor tyrosine kinases, most commonly AXL. The MITF-low/AXL-high/drug resistance phenotype was seen in roughly half of BRAF mutant and the majority of NRAS mutant melanoma cell lines. The dichotomous behavior of MITF in drug response was corroborated in vemurafenib-resistant biopsies, including MITF high and low clones in a relapsed patient. Drug cocktails containing AXL inhibitor enhanced melanoma cell elimination by BRAF or ERK inhibition. Our results demonstrate that a low MITF/AXL ratio predicts early resistance to multiple targeted drugs, and warrant clinical validation of AXL inhibitors to combat resistance of BRAF and NRAS mutant MITF-low melanomas. Experssion analysis by RNAseq of 14 melanoma cell lines.

2014-09-19 | E-GEOD-61544 | biostudies-arrayexpress

Integrated proteomics-based physical and functional mapping of AXL kinase signaling pathways and inhibitors define its role in cell migration: BioID

Project description:To better understand the signaling complexity of AXL, a member of the TAM family of receptor tyrosine kinases, we created a physical and functional map of AXL signaling interactions, phosphorylation events, and target-engagement of three AXL tyrosine kinase inhibitors (TKI). We assessed AXL protein-complexes using BioID, effects of AXL TKI on global phosphoproteins using mass spectrometry, and target engagement of AXL TKI using activity-based protein profiling. BioID identifies AXL-interacting proteins that are mostly involved in cell adhesion/migration. Global phosphoproteomics reveal that AXL inhibition deregulates phosphorylation of peptides involved in phosphatidylinositol-mediated signaling and cell adhesion/migration. Comparison of three AXL inhibitors reveals that TKI RXDX-106 inhibits pAXL, pAKT and migration/invasion of these cells without reducing their viability, while Bemcentinib exerts AXL-independent phenotypic effects. Proteomic characterization of these TKIs reveals that they inhibit diverse targets in addition to AXL, with Bemcentinib having the most off-targets. AXL and EGFR TKI co-treatment did not reverse resistance in cell line models of Erlotinib resistance. However, a unique vulnerability was identified in one persister clone, wherein combination of Bemcentinib and Erlotinib inhibited cell viability and signaling. We also show that AXL is overexpressed in ~30-40% of NSCLC but rarely in SCLC. NSCLC cells have a wide range of AXL protein expression, with basal activation detected rarely. Overall, we evaluate the mechanisms of action of AXL in lung cancer which can be used to establish assays to measure drug targetable active AXL complexes in patient tissues and inform the strategy for targeting its signaling network as an anticancer therapy.

2022-10-14 | PXD023911 | Pride

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