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Inhibition of AXL Receptor Tyrosine Kinase Enhances Brown Adipose Tissue Functionality in mice.

ABSTRACT: Inhibition of AXL Receptor Tyrosine Kinase Enhances Brown Adipose Tissue Functionality in mice.

PROVIDER: PRJNA966105 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24392383.fastq.gz	Fastqsanger.gz
	SRR24392284.fastq.gz	Fastqsanger.gz
	SRR24392384.fastq.gz	Fastqsanger.gz
	SRR24392285.fastq.gz	Fastqsanger.gz
	SRR24392385.fastq.gz	Fastqsanger.gz

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Inhibition of AXL Receptor Tyrosine Kinase Enhances Brown Adipose Tissue Functionality in mice [NovaSeq]

Project description:To identify transcriptomic differences in interscapular brown adipose tissue depots from HFD-challenged wild-type (Axl-floxed Cre-) vs. iFAXLKO (Axl-floxed Cre+) mice

2023-06-22 | GSE231470 | GEO

Inhibition of AXL Receptor Tyrosine Kinase Enhances Brown Adipose Tissue Functionality in mice [HiSeq]

Project description:To identify transcriptomic differences in interscapular brown adipose tissue depots from HFD-challenged wild-type (WT) vs. Axl KO (whole-body Axl Receptor knockout) mice

2023-06-22 | GSE231469 | GEO

Inhibition of AXL Receptor Tyrosine Kinase Enhances Brown Adipose Tissue Functionality in mice [HiSeq]

Project description:Inhibition of AXL Receptor Tyrosine Kinase Enhances Brown Adipose Tissue Functionality in mice [HiSeq]

| PRJNA966107 | ENA

Inhibition of AXL Receptor Tyrosine Kinase Enhances Brown Adipose Tissue Functionality in mice [NovaSeq]

Project description:Inhibition of AXL Receptor Tyrosine Kinase Enhances Brown Adipose Tissue Functionality in mice [NovaSeq]

| PRJNA966108 | ENA

Inhibition of AXL Receptor Tyrosine Kinase Enhances Brown Adipose Tissue Functionality in mice.

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-06-22 | GSE231471 | GEO

Identification of the receptor tyrosine kinase AXL in triple negative breast cancer as a novel target for the human miR-34a microRNA

Project description:This SuperSeries is composed of the following subset Series: GSE21719: Identification of the receptor tyrosine kinase AXL in triple negative breast cancer as a novel target for the human miR-34a microRNA (miRNA study) GSE21832: Identification of the receptor tyrosine kinase AXL in triple negative breast cancer as a novel target for the human miR-34a microRNA (gene expression) Refer to individual Series

2010-12-31 | E-GEOD-21834 | biostudies-arrayexpress

The effect of inhibition of receptor tyrosine kinase AXL on DNA damage response in ovarian cancer

Project description:To explore molecular alterations upon AXL inhibition and the functions that might be regulated by AXL and SAM68

2023-06-28 | GSE233776 | GEO

AXL and MERTK receptor tyrosine kinases inhibition protects against pancreatic necrosis via limiting CXCL2-mediated neutrophil infiltration

Project description:We aimed to investigate the strategies to protect against pancreatitis severity and we focused on AXL and MERTK tyrosine kinases receptors, which are the negative regulator of the innate immune response. In order to investigate the underlying mechanism of AXL and MERTK in mediating pancreatic necrosis, we performed high-throughput mRNA sequencing on the pancreatic tissues of 6 C57BL/6J wild type mice and 6 Axl-/-Mertk-/- mice under hyperstimulation of caerulein.

2024-12-15 | GSE191008 | GEO

The effect of inhibition of receptor tyrosine kinase AXL on DNA damage response in ovarian cancer

Project description:AXL is a receptor tyrosine kinase that is often overexpressed in cancers. It contributes to pathophysiology in cancer progression and therapeutic resistance, making it an emerging therapeutic target. The first-in-class AXL inhibitor bemcentinib (R428/BGB324) has been granted fast track designation by the U.S. Food and Drug Administration (FDA) in STK11-mutated advanced metastatic non-small cell lung cancer and was also reported to show selective sensitivity towards ovarian cancers (OC) with a Mesenchymal molecular subtype. In this study, we further explored AXL’s role in mediating DNA damage responses by using OC as a disease model. AXL inhibition using R428 resulted in the increase of DNA damage with the concurrent upregulation of DNA damage response signalling molecules. Furthermore, AXL inhibition rendered cells more sensitive to the inhibition of ATR, a crucial mediator for replication stress. Combinatory use of AXL and ATR inhibitors showed additive effects in OC. Through SILAC co-immunoprecipitation mass spectrometry, we identified a novel binding partner of AXL, SAM68, whose loss in OC cells harboured phenotypes in DNA damage responses similar to AXL inhibition. In addition, AXL- and SAM68-deficiency or R428 treatment induced elevated levels of cholesterol and upregulated genes in the cholesterol biosynthesis pathway. There might be a novel protective role of cholesterol in shielding cancer cells against DNA damage induced by AXL inhibition or SMA68 deficiency.

2023-06-22 | PXD042572 | Pride

Quantitative tyrosine phosphoproteome profiling of GAS6-AXL signaling network

Project description:Overexpression and amplification of AXL receptor tyrosine kinase (RTK) has been found in several hematologic and solid malignancies. Activation of AXL by its ligand GAS6 can enhance tumor-promoting processes such as proliferation, migration, invasion, and survival. Despite the important role of AXL in cancer development, a deep and quantitative mapping of its signaling transduction has not been performed. Here, we used a mass spectrometry-based quantitative proteomic approach to characterize the temporal dynamics of the phosphotyrosine proteome of MDA-MB-231 cells stimulated with GAS6

2021-08-24 | PXD025457 | Pride

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