|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for AXL(NM_021913.4) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
The protein encoded by this gene is a member of the receptor tyrosine kinase subfamily. Although it is similar to other receptor tyrosine kinases, this protein represents a unique structure of the extracellular region that juxtaposes IgL and FNIII repeats. It transduces signals from the extracellular matrix into the cytoplasm by binding growth factors like vitamin K-dependent protein growth-arrest-specific gene 6. It is involved in the stimulation of cell proliferation and can also mediate cell aggregation by homophilic binding. Alternatively spliced transcript variants encoding different isoforms have been identified.
Gene References into function
- Data suggest that Gas6 and Axl signal transduction is aberrantly stimulated in endometriotic endometria, and is plausibly related to its growth potential.
- Acidification prevents vascular endothelial cell apoptosis by Axl activation
- Interaction of Axl receptor tyrosine kinase with C1-TEN (C1 domain-containing phosphatase and TENsin homologue).
- Axl and Gas6 expression might be involved in childhood thyroid tumorigenesis around Chernobyl.
- Gas6 receptors were not upregulated in any of the allograft groups, except for the Axl receptor, which increased only in acute tubular necrosis.
- We found that there was a significant increase in the steady-state levels of Axl mRNA in the RCC compared with the normal kidney pair
- Axl pathway mediates increased survival of uveal melanoma cells
- GAS6/Axl signaling is involved in human renal disease.
- Gas6-Axl interactions can rescue endothelial cells from apoptosis.
- Axl stimulation by GAS6 results in inhibition of the ligand-dependent activation of vascular endothelial growth factor (VEGF) receptor 2 and the consequent activation of an angiogenic program in vascular endothelial cells
- Axl overexpression and activation by Gas6 could be involved in progression of prostate neoplastic disease
- Axl, Sky and Mer are Gas6 receptors that enhance platelet activation and regulate thrombotic responses
- This report demonstrates that Gas6-induced downregulation of Axl is blocked by inhibitors of endocytosis and lysosomal degradation, but not by inhibitors of proteosomal activity.
- Results identify and characterise a novel interaction between RanBPM and the related receptor tyrosine kinases, Axl and Sky.
- Over-expression of axl is associated with lung adenocarcinoma and with tumor progression
- The crystal structure at 3.3 A resolution of a minimal human Gas6/Axl complex reveals an assembly of 2:2 stoichiometry.
- Suppression of Gas6 using small interfering RNA and the Axl-extracellular domain abolished the preventive effect of statins on Pi-induced apoptosis and calcification.
- Identification, functional manipulation, in vitro and in vivo validation, and preclinical therapeutic inhibition of a target receptor tyrosine kinase mediating glioma growth and invasion.
- Overexpression of the Axl tyrosine kinase receptor is associated with the development of squamous cell skin cancers
- These results implicate Twist proteins in regulation of TNFalpha production by antiinflammatory factors and pathways, and provide a mechanism by which type I IFNs and Axl receptors suppress inflammatory cytokine production.
- Here we show the involvement of members of the Tyro3 receptor tyrosine kinase family-Axl, Dtk, and Mer-in cell entry of filoviruses.
- Signaling through Axl inhibits vascular calcification in vitro.
- Axl and Gas6 are frequently overexpressed in both glioma and vascular cells and predict poor prognosis in GBM patients.
- coordination of ERK signaling and NF-kappaB and Brg-1 activation are indispensable to regulation of Axl-dependent MMP-9 gene transcription
- Possible strategies for targeted inhibition of the TAM family in the treatment of human cancer.
- Activation of Axl may be a protective mechanism against hypertonicity-induced apoptosis. Our results identify Axl as an important element of osmotic stress-induced signalling.
- In human endometriosis, the PI3K-Akt and MAPK signaling pathways may be activated via overexpression of AXL and SHC1, respectively.
