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抗Human AXL 抗体:
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Human Polyclonal AXL Primary Antibody for BR, CyTOF - ABIN5012837
Gould, Baxi, Schroeder, Peng, Leadley, Peterson, Perrin: Gas6 receptors Axl, Sky and Mer enhance platelet activation and regulate thrombotic responses. in Journal of thrombosis and haemostasis : JTH 2005
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Human Polyclonal AXL Primary Antibody for IHC - ABIN965632
Partanen, Mäkelä, Alitalo, Lehväslaiho, Alitalo: Putative tyrosine kinases expressed in K-562 human leukemia cells. in Proceedings of the National Academy of Sciences of the United States of America 1991
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Human Polyclonal AXL Primary Antibody for IHC - ABIN965631
OBryan, Frye, Cogswell, Neubauer, Kitch, Prokop, Espinosa, Le Beau, Earp, Liu: axl, a transforming gene isolated from primary human myeloid leukemia cells, encodes a novel receptor tyrosine kinase. in Molecular and cellular biology 1991
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Mouse (Murine) Monoclonal AXL Primary Antibody for CyTOF, FACS - ABIN4899408
Fujimori, Grabiec, Kaur, Bell, Fujino, Cook, Svedberg, MacDonald, Maciewicz, Singh, Hussell: The Axl receptor tyrosine kinase is a discriminator of macrophage function in the inflamed lung. in Mucosal immunology 2015
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Human Monoclonal AXL Primary Antibody for ELISA, WB - ABIN965629
Rual, Venkatesan, Hao, Hirozane-Kishikawa, Dricot, Li, Berriz, Gibbons, Dreze, Ayivi-Guedehoussou, Klitgord, Simon, Boxem, Milstein, Rosenberg, Goldberg, Zhang, Wong, Franklin, Li, Albala, Lim et al.: Towards a proteome-scale map of the human protein-protein interaction network. ... in Nature 2005
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Human Monoclonal AXL Primary Antibody for ELISA, WB - ABIN968973
Budagian, Bulanova, Orinska, Duitman, Brandt, Ludwig, Hartmann, Lemke, Saftig, Bulfone-Paus: Soluble Axl is generated by ADAM10-dependent cleavage and associates with Gas6 in mouse serum. in Molecular and cellular biology 2005
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Human Monoclonal AXL Primary Antibody for IF, ELISA - ABIN965630
Green, Ikram, Vyas, Patel, Proby, Ghali, Leigh, OToole, Storey: Overexpression of the Axl tyrosine kinase receptor in cutaneous SCC-derived cell lines and tumours. in British journal of cancer 2006
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Human Polyclonal AXL Primary Antibody for IHC, IHC (p) - ABIN4282541
Pinato, Mauri, Lloyd, Vaira, Casadio, Boldorini, Sharma: The expression of Axl receptor tyrosine kinase influences the tumour phenotype and clinical outcome of patients with malignant pleural mesothelioma. in British journal of cancer 2013
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Human Monoclonal AXL Primary Antibody for FACS - ABIN4895644
Yumoto, Eber, Wang, Cackowski, Decker, Lee, Nobre, Aguirre-Ghiso, Jung, Taichman: Axl is required for TGF-β2-induced dormancy of prostate cancer cells in the bone marrow. in Scientific reports 2016
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Human Monoclonal AXL Primary Antibody for FACS - ABIN4895642
Zheng, Hedl, Abraham: TAM receptor-dependent regulation of SOCS3 and MAPKs contributes to proinflammatory cytokine downregulation following chronic NOD2 stimulation of human macrophages. in Journal of immunology (Baltimore, Md. : 1950) 2015
Study using gastric cancer (GC) tissue samples and mouse xenograft model showed that GAS6-AS1 can control the expression of its cognate sense gene GAS6 at the transcriptional or translational levels by forming a RNA-RNA duplex, significantly driving the aggressive GC phenotype, and consequently inducing an increase of AXL level and promoting AXL signaling pathway activation.
We emphasize a correlation between free Gas6 and free sAxl levels favoring abundant Gas6/Axl signaling in advanced fibrosis and hepatocellular carcinoma (HCC). The raised scenario provides a solid basis for theranostics allowing the use of sAxl as an accurate diagnostic biomarker of liver cirrhosis and HCC, as well as Axl receptor signaling for therapeutic intervention in stratified HCC patients.
Results found that prenatal tobacco smoke exposure was associated with the regulation of AXL, a receptor tyrosine kinase of the TAM family that plays an important role in suppressing Toll-like receptor-induced inflammation. Moreover, AXL methylation and tobacco smoke exposure during fetal development may act synergistically to modify the risk of bronchitis symptoms in childhood.
AXL is a key upstream effector of AKT pathway-associated resistance to BRAF inhibitors in melanomas with wildtype PTEN, but not in melanomas with impaired PTEN.The activated AXL kinase is required for acquired resistance to BRAF inhibitors in melanoma with wildtype PTEN.
sAXL is widely expressed in malignant effusions, particularly in ovarian and breast carcinoma and in malignant mesothelioma. sAXL is overexpressed in HGSC compared to LGSC and its levels are lower following exposure to chemotherapy.
AXL receptor tyrosine kinase (Axl) expression was induced by E6 protein, human papillomavirus-16 (HPV16E6) in cervical cancer cells, suggesting that blockade of Axl signalling might be an effective way to reduce the progression of cervical cancer.
AXL was highly expressed in clinical specimens of EGFR-mutated lung cancers and its high expression was associated with a low response rate to EGFR-tyrosine kinase inhibitor. These results indicated pivotal roles for AXL and its inhibition in the intrinsic resistance to osimertinib and the emergence of osimertinib-tolerant cells.
Axl/Akt/NF-kappaB signaling participates in mediating the effect of mineral trioxide aggregate on macrophage polarization.
The role of AXL in the esophageal adenocarcinoma cell invasion through upregulation of extracellular acidification, lysosomes peripheral distribution, and exocytosis.
Decreased ARL2 expression level was clinically correlated to the higher grades and poorer outcomes of glioma patients. ARL2 overexpression attenuated the proliferation, clone formation, migration, invasive and tumorigenic capabilities of glioma cells by regulating the expression of receptor tyrosine kinase AXL.
Axl binds to and phosphorylates TNS2 and that Axl/TNS2/IRS-1 cross-talk may potentially play a critical role in glucose metabolism of cancer cells.
AXL expression is regulated by miR-34a.miR-34a regulates dendritic cells activation by targeting AXL.AXL expression is reduced in rheumatoid arthritis CD1c+ dendritic cells.
Axl induction during viral infections contributes to maintaining macrophage capacity to engulf apoptotic cells, which may have important consequences for resolution of anti-viral immune responses.
Serum soluble AXL is not a helpful biomarker for cardiovascular complications after heart transplantation.
miR-34a is an oncogenic miRNA, downregulated in the distinct breast cancer subtypes. It also targets MET and AXL 3'-UTRs in triple-negative breast cancer.
identify the receptor tyrosine kinase Axl as a novel target of ZNF224 transcriptional repression activity.
Findings suggest that METTL3 plays very important oncogenic roles in ovarian carcinoma development and/or aggressiveness by stimulating AXL translation and EMT.
Co-expression of CDCP1 and AXL is often observed in EGFR-mutation-positive tumors, limiting the efficacy of EGFR TKIs. Co-treatment with EGFR TKI and TPX-0005 warrants testing.
This study demonstrates that motility behavior of AXL-expressing tumor cells can be elicited by Gas6-bearing apoptotic bodies generated from tumor treatment with therapeutics that produce killing of a portion of the tumor cells present but not all, hence generating potentially problematic invasive and metastatic behavior of the surviving tumor cells
Results show that average methylation in AXL at birth was associated with higher risk for asthma-related phenotypes in childhood, especially wheezing. The effects of average AXL methylation on wheezing symptoms were magnified in girls compared to boys.
Tyro3/Axl/Mertk-deficient mice develop bone marrow edema which is an early pathological marker in rheumatoid arthritis.
ALX-deficient macrophages have defective microparticle clearance resulting in lung inflammation and injury.
These results suggest a novel role for Axl in suppressing antigen presentation through MHCI, and enhancing cytokine release, which promotes a suppressive myeloid microenvironment.
AXL is not the key receptor for Zika virus infection using an Axl knockout mouse model.
present findings indicate that MafB enhances efferocytosis by regulating Axl expression in RAW264.7 macrophages
Study found that hematopoietic cell-Axl deficiency in Western-type diet-fed Ldlr(-/-) mice does not affect the progression of advanced atherosclerosis or lesional processes associated with TAM receptor signaling.
This study demonstrated that the Gas6(-/-) Axl(-/-) double knockout (DKO) mice showed axonal damage, motor deficits, prolonged neuroinflammation, and less remyelination following cuprizone exposure.
These results demonstrate that AXL is essential for limiting the immunosuppressive effects of type I interferons and enabling the induction of protective antiviral adaptive immunity.
GAS6-AXL signaling-mediated autophagy induction in murine macrophages ameliorates hepatic inflammatory responses by inhibiting NLRP3 inflammasome activation.
Both Axl+/- and Axl-/- suckling mice supported the replication of Zika virus.
reciprocal activation of Axl and Mer receptor tyrosine kinases has a major impact on the outcome of renal inflammation.
Axl is critical for survival of T lymphocytes, especially during vascular remodeling in hypertension.
Axl, Mertk and Tyro3 receptors are not required for Zika virus entry and infection.
Axl plays an essential role in the regulation of NK cell development as well as natural killer effector function.
Matrix metalloproteases ADAM10 and TACE (ADAM17) cleave AXL receptor tyrosine kinase (Axl) in lupus-prone leukocytes.
Gas6/Axl and Akt/FoxO1a were involved in protective effects of testosterone on VSMCs senescence and collagen synthesis.
Axl allows specific identification of airway macrophages, and that its expression is critical for macrophage functional compartmentalization in the airspaces or lung interstitium.
results establish TAM receptors as both controllers of microglial physiology and potential targets for therapeutic intervention in central nervous system disease
These results suggest that TAM receptors support NSCs survival, proliferation and differentiation by regulating expression of neurotrophins, especially the nerve growth factor.
Gas6-induced Axl signaling is a critical driver of pancreatic cancer progression.
activation of receptor tyrosine kinase Axl inhibits the osteogenic differentiation of vascular pericytes.
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.
, AXL transforming sequence/gene
, tyrosine-protein kinase receptor UFO
, adhesion-related kinase
, ufo oncogene homolog