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anti-Mouse (Murine) GAS6 Antibodies:
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Human Polyclonal GAS6 Primary Antibody for IHC, IHC (p) - ABIN4313581
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
Gas6 stimulates angiogenesis of human retinal endothelial cells and of zebrafish embryos via ERK1/2 signaling.
Genetic deletion of Gas6 or Mer is protective against silica-induced lung inflammation and fibrosis in mice.
MerTK ligands Gas6 and Protein S are expressed in both RPE cells and photoreceptors, and at least one of them is required for phagocytosis to occur. With opposite effects on RPE phagocytosis and changes in their expression levels around the time of POS uptake, Gas6 and Protein S may contribute to the tight control of the acute phagocytic peak in the retina. Review.
Disinhibiation of Gas6 binding to Tyro3 due to PGRN reduction results in activation of PKCalpha via PLCgamma, inducing tau phosphorylation at Ser203, mislocalization of tau to dendritic spines, and spine loss.
Here, the mechanism by which norepinephrine (NE)regulates prostate cancer DTCs in the marrow is explored. NE directly stimulated prostate cancer cell proliferation through beta2-adrenergic receptors (ADRB2).. NE also altered prostate cancer proliferation in the marrow niche by indirectly downregulating the secretion of the dormancy inducing molecule growth arrest specific-6 (GAS6) expressed by osteoblasts.
This study demonstrated that the Gas6(-/-) Axl(-/-) double knockout (DKO) mice showed axonal damage, motor deficits, prolonged neuroinflammation, and less remyelination following cuprizone exposure.
The possibility that the Gas6-Mer-PI3K/Akt-STAT1-LXR-Arg2 pathway plays an essential role for resolving inflammatory response in acute lung injury.
Taken together, in our study Gas6 fails to aggravate calcification against the previous assumption.
The present study provides evidence that the vitamin K-dependent protein growth arrest specific 6 (Gas6) promotes such repair in in vitro cultures of mouse optic nerve and cerebellum.
Gas6 specifically promotes the recruitment of inflammatory CCR2(hi)CX3CR1(lo) monocytes through the regulation of both CCR2 and CCL2 during deep venous thrombosis.
Gas6/Axl and Akt/FoxO1a were involved in protective effects of testosterone on VSMCs senescence and collagen synthesis.
Gas6-mediated uptake is not a means to clear the bulk of circulating membrane-derived microparticles (PMPs) but may serve to locally phagocytose PMPs generated at sites of platelet activation and as a way to effect endothelial responses.
Gas6-FoxO-1 signaling axis plays an important role in VCAM-1 expression in the context of venous thromboembolism by promoting bone marrow mononuclear cell-endothelial cell adhesion.
Gas6 and Axl serum levels increase in parallel to chronic liver disease progression inactivation.
Gas6, through upregulation of Ptges/PGE2, contributes to cancer-induced venous thrombosis.
Gas6-induced Axl signaling is a critical driver of pancreatic cancer progression.
Gas6/Axl signaling is essential for delaying the cellular senescence process regulated by the PI3K/Akt/FoxO signaling pathway.
The up-regulation of Gas6/Axl signaling is a protective mechanism which reduces tubulo-interstitial apoptosis and slows progression to end-stage renal failure.
Optimal TAM signaling requires coincident TAM ligand engagement of both its receptor and the phospholipid phosphatidylserine regulating TAM receptor tyrosine kinases Tyro3, Axl, and Mer and their ligands Gas6 and Protein S.
Inhibition of the Gas6 receptor Mer or therapeutic targeting of Gas6 by warfarin reduced myeloma burden and improved survival in a systemic model of myeloma.
data are consistent with Growth arrest-specific protein 6 being neuroprotective during experimental autoimmune encephalomyelitis by dampening the inflammatory response, thereby preserving axonal integrity and myelination.
Growth arrest-specific gene 6 transfer promotes mesenchymal stem cell survival and cardiac repair under hypoxia and ischemia via enhanced autocrine signaling and paracrine action
Macrophage-derived Gas6 is a critical regulator of the transition from premalignant to invasive cancer.
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.
findings suggest that Gas6 may play a role in human atherosclerotic plaque remodeling
Gas6 plays a role in the development and progression of oral squamous cell carcinoma.
N: Down-regulation of the Gas6 gene enhanced the expression of ICAM-1, E-selectin, IL-8 and MCP-1 in HUVECs after P.g- LPS stimulating, while up-regulaiton of the Gas6 gene weakened the expression of ICAM-1, E-selectin, IL-8 and MCP-1 in HUVECs after P.g-LPS stimulating,suggesting that Gas6 may play a role in the process of endothelial cell adhesion.
Growth Arrest-Specific 6(GAS6) levels increased significantly after vitamin K1 prophylaxis in preterm newborns but not in term infants
Higher levels of Gas6 in plasma are obviously correlated with acute lung injury (ALI) development. An early increase in the plasma Gas6 level suggests that endothelial injury is a key link in the pathogenesis of ALI.
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
Self-sustaining cells are characterized by excessive GAS6 secretion and TAM-PDK-RSK-mTOR pathway activation.
The anti-angiogenic effect of luteolin may be associated with the inhibition of the Gas6/Axl pathway and its downstream phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathways.
TWIST1, in part via GAS6 and L1CAM, led to higher expression and activation of Akt upon cisplatin treatment, and inhibition of Akt activation sensitized cells to cisplatin.
Gas6 bound to the fiber proteins of adenovirus and suppressed IFN beta production.
Protein S and Gas6 mediates phagocytosis of HIV-1-infected cells by bridging receptor tyrosine kinase Mer to phosphatidylserine exposed on infected cells.
A critical role for GAS6 in epithelial cells in maintaining oral homeostasis.
AXL is the only relevant Zika virus entry cofactor expressed on fetal endothelial cells, and that when produced in mammalian cells, only Zika virus, but not West Nile virus or dengue virus, can use AXL, because it more efficiently binds Gas6.
The plasma concentrations of Gas6 and Axl are lowered in rheumatoid arthritis patients.
Suppression of AXL by shRNA and inhibitor prolonged survival of chronic myelogenous leukemia (CML) mice and reduced the growth of leukemia stem cells ( LSCs) in mice. Gas6/AXL ligation stabilizes beta-catenin in an AKT-dependent fashion in human CML CD34(+) cells. Our findings improve the understanding of LSC regulation and validate Gas6/AXL as a pair of therapeutic targets to eliminate CML LSCs
AXL+ and GAS6+ expression is relevant to a poor prognosis in resected lung adenocarcinoma (AD)patients at stage I. AXL/GAS6 might serve as crucial predictive and prognostic biomarkers and targets to identify individuals at high risk of post-operative death.
The results imply that the GAS6 gene can be considered a potential candidate for meat quality trait selection and fat deposition in pigs.
This gene product is a gamma-carboxyglutamic acid (Gla)-containing protein thought to be involved in the stimulation of cell proliferation, and may play a role in thrombosis. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
growth arrest specific 6
, growth arrest-specific protein 6
, growth arrest-specific 6
, growth arrest-specific protein 6-like
, AXL receptor tyrosine kinase ligand
, GAS 6
, growth-potentiating factor
, AXL stimulatory factor