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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.
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.
These results demonstrate that Gas6 enhances several features of fungal allergic airway disease.
The expression of TAM receptor tyrosine kinases and their ligand Gas6 is markedly downregulated in psoriatic epidermis. These data are in concordance with earlier study, demonstrating that TAM-deficient mice develop systemic autoimmunity.
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.
Taken together, our data indicate that elevated plasma Gas6 levels is associated with the severity of disease during HTNV infection in humans, suggesting that Gas6 may play an important role by binding with Tyro3 on monocytes.
Study detected an inverse correlation between CSF Gas6 levels at Alzheimer's disease (AD) diagnosis and both disease duration and decrease in the MMSE score two years later. Conversely,no correlation was found between CSF Gas6 and both AD biomarkers and years of formal schooling. Results suggest that upregulation of CSF Gas6 may be part of a defensive response aimed at counteracting AD progression.
Upon chemotherapy macrophages increase Gas6 synthesis, which significantly attenuates the cytotoxic effect of 5-FU chemotherapy on colorectal cancer cells.
These results show that TYRO3, AXL and GAS6 are expressed at higher levels in LMS and expression of its ligands correlates to a worse PFS in LMS patients.
these data suggest that endogenous GAS6 and Mer receptor signaling contribute to the establishment of prostate cancer stem cells in the bone marrow microenvironment
The GAS6-AXL signaling network is a mesenchymal (Mes) molecular subtype-specific therapeutic target for ovarian cancer
The expression of AXL was positively associated with GAS6 expression (P < 0.001), and tumor differentiation (P = 0.014) in advanced NSCLC with metastases. AXL expression displayed no association with gender, age, smoking history, pathology, T stage, N stage, CEA, and LDH.
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