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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Growth arrest-specific 6

Gas6
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. [provided by RefSeq, Jan 2009] (from NCBI)
Top mentioned proteins: Apaf-1, TIF, CAN, HAD, Akt
Papers on Gas6
Negative feedback regulation of AXL by miR-34a modulates apoptosis in lung cancer cells.
New
Chuang et al., Taiwan. In Rna, Feb 2016
Both the GAS6-binding domain and the kinase domain of AXL, particularly the Y779 tyrosine phosphorylation site, are shown to be crucial for this autoregulation.
Growth Arrest-Specific 6 Exacerbates Pressure Overload-Induced Cardiac Hypertrophy.
New
Xu et al., Shanghai, China. In Hypertension, Jan 2016
Growth arrest-specific 6 (GAS6) is a member of the vitamin K-dependent protein family that is involved in the regulation of the cardiovascular system, including vascular remodeling, homeostasis, and atherosclerosis.
ALK inhibitor resistance in ALK(F1174L)-driven neuroblastoma is associated with AXL activation and induction of EMT.
New
George et al., Boston, United States. In Oncogene, Dec 2015
AXL activation in resistant cells was mediated through increased expression of the active form of its ligand, GAS6, that also served to stabilize the AXL protein.
MERTK rs4374383 polymorphism affects the severity of fibrosis in non-alcoholic fatty liver disease.
New
Craxì et al., Palermo, Italy. In J Hepatol, Nov 2015
MERTK expression was analysed in mouse models of fibrosis, and the effect of the MERTK ligand GAS6 were investigated in human HSC.
AXL is a potential therapeutic target in dedifferentiated and pleomorphic liposarcomas.
Torres et al., Houston, United States. In Bmc Cancer, 2014
A panel of DDLPS and PLS cell lines were interrogated via western blot for AXL expression and activity and by ELISA for growth arrest-specific 6 (GAS6) production.
Whole-genome cartography of p53 response elements ranked on transactivation potential.
Inga et al., Trento, Italy. In Bmc Genomics, 2014
Based on the mapping of predicted functional REs near TSS, we examined expression changes of thirteen genes as a function of different p53-inducing conditions, providing further evidence for PDE2A, GAS6, E2F7, APOBEC3H, KCTD1, TRIM32, DICER, HRAS, KITLG and TGFA p53-dependent regulation, while MAP2K3, DNAJA1 and potentially YAP1 were identified as new direct p53 target genes.
TAM receptor signaling in immune homeostasis.
Review
Impact
Ghosh et al., In Annu Rev Immunol, 2014
The TAM receptor tyrosine kinases (RTKs)-TYRO3, AXL, and MERTK-together with their cognate agonists GAS6 and PROS1 play an essential role in the resolution of inflammation.
The TAM family: phosphatidylserine sensing receptor tyrosine kinases gone awry in cancer.
Review
Impact
Earp et al., In Nat Rev Cancer, 2014
For example, the protein ligand, growth arrest-specific protein 6 (GAS6), binds to phosphatidylserine (PtdSer) that is externalized on apoptotic cell membranes, which activates MERTK on macrophages.
The Involvement of GAS6 Signaling in the Development of Obesity and Associated Inflammation.
Review
Hsieh et al., Taipei, Taiwan. In Int J Endocrinol, 2014
Growth arrest-specific 6 (GAS6), a vitamin K-dependent protein, plays a role in the survival, proliferation, migration, differentiation, adhesion, and apoptosis of cells.
Characterization of porcine GAS6 cDNA gene and its expression analysis in weaned piglets.
Ma et al., Changsha, China. In Genet Mol Res, 2014
The growth arrest-specific 6 gene (GAS6) is a member of the family of plasma vitamin K-dependent proteins, which are able to bind to phospholipids using an N-terminal gamma-carboxyglutamic acid domain.
AXL kinase as a novel target for cancer therapy.
Review
Halmos et al., Guangzhou, China. In Oncotarget, 2014
The AXL receptor tyrosine kinase and its major ligand, GAS6 have been demonstrated to be overexpressed and activated in many human cancers (such as lung, breast, and pancreatic cancer) and have been correlated with poor prognosis, promotion of increased invasiveness/metastasis, the EMT phenotype and drug resistance.
DNA methylation signatures for prediction of biochemical recurrence after radical prostatectomy of clinically localized prostate cancer.
Impact
Sørensen et al., Århus, Denmark. In J Clin Oncol, 2013
RESULTS: Hypermethylation of AOX1, C1orf114, GAS6, HAPLN3, KLF8, and MOB3B was highly cancer specific (area under the curve, 0.89 to 0.98).
Non-invasive analysis of acquired resistance to cancer therapy by sequencing of plasma DNA.
Impact
Rosenfeld et al., Cambridge, United Kingdom. In Nature, 2013
These included an activating mutation in PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha) following treatment with paclitaxel; a truncating mutation in RB1 (retinoblastoma 1) following treatment with cisplatin; a truncating mutation in MED1 (mediator complex subunit 1) following treatment with tamoxifen and trastuzumab, and following subsequent treatment with lapatinib, a splicing mutation in GAS6 (growth arrest-specific 6) in the same patient; and a resistance-conferring mutation in EGFR (epidermal growth factor receptor; T790M) following treatment with gefitinib.
Activation of the AXL kinase causes resistance to EGFR-targeted therapy in lung cancer.
Impact
Bivona et al., Cleveland, United States. In Nat Genet, 2012
Increased expression of AXL and, in some cases, of its ligand GAS6 was found in EGFR-mutant lung cancers obtained from individuals with acquired resistance to TKIs.
Hypoxia stabilizes GAS6/Axl signaling in metastatic prostate cancer.
GeneRIF
Taichman et al., Ann Arbor, United States. In Mol Cancer Res, 2012
Data show that growth arrest-specific 6 (GAS6) and receptor tyrosine kinase Axl is colocalize with hypoxia-inducible factor-1alpha (Hif-1alpha) in both primary tumors and bone metastasis in prostate tumor tissue microarrays samples.
Growth arrest-specific gene 6 (gas6) and vascular hemostasis.
Review
Blostein et al., Montréal, Canada. In Adv Nutr, 2012
Gas6 (growth arrest-specific 6) belongs structurally to the family of plasma vitamin K-dependent proteins.
The growth arrest-specific 6 (Gas6) gene polymorphism c.834+7G>A is associated with type 2 diabetes.
GeneRIF
Hung et al., Taipei, Taiwan. In Diabetes Res Clin Pract, 2012
The Gas6 c.843+7AA genotype and A allele are less prevalent in type 2 diabetes, which may have a protective role for type 2 diabetes.
Toll-like receptor-mediated inhibition of Gas6 and ProS expression facilitates inflammatory cytokine production in mouse macrophages.
GeneRIF
Han et al., Beijing, China. In Immunology, 2012
A self-regulatory mechanism of Toll-like receptor signalling through the suppression of Gas6 and ProS expression is described.
Increased secretion of Gas6 by smooth muscle cells in human atherosclerotic carotid plaques.
GeneRIF
Borgel et al., Châtenay-Malabry, France. In Thromb Haemost, 2012
Gas6 acts as a protective factor, in part by reducing the pro-inflammatory phenotype of vascular smooth muscle cells
Prolonged exposure to a Mer ligand in leukemia: Gas6 favors expression of a partial Mer glycoform and reveals a novel role for Mer in the nucleus.
GeneRIF
Graham et al., Aurora, United States. In Plos One, 2011
The present study explores Mer behavior following prolonged exposure to Gas6.
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