Recombinant Human GAS6 (C-6His) Cat# C3282– 50 Ug Storage -20°C for 2 Years

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Recombinant Human GAS6 (C-6His) Cat# C3282– 50 Ug Storage -20°C for 2 Years

Datasheet Technical support: [email protected] Phone: 886-3-2870051 Ver.1 Date : 20180222 Recombinant Human GAS6 (C-6His) Cat# C3282– 50 ug Storage -20°C for 2 years INTFORMATION Product Name Recombinant Human GAS6 (C-6His) Cat NO. C3282 Size 50 ug Uniprot Q14393 Recombinant Human Growth Arrest-specific Protein 6 is produced by our Description Mammalian expression system and the target gene encoding Ala31-Ala678 is expressed with a 6His tag at the C-terminus. Purity Greater than 95% as determined by reducing SDS-PAGE. Endotoxin Less than 0.1 ng/ug (1 EU/ug) as determined by LAL test. Formulation Supplied as a 0.2 μm filtered solution of PBS, 10% Glycerol, pH 7.4. Molecular Weight 72.7 kDa Application Molecular Weight 80-90 kDa, reducing conditions Store at < -20°C, stable for 6 months after receipt. Please minimize freeze-thaw Storage cycles. AXLLG; AXLLGAXL stimulatory factor; AXSFAXL receptor tyrosine kinase ligand; Alias Gas6; GAS-6; growth arrest-specific 6; growth arrest-specific protein 6 GAS6 (Growth arrest-specific protein 6) is also known as AXL receptor tyrosine kinase ligand, AXLLG, is a multimodular protein that is up-regulated by a wide variety of cell types in response to growth arrest. Gas6 binds and induces signaling through the receptor tyrosine kinases Axl, Dtk, and Mer whose signaling is implicated in cell growth and survival, cell adhesion and cell Background migration. GAS6/AXL signaling plays a role in various processes such as endothelial cell survival during acidification by preventing apoptosis, optimal cytokine signaling during human natural killer cell development, hepatic regeneration, gonadotropin-releasing hormone neuron survival and migration, platelet activation, or regulation of thrombotic responses. ACE BIOLABS CO., LTD. www.acebiolab.com 6F., No 68, Qingsheng 2nd St., Dayuan Dist., Taoyuan City33743, Taiwan. Image PRODUCT USE LIMITATION These products are intended for research use only. ACE BIOLABS CO., LTD. www.acebiolab.com 6F., No 68, Qingsheng 2nd St., Dayuan Dist., Taoyuan City33743, Taiwan. .

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Vitamin K Dependent Actions of Gas6
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Digital.CSIC Vitamin K dependent actions of Gas6. Lola Bellido-Martín, Pablo García de Frutos Department of Cell Death and Proliferation, Institute for Biomedical Research of Barcelona, IIBB-CSIC-IDIBAPS, Barcelona, Spain. Correspondence to: Pablo García de Frutos, Institute for Biomedical Research of Barcelona (IIBB-CSIC-IDIBAPS), Roselló 161 p6, 08036 Barcelona, Spain Tel: +34 933632382 Fax: +34 933638301 Email: [email protected] Abstract GAS6 (growth arrest-specific gene 6) is the last addition to the family of plasma vitamin K- dependent proteins. Gas6 was cloned and characterized in 1993 and found to be similar to the plasma anticoagulant protein S. Soon after it was recognized as a growth factor-like molecule, as it interacted with receptor tyrosine kinases of the TAM family; Tyro3, Axl and MerTK. Since then, the role of Gas6, protein S and the TAM receptors has been found to be important in inflammation, hemostasis and cancer, making this system an interesting target in biomedicine. Gas6 employs a unique mechanism of action, interacting through its vitamin K- dependent Gla module with phosphatidylserine-containing membranes and through its carboxy-terminal LG domains with the TAM membrane receptors. The fact that these proteins are affected by anti-vitamin K therapy is discussed in detail. Article Outline I. Introduction. II. Gas6 structure. III. Cellular effects of Gas6. IV. Interaction with TAM receptor molecules and signal transduction in the Gas6/TAM ligand/receptor system. V. Role of the Gas6/TAM system in vascular biology.
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Role of Vitamin K-Dependent Factors Protein S and GAS6 and TAM Receptors in SARS-Cov-2 Infection and COVID-19-Associated Immunothrombosis
cells Review Role of Vitamin K-Dependent Factors Protein S and GAS6 and TAM Receptors in SARS-CoV-2 Infection and COVID-19-Associated Immunothrombosis Anna Tutusaus 1 , Montserrat Marí 1 , José T. Ortiz-Pérez 2,3 , Gerry A. F. Nicolaes 4, Albert Morales 1,5,* and Pablo García de Frutos 1,3,* 1 Department of Cell Death and Proliferation, IIBB-CSIC, IDIBAPS, 08036 Barcelona, Spain; [email protected] (A.T.); [email protected] (M.M.) 2 Clinic Cardiovascular Institute, Hospital Clinic Barcelona, 08036 Barcelona, Spain; [email protected] 3 Centro de Investigación Biomédica en Red sobre Enfermedades Cardiovasculares (CIBERCV), 28029 Madrid, Spain 4 Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, 6200 MD Maastricht, The Netherlands; [email protected] 5 Barcelona Clinic Liver Cancer (BCLC) Group, Liver Unit, Hospital Clínic, CIBEREHD, 08036 Barcelona, Spain * Correspondence: [email protected] (A.M.); [email protected] (P.G.d.F.); Tel.: +34-93-3638300 (A.M. & P.G.d.F.) Received: 2 September 2020; Accepted: 26 September 2020; Published: 28 September 2020 Abstract: The vitamin K-dependent factors protein S (PROS1) and growth-arrest-speciﬁc gene 6 (GAS6) and their tyrosine kinase receptors TYRO3, AXL, and MERTK, the TAM subfamily of receptor tyrosine kinases (RTK), are key regulators of inﬂammation and vascular response to damage. TAM signaling, which has largely studied in the immune system and in cancer, has been involved in coagulation-related pathologies. Because of these established biological functions, the GAS6-PROS1/TAM system is postulated to play an important role in SARS-CoV-2 infection and progression complications.
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Crystal Structure of the Kinase Domain of Mertk in Complex with AZD7762 Provides Clues for Structure-Based Drug Development
International Journal of Molecular Sciences Article Crystal Structure of the Kinase Domain of MerTK in Complex with AZD7762 Provides Clues for Structure-Based Drug Development Tae Hyun Park 1,2 , Seung-Hyun Bae 1,3 , Seoung Min Bong 1, Seong Eon Ryu 2, Hyonchol Jang 1,3 and Byung Il Lee 1,3,* 1 Research Institute, National Cancer Center, Goyang, 10408 Gyeonggi, Korea; [email protected] (T.H.P.); [email protected] (S.-H.B.); [email protected] (S.M.B.); [email protected] (H.J.) 2 Department of Bioengineering, Hanyang University, 04763 Seoul, Korea; [email protected] 3 Department of Cancer Biomedical Science, National Cancer Center Graduate School of Cancer Science and Policy, Goyang, 10408 Gyeonggi, Korea * Correspondence: [email protected]; Tel.: +82-31-920-2223; Fax: +82-31-920-2006 Received: 29 August 2020; Accepted: 21 October 2020; Published: 23 October 2020 Abstract: Aberrant tyrosine-protein kinase Mer (MerTK) expression triggers prosurvival signaling and contributes to cell survival, invasive motility, and chemoresistance in many kinds of cancers. In addition, recent reports suggested that MerTK could be a primary target for abnormal platelet aggregation. Consequently, MerTK inhibitors may promote cancer cell death, sensitize cells to chemotherapy, and act as new antiplatelet agents. We screened an inhouse chemical library to discover novel small-molecule MerTK inhibitors, and identiﬁed AZD7762, which is known as a checkpoint-kinase (Chk) inhibitor. The inhibition of MerTK by AZD7762 was validated using an in vitro homogeneous time-resolved ﬂuorescence (HTRF) assay and through monitoring the decrease in phosphorylated MerTK in two lung cancer cell lines.
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Axl and Growth Arrest ^ Specific Gene 6 Are Frequently Overexpressed In
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Description: Uniprot:P30530 Alternative Names： Specificity
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www.nature.com/bjc ARTICLE Cellular and Molecular Biology TYRO3 as a molecular target for growth inhibition and apoptosis induction in bladder cancer Florent Dufour1,2, Linda Silina1,2, Hélène Neyret-Kahn1,2, Aura Moreno-Vega1,2, Clémentine Krucker1,2, Narjesse Karboul1,2, Marion Dorland-Galliot1,2, Pascale Maillé3, Elodie Chapeaublanc1,2, Yves Allory1,4, Nicolas Stransky1,2, Hélène Haegel5, Thierry Menguy5, Vanessa Duong5, François Radvanyi1,2 and Isabelle Bernard-Pierrot1,2 BACKGROUND: Muscle-invasive bladder cancer (MIBC) is an aggressive neoplasm with poor prognosis, lacking effective therapeutic targets. Oncogenic dependency on members of the TAM tyrosine kinase receptor family (TYRO3, AXL, MERTK) has been reported in several cancer types, but their role in bladder cancer has never been explored. METHODS: TAM receptor expression was evaluated in two series of human bladder tumours by gene expression (TCGA and CIT series), immunohistochemistry and western blotting analyses (CIT series). The role of the different TAM receptors was assessed by loss-of-function experiments and pharmaceutical inhibition in vitro and in vivo. RESULTS: We reported a signiﬁcantly higher expression of TYRO3, but not AXL or MERTK, in both non-MIBCs and MIBCs, compared to normal urothelium. Loss-of-function experiments identiﬁed a TYRO3-dependency of bladder carcinoma-derived cells both in vitro and in a mouse xenograft model, whereas AXL and MERTK depletion had only a minor impact on cell viability. Accordingly, TYRO3-dependent bladder tumour cells were sensitive to pharmacological treatment with two pan-TAM inhibitors. Finally, growth inhibition upon TYRO3 depletion relies on cell cycle inhibition and apoptosis associated with induction of tumour-suppressive signals.
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