R&D Systems代理854-AX-100 Recombinant Mouse Axl Fc Chimera Protein, CF (100 UG)

2025-06-27

货号:854-AX-100

品牌:R&D Systems

规格:100ug

目录价:¥4760.00

市场价格:¥3808.00

会员价格:¥3808.00

  • 到货时间:3~4周

    金山科研平台,产品价格货期咨询微信:jinshanbio Source:Mouse myeloma cell line, NS0-derived Accession #:Q80YQ3 N-terminal Sequence Analysis:His20 Structure:Disulfide-linked homodimer Purity:>90%, by SDS-PAGE under reducing conditions and visualized by silver stain. Predicted Molecular Mass:73.8 kDa (monomer) SDS-PAGE:100-110 kDa, reducing conditions Activity:Measured by its binding ability in a functional ELISA.When Recombinant Mouse Axl FcChimera is coated at 2 µg/mL (100 µL/well), the concentration of Recombinant Mouse Gas6 (Catalog# 986‑GS) that produces 50%optimal binding response is typically 0.4‑2ng/mL. Formulation:Lyophilized from a 0.2 µm filtered solution in PBS.See Certificate of Analysis for details. Molecule Information: Axl Long Name: Axl Receptor Tyrosine Kinase Aliases: Ark; Ufo Entrez Gene IDs: 558 (Human); 26362 (Mouse) Background: Axl Axl, also known as Ark and Ufo, is an 894 amino acid (aa) member of the TAM subfamily of receptor tyrosine kinases that also includes Mer and Dtk. Human Axl has a predicted molecular weight of approximately 98 kDa and shares 88% aa sequence identity with the mouse and rat orthologs. Axl was originally identified in primary human myeloid leukemia cells, but it is also ubiquitously expressed in epithelial, mesenchymal, and hematopoietic cells. Structurally, Axl is composed of two immunoglobulin-like domains and two fibronectin type III domains in the extracellular region, and a cytoplasmic kinase domain. Gas6 and Protein S/PROS1 bind and activate Axl. Axl signaling can promote cellular proliferation, survival, and migration via activation of the MAPK, FAK, and PI 3-Kinase/Akt pathways. Interestingly, Axl can be cleaved near the cell membrane, producing a soluble form that is present in serum and plasma where it binds Gas6 and presumably blocks its ability to activate full-length Axl. The expression and activity of Axl has been associated with several disease states, including autoimmunity and cancer. Loss of Axl has been reported to promote the progression of experimental autoimmune encephalomyelitis in mice. With respect to cancer, Axl expression has been shown to promote glioma invasiveness and may provide one mechanism of drug resistance in non-small cell lung cancers.

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