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Price
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납기 |
재고 |
DataSheet |
주문/견적 |
| LCA-44-32660 |
34-5900 |
Anti-Axin Polyclonal Antibody, Unconjugated, Clone ZMD.195/100 ug/Human. The sequence used for this antibody shares 86% sequence homology with mouse, rat, and chicken Axin./Request Info |
1/EA |
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문의 |
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Subject
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Anti-Axin Polyclonal Antibody, Unconjugated, Clone ZMD.195 |
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Description
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100 ug / Human. The sequence used for this antibody shares 86% sequence homology with mouse, rat, and chicken Axin./Request Info |
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Clonality
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Poly |
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Company
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Invitrogen |
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Application
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WB |
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Conjugation
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Unconjugated |
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Immunogen
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Axin |
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Contents
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The Axin (axis inhibition) protein is an ~120-130 kDa negative regulator of Wnt pathway signaling. The Wnt pathway is essential for embryonic axis development in amphibians, Drosophila, and mammals; Axin has been shown to inhibit dorsal axial development. In vertebrates, Wnt signaling occurs when the frizzled receptor transduces a signal to the Dishevelled protein, triggering glycogen synthase kinase-3 (GSK-3) inactivation and the accumulation of b-catenin. Axin binds directly to GSK-3b, b-catenin, and the adenomatous polyposis coli (APC) tumor suppressor protein at separate binding sites; these four proteins form a tetrameric complex that regulates b-catenin stability and signaling.In addition to its role in Wnt signaling, Axin has been implicated in tumorigenesis, particularly via its interaction with APC. Inactivation of the APC protein is responsible for both inherited and sporadic forms of colon cancer, as the result of mutant APC’s inability to downregulate b-catenin. This lack of b-catenin downregulation by mutant APC may be partially explained by several observations about Axin: 1) overexpression of Axin produces downregulation of b-catenin in colon cancer cells, and 2) the binding sites for Axin on APC are typically deleted by cancer-associated mutations in the APC gene. The lack of Axin binding sites on mutant APC may thus contribute directly to the initiation and progression of colon cancer. However, mutations in the Axin gene itself are not associated with pediatric renal tumors. In transgenic mice, Axin expression impairs mammary gland and lymphoid organ development, inducing massive levels of apoptosis in the spleen and thymus. This finding has proposed Axin as a tumor suppressor protein that controls cell survival, growth, and differentiation through the regulation of apoptosis. Axin is ubiquitously expressed in almost all tissues, from early development to adulthood. Studies of mutant Axin protein have demonstrated that the phosphorylated form of Axin is more stable than the unphosphorylated form. Other signal transduction pathways in which Axin is involved are the JNK mitogen-associated protein kinase cascade, wherein Axin functions as a scaffold for JNK activation, and the TGF-b signaling pathway, in which Axin acts as an adapter protein for Smad3, enhancing the transcriptional activity of TGF-b. Axin has also demonstrated binding to g-catenin (plakoglobin and, through its C-terminal region, to the catalytic subunit of protein phosphatase 2A and to itself in the formation of dimers or multimers. |
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