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Sino Biological Inc. liefert PIK3IP1 Protein mit höherer Qualität und günstiger Kosten im Vergleich mit anderen globalen Lieferanten.
Weitere Informationen über PIK3IP1 Protein lesen Sie bitte: http://www.sinobiological.com/PIK3IP1-Protein-g-9981.html
| Synonym | PIK3IP1, HGFL |
| Protein Construction | A DNA sequence encoding the human PIK3IP1 (AAH11049.1)(Met1-Thr168) was expressed, fused with the Fc region of human IgG1 at the C-terminus. |
| Source | Human |
| Expression Host | Human Cells |
| Purity | > 85 % as determined by SDS-PAGE | SDS-PAGE:![]() PIK3IP1 protein |
| Endotoxin | < 1.0 EU per μg of the protein as determined by the LAL method | |
| Stability | Samples are stable for up to twelve months from date of receipt at -70℃ | |
| Predicted N terminal | Ser 22 | |
| Molecular Mass | The recombinant human PIK3IP1/Fc is a disulfide-linked homodimer. The reduced monomer comprises 388 amino acids and has a predicted molecular mass of 42.7 kDa. The apparent molecular mass of the protein is approximately 55 kDa in SDS-PAGE under reducing conditions. | |
| Formulation | Lyophilized from sterile PBS, pH7.4.
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| Storage | Store it under sterile conditions at -70℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles. |
| Reconstitution | A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information. |
PIK3IP1 contains 1 kringle domain and is a negative regulator of phosphatidylinositol-3-kinase (PI3K), suppresses the development of hepatocellular carcinoma. In most cell types, PI3K functions as a regulator of cell division, motility, metabolism and survival in. Proper liver function and development highly depend on intact PI3K signal transduction. Aberrant PI3K pathway signaling in the liver can cause hepatocellular carcinoma. PI3K signaling is involved in the homeostasis of lipid and glucose metabolism. Activation of the PI3K pathway induces lipogenesis and glycogenesis in the liver, since both Akt overexpressing transgenic mice and PTEN knockout mice develop fatty liver and hypoglycemia. PIK3IP1 overexpression can contribute to glucose homeostasis and fatty deposition.