Background[1-3]
Phosphatidylinositol kinase (PI3KB) antibodies are a type of polyclonal antibody that can specifically bind to PI3KB. They are mainly used in immunological experiments to detect PI3KB in vitro.
Phosphatidylinositol kinase is the collective name for phosphatidylinositol 3-kinase, phosphatidylinositol 4-kinase and phosphatidylinositol 4-phosphate 5-kinase. Enzymes that specifically catalyze the phosphorylation of the 3, 4 or 5 hydroxyl groups on the 1-phosphatidyl-1D-inositol ring, respectively.
Phosphatidylinositol is mainly composed of two parts, one is 1,2-diglycerol phosphate, and the other is inositol. In cells, it plays a very important role in cell morphology, metabolic regulation, signal transduction and various physiological functions of cells.
The phosphatidylinositol 3-kinase (PI3K) pathway is one of the main pathways that regulates cell growth, proliferation, metabolism, survival and angiogenesis.
Many cancer studies have shown that in cancer patients, proteins involved in PI3K/Akt signal transduction have higher expression changes, mutations and translocations than other proteins. This pathway is one of the most overactive in cancer patients, making it an obvious target for treating the disease.
Akt, also known as PKB, is a serine/threonine protein kinase consisting of a PH domain, a kinase catalytic domain and a regulatory domain.
Akt has three isoforms: Akt1, Akt2 and Akt3, which are expressed at different levels in various tissues. In addition to being a major component of the PI3K silicone signaling pathway, AKT also plays an important role in a variety of signaling networks (such as cytokines, NK-κB, GPCRs, and integrins).
Activated PI3K produces the second messenger phosphoinositide 3,4,5-trisphosphate (PIP3), which binds to Akt and phosphoinositide-dependent kinase (PDK1), changing the protein structure of Akt and displacing it to the cell membrane, leading to Akt activation.
Phosphorylation of Thr308 and Ser473 on Akt can fully activate it and downregulate PTEN, PPA2 and mTOR. PI3K/PTEN/Akt and mTOR have become targets for the treatment of cancer, diabetes, neurological disorders, etc.
Apply[4][5]
For research on the expression and significance of phosphatidylinositol 3-kinase and protein kinase B in pediatric hemangiomas
To explore the role of phosphatidylinositol 3-kinase (P13K) and protein kinase B (Akt) in the occurrence, development and regression of pediatric hemangiomas.
Methods: Collect specimens pathologically diagnosed as hemangioma, classify and stage the hemangioma based on the classification method and the expression of proliferating cell nuclear antigen (PCNA), extract 20 cases of hemangioma in the proliferative stage and the regression stage, and use immunohistochemistry The expression levels of phosphatidylinositol 3-kinase and protein kinase B in hemangioma tissues were detected, and image analysis was performed.
Quantitative PCR was used to detect the mRNA expression of phosphatidylinositol 3-kinase and protein kinase B in hemangioma tissues.
Results: 1. All 20 cases of hemangiomas in the proliferative stage expressed PI3Kp85 and p-Akt. The expression rates of PI3Kp85 and p-Akt in the 20 cases of hemangiomas in the involution stage were 14 cases (70%) and 12 cases (60%) respectively. The differences were all statistically significant (P<0.05); the expression intensity of PI3Kp85 (?) in hemangiomas in the proliferative phase was 1 case (+), 7 cases (++), and 12 cases (+++), and the expression intensity of PI3Kp85 in hemangioma in the involution phase was The expression intensity of (?) spoon was 6 cases (-), 8 cases (+), 5 cases (++), and 1 case (+++), with significant statistical differences (P<0.01); proliferative phase hemangioma p The expression intensity of -Akt was 2 cases (+), 11 cases (++), and 7 cases (+++). The expression intensity of p-Akt in involutional hemangioma was 8 cases (-), 9 cases (+), 3 cases (++), the statistical difference is large (P<0.01).
2. The integrated optical densities of PI3Kp85 and p-Akt in 20 cases of hemangiomas in the proliferative stage were 191.23±40.45 and 178.73±38.49 respectively. The integrated optical densities of PI3Kp85 and P-Akt in hemangiomas in the degenerative stage were 46.63±13.08 and 64.93±21.22 respectively. , the statistical differences are all large (P<0.01). There was a positive correlation between the expression of PI3Kp initiator 85 and p-Akt (r=0.553, P<0.05).
3. The relative expression values of PI3Kp85mRNA and p-AktmRNA in 20 cases of hemangiomas in the proliferative stage were 0.0807±0.0136 and 0.0841±0.0137 respectively. The integrated optical densities of PI3Kp85 and P-Akt in hemangiomas in the involutional stage were 0.0203±0.0098 and 0.0324±0.0178 respectively. , the statistical differences are all large (P<0.01). There was a positive correlation between the expressions of PI3Kp85mRNA and P-AktmRNA (r=0.5503P<0.01).
