INT112868
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Expression of proliferating cell nuclear antigen (PCNA) and cell cycle proteins cyclin D1 and p21 were not detectable in controls or after AAP alone. | |||||||||||||||
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Much more intense were the smoke-induced alterations of a variety of intermediate biomarkers, such as cytogenetic end points in pulmonary alveolar macrophages, bone marrow and peripheral blood erythrocytes; apoptosis, p53 oncoprotein, and proliferating cell nuclear antigen in the bronchial epithelium; bulky DNA adducts, 8-hydroxy-2-deoxyguanosine; multigene expression, and thiobarbituric acid-reactive aldehydes in whole lung and several other organs. | |||||||||||||||
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Expression of proliferating cell nuclear antigen (PCNA) and cell cycle proteins cyclin D1 and p21 were not detectable in controls or after AAP alone. | |||||||||||||||
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The induction of proliferation in a subset of bronchiolar cells and alveolar type II cells by Sox17 was associated with increased expression of several cyclin genes known to stimulate cell cycle progression. | |||||||||||||||
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Recent studies have shown that post-mitotic cells can reenter the cell cycle by blocking the expression of cyclin-dependent kinase inhibitors, supporting a role for this protein family in maintaining the balance between quiescence and proliferation [54]. | |||||||||||||||
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Together, these results demonstrate that Sox17 expression in adult mouse lung results in decreased levels of cyclin-dependent kinase inhibitors associated with G1 arrest and increased expression of cell cycle-promoting genes, providing insight into the molecular mechanisms that regulate Sox17-induced proliferation associated with the initiation of progenitor cell behavior in respiratory epithelial cells.
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B activation operates on cell growth through cyclin expression is indicated in certain cell types [16]. | |||||||||||||||
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We therefore examined if Fas activation and estrogen could interact to regulate the expression of cyclin A, PCNA and p21/waf-1 and compared the expression of these anti-apoptotic cell cycle proteins with other cell-cycle proteins. | |||||||||||||||
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We therefore hypothesized that in the context of Fas activation, estrogen would alter the expression of specific cell-cycle related proteins such as Cyclin-A [50], the Proliferating Cell Nuclear Antigen (PCNA, [51,52]) and p21/waf-1 [53], that also serve anti-apoptotic and DNA repair functions in addition to their roles in cell cycle. | |||||||||||||||
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In contrast, estrogen and sFasL, individually and together, induced cyclin-A expression, suggesting activation of compensatory survival mechanisms.
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nor sFasL alone or together altered the expression of cdk2 or cyclin E compared to control cultures (Figure 9). | |||||||||||||||
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Similarly, neither estrogen nor sFasL significantly altered the expression of Cyclin-dependent Kinase-1 (cdk1/cdc2) relative to control cultures, suggesting that that interactions between estrogen and Fas activation were not specifically related to cell cycle.
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Therefore, we examined the expression of cyclin-A following exposure to E2 and/or FasL. | |||||||||||||||
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Estrogen and sFasL separately and together induce expression of cyclin A.
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Both estrogen and sFasL alone led to a statistically significant increase in the expression of cyclin-A compared with controls at 12 hours post-treatment. | |||||||||||||||
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agonist increases the expression of the cyclin inhibitor p16, indicating that | |||||||||||||||
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Western blot analyses indicated that [6]-gingerol decreased both Cyclin A and Cyclin-dependent kinase (Cdk) expression. | |||||||||||||||
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Thus, the reduction of Cyclin or Cdk expressions results the blocking of Cyclin-Cdk complexes formation and that lowers the level of phospho-Rb. | |||||||||||||||
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Western blot analyses indicated that [6]-gingerol decreased the expression of Cyclin A and Cdks including Cdk2, Cdk4, and Cdk6 in BxPC-3. | |||||||||||||||
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Western blot analyses indicated that [6]-gingerol decreased both Cyclin A and Cyclin-dependent kinase (Cdk) expression. | |||||||||||||||
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