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| DC Field | Value | Language |
|---|---|---|
| dc.contributor.author | Jung, J. M. | en |
| dc.contributor.author | Li, H. | en |
| dc.contributor.author | Kobayashi, T. | en |
| dc.contributor.author | Kyritsis, A. P. | en |
| dc.contributor.author | Langford, L. A. | en |
| dc.contributor.author | Bruner, J. M. | en |
| dc.contributor.author | Levin, V. A. | en |
| dc.contributor.author | Zhang, W. | en |
| dc.date.accessioned | 2015-11-24T19:09:50Z | - |
| dc.date.available | 2015-11-24T19:09:50Z | - |
| dc.identifier.issn | 1044-9523 | - |
| dc.identifier.uri | https://olympias.lib.uoi.gr/jspui/handle/123456789/20755 | - |
| dc.rights | Default Licence | - |
| dc.subject | Brain Neoplasms/*drug therapy/pathology | en |
| dc.subject | Cell Cycle/drug effects/genetics | en |
| dc.subject | Cell Division/drug effects/genetics | en |
| dc.subject | Cyclin-Dependent Kinase Inhibitor p21 | en |
| dc.subject | Cyclin-Dependent Kinases/*antagonists & inhibitors | en |
| dc.subject | Cyclins/*pharmacology | en |
| dc.subject | Enzyme Inhibitors/*pharmacology | en |
| dc.subject | *Genes, p53 | en |
| dc.subject | Glioblastoma/*drug therapy/pathology | en |
| dc.subject | Humans | en |
| dc.subject | Mutation | en |
| dc.subject | Transfection | en |
| dc.subject | Tumor Cells, Cultured | en |
| dc.title | Inhibition of human glioblastoma cell growth by WAF1/Cip1 can be attenuated by mutant p53 | en |
| heal.type | journalArticle | - |
| heal.type.en | Journal article | en |
| heal.type.el | Άρθρο Περιοδικού | el |
| heal.identifier.secondary | http://www.ncbi.nlm.nih.gov/pubmed/8547219 | - |
| heal.language | en | - |
| heal.access | campus | - |
| heal.recordProvider | Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής | el |
| heal.publicationDate | 1995 | - |
| heal.abstract | The WAF1/Cip1 protein is an important regulator at the G1 checkpoint in the cell cycle. The WAF1/Cip1 protein binds to the cyclin-dependent kinase complexes and inhibits the kinase activity that is required for cell cycle progression. We investigated the expression of WAF1/Cip1 protein in 14 glioblastoma cell lines and found that WAF1/Cip1 expression was detectable in many of the cell lines, even when mutant p53 was present. We also showed that WAF1/Cip1 protein level was very low in LN-Z308 cells that do not express endogenous p53. Transfection of the wild-type p53 into this cell line activated WAF1/Cip1 expression and inhibited cell growth. In contrast, transfection of the p53 mutant 248Trp failed to activate WAF1/Cip1 expression. Transfection of WAF1/Cip1 alone also inhibited LN-Z308 cell proliferation. However, cotransfection of the p53 mutant 248Trp with WAF1/Cip1 attenuated the growth-suppression effect of WAF1/Cip1. Our analysis with Western blot showed that the levels of cyclin E increased in cells transfected with p53 mutants. We conclude that p53 mutants may counter the negative regulators, such as WAF1/Cip1, by the elevation of positive cell cycle regulators, and the presence of WAF1/Cip1 in tumor cells is not sufficient for growth inhibition. | en |
| heal.journalName | Cell Growth Differ | en |
| heal.journalType | peer-reviewed | - |
| heal.fullTextAvailability | TRUE | - |
| Appears in Collections: | Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ | |
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