Loss of p14(ARF) confers resistance to heat shock- and oxidative stress-mediated cell death by upregulating beta-catenin
dc.contributor.author | Damalas, A. | en |
dc.contributor.author | Velimezi, G. | en |
dc.contributor.author | Kalaitzakis, A. | en |
dc.contributor.author | Liontos, M. | en |
dc.contributor.author | Papavassiliou, A. G. | en |
dc.contributor.author | Gorgoulis, V. | en |
dc.contributor.author | Angelidis, C. | en |
dc.date.accessioned | 2015-11-24T19:06:10Z | |
dc.date.available | 2015-11-24T19:06:10Z | |
dc.identifier.issn | 1097-0215 | - |
dc.identifier.uri | https://olympias.lib.uoi.gr/jspui/handle/123456789/20308 | |
dc.rights | Default Licence | - |
dc.subject | *Apoptosis | en |
dc.subject | Blotting, Western | en |
dc.subject | Cell Proliferation | en |
dc.subject | Flow Cytometry | en |
dc.subject | Gene Expression Regulation, Neoplastic | en |
dc.subject | HSP72 Heat-Shock Proteins/genetics/*metabolism | en |
dc.subject | *Heat-Shock Response | en |
dc.subject | Humans | en |
dc.subject | Immunoprecipitation | en |
dc.subject | Luciferases/metabolism | en |
dc.subject | Neoplasms/genetics/metabolism/pathology | en |
dc.subject | *Oxidative Stress | en |
dc.subject | RNA, Messenger/genetics | en |
dc.subject | RNA, Small Interfering/genetics | en |
dc.subject | Reverse Transcriptase Polymerase Chain Reaction | en |
dc.subject | Tumor Cells, Cultured | en |
dc.subject | Tumor Suppressor Protein p14ARF/antagonists & inhibitors/genetics/*metabolism | en |
dc.subject | Up-Regulation | en |
dc.subject | beta Catenin/genetics/*metabolism | en |
dc.title | Loss of p14(ARF) confers resistance to heat shock- and oxidative stress-mediated cell death by upregulating beta-catenin | en |
heal.abstract | The p14(ARF) is a key tumor suppressor induced mainly by oncogenic stimuli. Although p14(ARF) does not seem to respond to DNA damage, there are very few data regarding its role in other forms of stress, such as heat shock (HS) and oxidative stress (OS). Here, we report that suppression of p14(ARF) increased resistance to cell death when cells were treated with H(2) O(2) or subjected to HS. In this setting, protection from cell death was mediated by elevated levels and activity of beta-catenin, as downregulation of beta-catenin alleviated the protective role of p14(ARF) silencing. Moreover, Hsp70 was shown to regulate beta-catenin protein levels by interacting with p14(ARF) , suggesting that Hsp70, p14(ARF) and beta-catenin form a regulatory network. This novel pathway triggers cell death signals when cells are exposed to HS and OS. | en |
heal.access | campus | - |
heal.fullTextAvailability | TRUE | - |
heal.identifier.primary | 10.1002/ijc.25510 | - |
heal.identifier.secondary | http://www.ncbi.nlm.nih.gov/pubmed/20549705 | - |
heal.identifier.secondary | http://onlinelibrary.wiley.com/store/10.1002/ijc.25510/asset/25510_ftp.pdf?v=1&t=h0dnm3ch&s=b5f169b405f087425a8f2063963cd2f6259f404d | - |
heal.journalName | Int J Cancer | en |
heal.journalType | peer-reviewed | - |
heal.language | en | - |
heal.publicationDate | 2011 | - |
heal.recordProvider | Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής | el |
heal.type | journalArticle | - |
heal.type.el | Άρθρο Περιοδικού | el |
heal.type.en | Journal article | en |
Αρχεία
Φάκελος/Πακέτο αδειών
1 - 1 of 1
Φόρτωση...
- Ονομα:
- license.txt
- Μέγεθος:
- 1.74 KB
- Μορφότυπο:
- Item-specific license agreed upon to submission
- Περιγραφή: