Please use this identifier to cite or link to this item:
https://hdl.handle.net/2440/52397
Citations | ||
Scopus | Web of Science® | Altmetric |
---|---|---|
?
|
?
|
Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Neilsen, P. | - |
dc.contributor.author | Cheney, K. | - |
dc.contributor.author | Li, C. | - |
dc.contributor.author | Chen, D. | - |
dc.contributor.author | Noll, J. | - |
dc.contributor.author | Schulz, R. | - |
dc.contributor.author | Powell, J. | - |
dc.contributor.author | Kumar, R. | - |
dc.contributor.author | Callen, D. | - |
dc.date.issued | 2008 | - |
dc.identifier.citation | Journal of Cell Science, 2008; 121(21):3541-3552 | - |
dc.identifier.issn | 0021-9533 | - |
dc.identifier.issn | 1477-9137 | - |
dc.identifier.uri | http://hdl.handle.net/2440/52397 | - |
dc.description.abstract | The ability of p53 to act as a transcription factor is critical for its function as a tumor suppressor. Ankyrin repeat domain 11, ANKRD11 (also known as ANR11 or ANCO1), was found to be a novel p53-interacting protein that enhanced the transcriptional activity of p53. ANKRD11 expression was shown to be downregulated in breast cancer cell lines. Restoration of ANKRD11 expression in MCF-7 (wild-type p53) and MDA-MB-468 (p53(R273H) mutant) cells suppressed their proliferative and clonogenic properties through enhancement of CDKN1A (p21(waf1)/CIP1) expression. ShRNA-mediated silencing of ANKRD11 expression reduced the ability of p53 to activate CDKN1A expression. ANKRD11 was shown to associate with the p53 acetyltransferases and cofactors, P/CAF and hADA3. Exogenous ANKRD11 expression enhanced the levels of acetylated p53 in both MCF-7 and MDA-MB-468 cells. ANKRD11 enhanced the DNA-binding properties of mutant p53(R273H) to the CDKN1A promoter, suggesting that ANKRD11 can mediate the restoration of normal p53 function in some cancer-related p53 mutations. In addition, ANKRD11 itself was found to be a novel p53 target gene. These findings demonstrate a role for ANKRD11 as a p53 coactivator and suggest the involvement of ANKRD11 in a regulatory feedback loop with p53. | - |
dc.description.statementofresponsibility | Paul M. Neilsen, Kelly M. Cheney, Chia-Wei Li, J. Don Chen, Jacqueline E. Cawrse, Renée B. Schulz, Jason A. Powell, Raman Kumar and David F. Callen | - |
dc.language.iso | en | - |
dc.publisher | Company of Biologists Ltd | - |
dc.source.uri | http://dx.doi.org/10.1242/jcs.026351 | - |
dc.subject | Acetylation | - |
dc.subject | Ankyrin repeat domain protein | - |
dc.subject | Breast cancer | - |
dc.subject | p53 | - |
dc.subject | p53 mutant rescue | - |
dc.title | Identification of ANKRD11 as a p53 coactivator | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1242/jcs.026351 | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | Noll, J. [0000-0001-7375-635X] | - |
dc.identifier.orcid | Callen, D. [0000-0002-6189-9991] | - |
Appears in Collections: | Aurora harvest Medicine publications |
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.