http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-7358335-B2
Outgoing Links
Predicate | Object |
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assignee | http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_1721d75f5bf603447ec5a26b5c1c0be0 |
classificationCPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N33-57496 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N33-574 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61P35-00 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61P35-02 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12P21-06 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12N9-64 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12N9-93 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C07K14-4747 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C07K14-47 |
classificationIPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C07K5-10 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/G01N33-53 |
filingDate | 2005-04-29-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
grantDate | 2008-04-15-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
inventor | http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_da381088754dd3e9ad0f74a429cf34cb |
publicationDate | 2008-04-15-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
publicationNumber | US-7358335-B2 |
titleOfInvention | ARF-BP1 as mediator of p53-dependent and independent tumor suppression and uses thereof |
abstract | The present invention relates to the mechanism of ARF-mediated cell growth suppression. ARF-BP1 is identified as a novel ubiquitin ligase, and a major component of ARF-containing nuclear complexes in human cells. The present invention discloses a novel mechanism of ARF-mediated p53 activation and that ARF-BP1 is a critical mediator of both p53-independent and p53-dependent tumor suppression functions of ARF. Inactivation of ARF-BP1 in normal cells stabilizes p53 and induces p53-dependent apoptosis. Inactivation of ARF-BP1, but not Mdm2, in p53-wildtype cells promotes cell growth inhibition in a manner reminiscent of ARF induction. ARF-BP1 directly binds and ubiquitinates p53 and inactivation of endogenous ARF-BP1 is crucial for ARF-mediated p53 stabilization in Mdm2-null cells. ARF-BP1 is advantageous over Mdm2 as a target for suppressing tumor cell growth regardless of p53 status. |
isCitedBy | http://rdf.ncbi.nlm.nih.gov/pubchem/patent/WO-2007100576-A3 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-2008187917-A1 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/DE-102008047128-A1 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/WO-2007100576-A2 |
priorityDate | 2004-09-15-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
type | http://data.epo.org/linked-data/def/patent/Publication |
Incoming Links
Total number of triples: 204.