Predicate |
Object |
assignee |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_6e089a1229311ed1e13567f1b6b91b75 |
classificationCPCInventive |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12N9-64 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N33-57496 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12N9-93 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N33-574 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61P35-02 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61P35-00 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C07K14-47 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C07K14-4747 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12P21-06 |
classificationIPCInventive |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C12N9-64 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C12Q1-68 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C07H21-04 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C12P21-06 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/G01N33-574 |
filingDate |
2005-04-29-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
inventor |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_c1d3c3aa504502037e92bc1dd0e3ede2 |
publicationDate |
2006-04-27-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
publicationNumber |
US-2006088847-A1 |
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/KR-101561965-B1 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-11740162-B2 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-2017241873-A1 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-11208685-B2 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-10371610-B2 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-11385144-B2 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-10345204-B2 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-2013097718-A1 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-11360005-B2 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-11366043-B2 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-11041842-B2 |
priorityDate |
2004-09-15-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
type |
http://data.epo.org/linked-data/def/patent/Publication |