http://rdf.ncbi.nlm.nih.gov/pubchem/patent/CA-2398580-A1
Outgoing Links
Predicate | Object |
---|---|
assignee | http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_18d92c46f60af8af24e262b67381d7eb |
classificationCPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12N9-1205 |
classificationIPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C12N9-12 |
filingDate | 2001-02-09-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
inventor | http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_3ae20325c041aed6df48530c90f0e6cd http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_e421a40bb6560bfd11074ed78df15353 http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_a706926c5c3cb30b022a6c04d4365bda |
publicationDate | 2001-08-16-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
publicationNumber | CA-2398580-A1 |
titleOfInvention | Cdk4 is a target of c-myc |
abstract | The prototypic oncogene c-MYC encodes a transcription factor, which can driv e proliferation by promoting cell cycle re-entry. However, the mechanisms through which c-MYC achieves these effects have been unclear. Using serial analysis of gene expression (SAGE), we have identified the cyclin dependent kinase 4 (CDK4) gene as a transcriptional target of c-MYC. c-MYC induced a rapid increase in CDK4 mRNA levels through four highly conserved c-Myc bindi ng sites (MBS) within the CDK4 promoter. Cell cycle progression is delayed in c - MYC-deficient RAT1 cells, and this delay was associated with a defect in CDK 4 induction. Ectopic expression of CDK4 in these cells partially alleviated th e growth defect. Thus CDK4 provides a direct link between the oncogenic effect s of c-MYC and cell cycle regulation. |
priorityDate | 2000-02-11-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
type | http://data.epo.org/linked-data/def/patent/Publication |
Incoming Links
Total number of triples: 122.