| Predicate |
Object |
| assignee |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_1fee896617d6bc402607c5a8588e8b80
http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_3eeb3ba1c10701bdc91e9a2f2d66a2cf
http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_7890dd06821659260c0ec965a05d6570 |
| classificationCPCAdditional |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12Q2600-136
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12Q2600-106
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12Q2600-178
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12Q2600-158 |
| classificationCPCInventive |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K45-06
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12Q1-6809
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12Q1-6886
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K31-7088 |
| classificationIPCInventive |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C12N5-00
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C07H21-02
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61N5-00
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-7088
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K33-24
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C12Q1-68
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-704 |
| filingDate |
2010-03-22-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| inventor |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_66cbcd93c827e2113513c0325c7fc815
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_5bddfb152f3b7be13305f4ecf13d734d
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_7f56b4f4c4ab8b0d2af3c145634a9cd0 |
| publicationDate |
2012-04-12-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| publicationNumber |
US-2012087992-A1 |
| titleOfInvention |
miRNAS AS THERAPEUTIC TARGETS IN CANCER |
| abstract |
Methods for modulating expression of a component of a cell, comprising contacting the cell with a nucleic acid comprising an miR-140 nucleic acid sequence in an amount sufficient to modulate the cellular component are provided. Overexpression of miR-140 inhibits cell proliferation in both U-2 OS (wt-p53) and HCT 116 (wt-p53) cell lines. Cells transfected with miR-140 are more resistant to chemotherapeutic agent methotrexate, mi-140 expression is related to HDAC4 protein expression. The claimed methods reduce the protein expression level of HDAC4 without degrading the target mRNA. |
| isCitedBy |
http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-2015151004-A1
http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-11584932-B2
http://rdf.ncbi.nlm.nih.gov/pubchem/patent/KR-20190086688-A
http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-11236337-B2
http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-10323067-B2
http://rdf.ncbi.nlm.nih.gov/pubchem/patent/WO-2018085198-A1
http://rdf.ncbi.nlm.nih.gov/pubchem/patent/KR-102502248-B1
http://rdf.ncbi.nlm.nih.gov/pubchem/patent/WO-2017214145-A1 |
| priorityDate |
2009-03-20-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| type |
http://data.epo.org/linked-data/def/patent/Publication |