| 序号 | 专利名 | 申请号 | 申请日 | 公开（公告）号 | 公开（公告）日 | 发明人 |
|---|---|---|---|---|---|---|
| 1 | Visualization of P-TEFb by Fluorescence Complementation | US14932611 | 2015-11-04 | US20160123957A1 | 2016-05-05 | Boris Peterlin; Koh Fujinaga |
| Provided herein is a novel assay for the quantification of P-TEFb activation in living cells. The invention, in one embodiment, comprises cells which express P-TEFb and a P-TEFb-phosphorylated or P-TEFb-binding species, for example the C terminal domain of RNA polymerase II. Each of the P-TEFb and P-TEFb-phosphorylated or P-TEFb-binding species comprises a complementary signal moiety, for example complementary fragments of a fluorescent protein, such that when the P-TEFb interacts with the P-TEFb-phosphorylated or P-TEFb-binding species, the signal moieties are in sufficiently close proximity to generate a detectable signal. | ||||||
| 2 | IN SITU VISUALIZATION OF KINASE ACTIVITY | US16326282 | 2017-08-17 | US20190185906A1 | 2019-06-20 | Peter Sicinski; Wojciech Michowski |
| Kinases can be engineered to utilize an ATP analog that is not readily utilized by wild-type kinases by introducing a mutation in the ATP-binding pocket. However, application of this method has been limited by the membrane impermeability of the ATP analog. Provided herein are methods for in situ visualization of substrates of an analog-sensitive kinase, the method comprising a mild fixation step. Also provided herein are kits comprising a fixative, an ATP analog, and an agent for detecting the substrates modified by the ATP analog. | ||||||
| 3 | METHOD AND KITS FOR IDENTIFYING OF CDK9 INHIBITORS FOR THE TREATMENT OF CANCER | US15301683 | 2015-04-02 | US20170173021A1 | 2017-06-22 | Scott William LOWE; Charles J. SHERR; Chun-Hao HUANG; Amaia LUJAMBIO |
| A method of determining sensitivity to cancer treatment includes the step of determining the presence of overexpression of MYC in a biological sample from a patient suffering from cancer, wherein the presence of overexpression of MYC indicates a sensitivity to a treatment by a CDK9 inhibitor and wherein the cancer is selected from the group consisting of carcinoma, leukemia, and lymphoma. | ||||||
| 4 | CDK MODULATORS AND METHODS FOR THE TREATMENT OF CANCER | US15368341 | 2016-12-02 | US20170157212A1 | 2017-06-08 | Katherine Jones; Seung Hyuk Choi |
| Disclosed is a polypeptide that includes amino acids 183-222 of CRIF, wherein the polypeptide does not include the full length CRIF1 amino acid sequence. Also disclosed is a nucleic acid molecule encoding this polypeptide, vectors including this nucleic acid molecule, and host cells transformed with these vectors. In some embodiments, methods are disclosed for treating a subject with cancer, comprising administering to the subject a therapeutically effective amount of an inhibitor of CDK12/CRIF1 interaction, thereby treating the cancer in the subject. In specific non-limiting examples, these methods can utilize CRIF1 polypeptides, nucleic acids encoding these polypeptides, and vectors including these nucleic acids. | ||||||
| 5 | METHOD AND KITS FOR IDENTIFYING OF CDK9 INHIBITORS FOR THE TREATMENT OF CANCER | EP15773170 | 2015-04-02 | EP3126525A4 | 2017-10-18 | LOWE SCOTT WILLIAM; SHERR CHARLES J; HUANG CHUN-HAO; LUJAMBIO AMAIA |
| A method of determining sensitivity to cancer treatment includes the step of determining the presence of overexpression of MYC in a biological sample from a patient suffering from cancer, wherein the presence of overexpression of MYC indicates a sensitivity to a treatment by a CDK9 inhibitor and wherein the cancer is selected from the group consisting of carcinoma, leukemia, and lymphoma. | ||||||
| 6 | AGENTS THAT INHIBIT P-TEFB INTERACTIONS AND METHODS OF USE THEREOF | PCT/US2008009298 | 2008-07-31 | WO2009020559A3 | 2009-04-09 | VERDIN ERIC M; BISGROVE DWAYNE A |
| The present invention provides methods of treating disorders associated with abnormal cellular growth and/or proliferation. The methods generally involve administering an agent that reduces interaction of BRD4 with P-TEFb. The present invention further provides methods of treating an immunodeficiency virus infection. The methods generally involve administering an agent that reduces interaction of BRD4 with P-TEFb and/or a viral protein. The present invention further provides methods of identifying an agent that reduces binding of BRD4 with P-TEFb. The present invention further provides BRD4 peptides and recombinant BRD4 polypeptides. | ||||||
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