Claims
- 1. A method of inhibiting the transcription of a gene, which is activated by AP-1 or an AP-1 component, comprising binding AP-1 or the component with a nuclear receptor so as to prevent the binding of AP-1 to the gene, wherein transcription is inhibited.
- 2. The method of claim 1, wherein the AP-1 component is a Jun protein.
- 3. The method of claim 1, wherein the nuclear receptor is a glucocorticoid receptor.
- 4. The method of claim 1, wherein the nuclear receptor is a vitamin D3 receptor.
- 5. The method of claim 1, wherein the nuclear receptor is an estrogen receptor.
- 6. The method of claim 1, wherein the gene is the gene encoding collagenase.
- 7. The method of claim 1, wherein the receptor is bound to its ligand.
- 8. The method of claim 1, wherein the nuclear receptor is a retinoic acid receptor.
- 9. The method of claim 8, wherein the retinoic acid receptor is selected from the group consisting of RAR.epsilon., RAR.alpha. RAR.beta., RAR.tau., and RXR.
- 10. The method of claim 1, wherein the nuclear receptor is a thyroid receptor.
- 11. The method of claim 10, wherein the thyroid receptor is selected from the group consisting of erbA-T and TR.alpha.-2.
- 12. A method of inhibiting the transcription of a gene which is activated by a nuclear receptor which binds AP-1 or an AP-1 component comprising binding the receptor with AP-1 or an AP-1 component so as to prevent the binding of the nuclear receptor to the gene, wherein transcription is inhibited.
- 13. A composition of matter comprising AP-1 or an AP-1 component bound to a nuclear receptor.
- 14. The composition of claim 13, wherein the AP-1 component is selected from the group consisting of a Jun and a Fos protein.
- 15. The composition of claim 13, wherein the nuclear receptor is a glucocorticoid receptor.
- 16. The composition of claim 13, wherein the nuclear receptor is a vitamin D3 receptor.
- 17. The composition of claim 13, wherein the nuclear receptor is an estrogen receptor.
- 18. The composition of claim 13, wherein the nuclear receptor is a retinoic acid receptor.
- 19. The composition of claim 18 wherein the retinoic acid receptor is selected from the group consisting of RAR.epsilon., RAR.alpha., RAR.beta. and RAR.tau. and RXR.
- 20. The composition of claim 13, wherein the nuclear receptor is a thyroid receptor.
- 21. The composition of claim 20, wherein the thyroid receptor is selected from the group consisting of erbA-T and TR.alpha.-2.
- 22. A method of promoting the transcription of a gene which is activated by AP-1 or an AP-1 component, comprising preventing the binding of AP-1 or an AP-1 component with a nuclear receptor thereby allowing AP-1 to bind the gene, wherein transcription is promoted.
Parent Case Info
This application is a continuation of U.S. Ser. No. 08/182,735, filed Jan. 14, 1994, now U.S. Pat. No. 5,643,720, which is a continuation of U.S. Ser. No. 08/032,726, filed Mar. 16, 1993, now abandoned, which is a continuation of U.S. Ser. No. 07/595,582, filed Oct. 10, 1990, now abandoned.
US Referenced Citations (1)
Number |
Name |
Date |
Kind |
5639592 |
Evans et al. |
Jun 1997 |
|
Foreign Referenced Citations (1)
Number |
Date |
Country |
0 552 202B1 |
Jan 1996 |
EPX |
Continuations (3)
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Number |
Date |
Country |
Parent |
182735 |
Jan 1994 |
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Parent |
032726 |
Mar 1993 |
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Parent |
595582 |
Oct 1990 |
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