40 results about "Steroids Receptors" patented technology

The invention relates to an insect steroid receptor protein which is capable of acting as a gene switch which is responsive to a chemical inducer enabling external control of the gene.

FK506 and geldanamycin promote nerve regeneration by a common mechanism that involves the binding of these compounds to polypeptide components of steroid receptor-complexes other than the steroid hormone binding portion of the complex (FKBP52 and hsp90, respectively). These and other agents cause hsp90 dissociation from steroid receptor complexes or block association of hsp90 with steroid receptor complexes.

The present invention provides a method of screening for a compound that binds to a selected nucleic acid comprising contacting compound fluorescently labeled by a fluorescent protein with a cell having a plurality of copies of the nucleic acid in an array such that the nucleic acid can be directly detected when bound by fluorescently labeled compound; and directly detecting the location of fluorescence within the cell, fluorescence aggregated at the site of the nucleic acid array indicating a compound that binds to the selected nucleic acid. In particular compounds such a transcription factors can be screened. Reagents for such method are provided including a mammalian cell having a plurality of steroid receptor response elements in an array such that the response element can be directly detected when bound by fluorescently labeled steroid receptor and a chimeric protein comprising a fluorescent protein fused to a steroid receptor.

The present invention provides a human cytokine/steroid receptor protein (CYSTAR) and polynucleotides which identify and encode CYSTAR. The invention also provides expression vectors, host cells, antibodies and antagonists. The invention also provides methods for the prevention and treatment of diseases associated with expression of CYSTAR, as well as diagnostic assays.

The present invention provides a novel steroid inducible expression system in a non-mammalian host cell (e.g., fungal) that is independent of metabolic and developmental regulation. The human estrogen receptor gene expressed in Aspergillus, under a constitutive promoter, was shown to be functional. A construct containing a promoter from Aspergillus, synthetic sequence containing the estrogen receptor biding sites (EREs) and a reporter gene was expressed in response to a hormone derivative inducer. In the absence of the inducer, the promoter is silent and depending on the type of construct and inducer concentration the expression level can be modulated from moderate to very strong.

Interaction of Rel proteins and steroid receptors is known to result in repression of target genes. Here we describe the discovery of a new mechanism in which Rel proteins and steroid receptors act synergistically to activate a regulatory element. This mechanism is shown to influence the expression of the brain-specific 5HT1A receptor wherein the estrogen receptor acts synergistically with the Nuclear Factor kappa B to enhance the activity of the promoter for the 5HT1A receptor gene. In addition, synergistic effects of Rel proteins with the mineralocorticoid receptor were observed, showing that synergism with Rel proteins may be expected for other steroid receptors as well. The synergism between Rel proteins and estrogen receptor or mineralocorticoid receptor provides a tool for the development of compounds that interact with the estrogen or mineralocorticoid receptor in such a way that only the synergistic effect is modulated whereas other effects are left intact. Such compounds would be invaluable for the development of medicaments for the treatment of diseases of the central nervous or cardiovascular system and other disorders in which Rel proteins play a role.

Methods for separation and synthesis of the optically active 7-thioester isomers and mono or bis-cyclopropyl derivatives of spironolactone are provided. Preferred stereoisomerically purified 7-thioester isomers and mono or bis-cyclopropyl derivatives of spironolactone have fewer effects mediated by gonadal steroid receptors relative to effect mediated by minteralocorticoid progesterone receptors, compared to the stereoisomerically unpurified form of the compound. These optically active compounds can be useful for obtaining reduction in moderate essential hypertension and it the treatment of congestive heart failure in humans with minimized undesirable side effects such as gynecomastia, tender breast enlargement and menstrual irregularities in women, and loss of libido in men.

The disclosure relates to anti-cancer compounds derived from nuclear steroid receptor binders, to products containing the same, as well as to methods of their use and preparation.

Mutants of steroid receptor ligand binding domains and synthetic ligands which have specific binding affinities for these receptors are provided. The use of these LBD-ligand combinations for construction of selective “molecular gene switches” is disclosed. Methods of regulating gene function using these switches are provided.

The present invention relates to fundamental discoveries for understanding the mechanism of non-gene targeting effects of steroids and its relation to gene targeting effects. It has been found that (i) non-gene targeting and gene targeting effects of steroids can be mediated through the same steroid receptors; (ii) both effects are ligand-induced; (iii) non-gene targeting effects occur is due to the ligand-inducing activity of the ligand-binding domain, which may be rapid and loose binding; (iv) gene targeting occurs due to the ligand of the DNA-binding domain of the steroid receptor induced activity, which is usually the result of a slower, stronger interaction; and (v) non-gene targeting of ligand interactions can be derived from gene targeting of ligand interactions separation so that selective reactions can be carried out. The present invention also discloses for the first time that certain steroids can induce non-gene targeting effects by binding to unrelated steroid receptors.

Compositions including at least one nuclear steroid family (NSF) receptor antagonist for the treatment or prevention of a coronavirus infection, such as SARS-CoV-2, and for the treatment of symptoms resulting from such infection. Also provided herein are methods of administering such compounds to a patient, either in a combination pharmaceutical formulation or in separate pharmaceutical formulations, to treat or prevent viral infections, including viral infections from coronaviruses such as SARS-CoV-2. Treatment decreases a viral load in a subject and/or may ameliorate symptoms associated with or produced by viral infection. Various administration modalities and mechanisms may be selected depending upon a condition of a patient and the patient's ability to be administered via a selected modality.

The invention features methods for treating and preventing a peripheral nerve sheath tumor in a mammal such as a human. The methods involve administering to the mammal a compound that modulates the biological activity of a gonatropic steroid receptor, such as the progesterone receptor in an amount sufficient to inhibit the growth of the peripheral nerve sheath tumor. The mammal may be administered with the compound alone or in combination with a second therapeutic regimen. Also disclosed are screening methods that make use of gonatropic steroid receptors for the identification of novel therapeutics for PNSTs.

The present invention relates to methods for the treatment of treatment-resistant depression (TRD), comprising the administration of compounds of formula (I), which are blocked in C₃ position and cannot metabolize in vivo into pregnenolone derivatives and which do not have significant affinity for steroid hormonal receptors and for all tested classical main receptors and receptors of neurotransmitters of the central nervous system.

The disclosure relates to anti-cancer compounds derived from nuclear steroid receptor binders, to products containing the same, as well as to methods of their use and preparation.