168 results about "Calmodulin" patented technology

It has been discovered that the stimulation of beta-adrenergic receptors, which activate cAMP formation, give rise to increased APP and GFAP synthesis in astrocytes. Hence, the in vitro or in vivo exposure of neuronal cells to certain compositions comprising beta-adrenergic receptor ligands or agonists, including, e.g., norepinephrine, isoproterenol and the like, increases APP mRNA transcription and consequent APP overproduction. These increases are blocked by beta-adrenergic receptor antagonists, such as propranolol. The in vitro or in vivo treatment of these cells with 8Br-cAMP, prostaglandin E2 (PG E2), forskolin, and nicotine ditartrate also increased APP synthesis, including an increase in mRNA and holoprotein levels, as well as an increase in the expression of glial fibrillary acidic protein (GFAP). Compositions and methods are disclosed of regulating APP overexpression and mediating reactive astrogliosis through cAMP signaling or the activation of beta-adrenergic receptors. It has further been found that the increase in APP synthesis caused by 8Br-cAMP, PG E2, forskolin, or nicotine ditartrate is inhibited by immunosuppressants or anti-inflammatory agents, such as cyclosporin A, and FK-506 (tacrolimus), as well as ion-channel modulators, including ion chelating agents such as EGTA, or calcium / calmodulin kinase inhibitors, such as KN93. The present invention has broad implications in the alleviation, treatment, or prevention of neurological disorders and neurodegenerative diseases, including Alzheimer's Disease.

It has been discovered that the stimulation of beta -adrenergic receptors, which activate cAMP formation, give rise to increased APP and GFAP synthesis in astrocytes. Hence, the in vitro or in vivo exposure of neuronal cells to certain compositions comprising beta -adrenergic receptor ligands or agonists, including, e.g., norepinephrine, isoproterenol and the like, increases APP mRNA transcription and consequent APP overproduction. These increases are blocked by beta -adrenergic receptor antagonists, such as propranolol. The in vitro or in vivo treatment of these cells with 8Br-cAMP, prostaglandin E2 (PG E2), forskolin, and nicotine ditartrate also increased APP synthesis, including an increase in mRNA and holoprotein levels, as well as an increase in the expression of glial fibrillary acidic protein (GFAP). Compositions and methods are disclosed of regulating APP overexpression and mediating reactive astrogliosis through cAMP signaling or the activation of beta -adrenergic receptors. It has further been found that the increase in APP synthesis caused by 8Br-cAMP, PG E2, forskolin, or nicotine ditartrate is inhibited by immunosuppressants or anti-inflammatory agents, such as cyclosporin A, and FK-506 (tacrolimus), as well as ion-channel modulators, including ion chelating agents such as EGTA, or calcium / calmodulin kinase inhibitors, such as KN93. The present invention has broad implications in the alleviation, treatment, or prevention of neurological disorders and neurodegenerative diseases, including Alzheimer's Disease.

It has been discovered that the stimulation of beta-adrenergic receptors, which activate cAMP formation, give rise to increased APP and GFAP synthesis in astrocytes. Hence, the in vitro or in vivo exposure of neuronal cells to certain compositions comprising beta-adrenergic receptor ligands or agonists, including, e.g., norepinephrine, isoproterenol and the like, increases APP mRNA transcription and consequent APP overproduction. These increases are blocked by beta-adrenergic receptor antagonists, such as propranolol. The in vitro or in vivo treatment of these cells with 8Br-cAMP, prostaglandin E2 (PG E2), forskolin, and nicotine ditartrate also increased APP synthesis, including an increase in mRNA and holoprotein levels, as well as an increase in the expression of glial fibrillary acidic protein (GFAP). Compositions and methods are disclosed of regulating APP overexpression and mediating reactive astrogliosis through cAMP signaling or the activation of beta-adrenergic receptors. It has further been found that the increase in APP synthesis caused by 8Br-cAMP, PG E2, or forskolin is inhibited by immunosuppressants, immunophilin ligands, or anti-inflammatory agents, such as cyclosporin A, and FK-506 (tacrolimus), as well as ion-channel modulators, including ion chelating agents such as EGTA, or calcium / calmodulin kinase inhibitors, such as KN93. The present invention has broad implications in the alleviation, treatment, or prevention of neurological disorders and neurodegenerative diseases, including Alzheimer's Disease.

Described herein are electromagnetic treatment devices for treatment of tissue. In particular, described herein are lightweight, wearable, low-energy variations that are specifically configured to specifically and sufficiently apply energy within a specific bandpass of frequencies of a target biological pathway, such as the binding of Calcium to Calmodulin, and thereby regulate the pathway. Methods and systems for treating biological tissue are also described.

It has been discovered that the stimulation of beta-adrenergic receptors, which activate cAMP formation, give rise to increased APP and GFAP synthesis in astrocytes. Hence, the in vitro or in vivo exposure of neuronal cells to certain compositions comprising beta-adrenergic receptor ligands or agonists, including, e.g., norepinephrine, isoproterenol and the like, increases APP mRNA transcription and consequent APP overproduction. These increases are blocked by beta-adrenergic receptor antagonists, such as propranolol. The in vitro or in vivo treatment of these cells with 8Br-cAMP, prostaglandin E2 (PG E2), forskolin, and nicotine ditartrate also increased APP synthesis, including an increase in mRNA and holoprotein levels, as well as an increase in the expression of glial fibrillary acidic protein (GFAP). Compositions and methods are disclosed of regulating APP overexpression and mediating reactive astrogliosis through cAMP signaling or the activation of beta-adrenergic receptors. It has further been found that the increase in APP synthesis caused by 8Br-cAMP, PG E2, or forskolin is inhibited by immunosuppressants, immunophilin ligands, or anti-inflammatory agents, such as cyclosporin A, and FK-506 (tacrolimus), as well as ion-channel modulators, including ion chelating agents such as EGTA, or calcium / calmodulin kinase inhibitors, such as KN93. The present invention has broad implications in the alleviation, treatment, or prevention of neurological disorders and neurodegenerative diseases, including Alzheimer's Disease.

Calmodulin-like polypeptides named rgs-CaM are disclosed. cDNAs coding rgs-CaM are also provided. In addition, methods of using rgs-CaM cDNAs and polypeptides for modulating gene expression in plants are also provided.

Apparatus and methods for delivering electromagnetic signals configured specifically to accelerate the asymmetrical kinetics of the binding of intracellular ions to their respective intracellular buffers, to enhance the biochemical signaling pathways plant animal and human molecules, cells, tissues, organs, portions of entire organisms and entire organisms employ for growth, repair and maintenance. Described herein are devices and methods that utilize repetitive bursts of waveforms configured to maximize the bound concentration of intracellular ions at their associated molecular buffers to enhance the biochemical signaling pathways living systems employ for growth, repair and maintenance. For example the systems and methods described herein may drive the binding of calcium to calmodulin (CaM), thereby enhancing the CaM-dependent nitric oxide (NO) / cyclic guanosine monophosphate (cGMP) signaling pathway.

Described herein are electromagnetic treatment devices for treatment of tissue. In particular, described herein are lightweight, wearable, low-energy variations that are specifically configured to specifically and sufficiently apply energy within a specific bandpass of frequencies of a target biological pathway, such as the binding of Calcium to Calmodulin, and thereby regulate the pathway. Methods and systems for treating biological tissue are also described.

Described herein are devices and methods for treating degenerative joint diseases with electromagnetic fields using one or more waveforms that are configured to modulate Ca2+ binding to calmodulin and thereby modulate calmodulin-dependent nitric oxide signaling within joint and other affected tissue for the purpose of reducing pain and inflammation, as well as enhancing the healing and regeneration of such tissue.

Apparatus and methods for delivering electromagnetic signals configured specifically to accelerate the asymmetrical kinetics of the binding of intracellular ions to their respective intracellular buffers, to enhance the biochemical signaling pathways plant animal and human molecules, cells, tissues, organs, portions of entire organisms and entire organisms employ for growth, repair and maintenance. Described herein are devices and methods that utilize repetitive bursts of waveforms configured to maximize the bound concentration of intracellular ions at their associated molecular buffers to enhance the biochemical signaling pathways living systems employ for growth, repair and maintenance. For example the systems and methods described herein may drive the binding of calcium to calmodulin (CaM), thereby enhancing the CaM-dependent nitric oxide (NO) / cyclic guanosine monophosphate (cGMP) signaling pathway.

The invention discloses a calmodulin gene. The calmodulin gene is cloned in a cryptococcus humicolus BSLL1-1 bacterial strain, wherein the nucleotide sequence of the calmodulin gene is as shown in SEQ ID NO:1; a protein with an amino acid sequence shown in SEQ ID NO:2 is encoded by the gene; the protein is expressed in escherichia coli and the gene is further successfully expressed in saccharomyces cerevisiae. The aluminum resistance of the saccharomyces cerevisiae is increased due to the gene; genetically engineered bacteria can adsorb (or absorb) activated aluminum in a culture medium; and the genetically engineered bacterial strain of the saccharomyces cerevisiae has the application potential of reducing the activated aluminum content in acid soil.

The present invention provides methods and compositions for promoting bone regeneration, comprising administration of calmodulin. The method of bone regeneration is applied to subjects having bone disorders characterized by decreased bone mass such as osteopenia and osteoporosis, as well as those suffering from non-union fractures and osteochondrosis.

The presently-disclosed subject matter includes fluorescent protein-based indicators for detecting ions, small molecule analytes, or combinations thereof. In some embodiments the indicators include a polypeptide, which itself includes a fluorescent polypeptide, a compound-binding polypeptide, and a polypeptide target of the compound-binding polypeptide. In some embodiments the polypeptide includes an EosFP polypeptide, a calmodulin polypeptide, and a M13 polypeptide, or fragments and / or variants thereof. The presently-disclosed subject matter also includes methods for detecting calcium in a sample with embodiments of the present polypeptides. In some embodiments the present indicators experience a permanent shift from green to red fluorescent when exposed to an detecting substance, such as calcium.

The invention provides micromolecular protein used for indicating calcium ions and an application of the micromolecular protein. The amino acid sequence of the micromolecular protein is shown in SEQ ID NO.1. The gene encoded micromolecular protein is named as GEM and is blended with CaM (calmodulin) and myosin light-chain kinase M13, and numerous defects in existing calcium imaging technologies can be overcome. A new calcium imaging technology which takes the whole situation and the microscopic situation into consideration and can record activity in brains of experiment animals freely moving in the true sense can be obtained with the adoption of the micromolecular protein, and the micromolecular protein has broad application prospects and huge market value.

The present invention provides methods and compositions for promoting bone regeneration, comprising administration of calmodulin. The method of bone regeneration is applied to subjects having bone disorders characterized by decreased bone mass such as osteopenia and osteoporosis, as well as those suffering from non-union fractures.