57 results about "Apoptotic programmed cell death" patented technology

A method and system for non-ablative acne treatment and prevention is disclosed. The method utilizes ultrasound energy which is targeted at a region of interest to treat existing acne and prevent future acne from forming. The application of ultrasound energy causes numerous physiological effects that treat acne. Some of these physiological effects comprise reducing sebum, increasing perfusion at the region of interest, denaturing proteins at the region of interest, creating an uninhabitable environment at the region of interest, initiating programmed cell death at the region of interest and the initiation of mechanical effects at the region of interest.

The present invention provides compounds, which have activity for modulating protein kinase enzymatic activity and are potentially useful for modulating cellular activities such as, e.g., proliferation, differentiation, programmed cell death, migration and chemoinvasion. The present invention also provides compositions containing such compounds, and methods for producing and using such compounds and compositions.

Regulation of expression of programmed cell death, including senescence, in plants is achieved by integration of a gene or gene fragment encoding senescence-induced deoxyhypusine synthase, senescence-induced eIF-5A or both into the plant genome in antisense orientation. Plant genes encoding senescence-induced deoxyhypusine synthase and senescence-induced eIF-5A are identified and the nucleotide sequences of each, alone and in combination are used to modify senescence in transgenic plants.

The present invention relates to compounds of the Formula (I) and (II) wherein R, R21, R25-R33, m, n, X21-X23, and Q1 are defined herein. The compounds modulate protein kinase enzymatic activity to modulate cellular activities such as proliferation, differentiation, programmed cell death, migration and chemoinvasion. Compounds of the invention inhibit, regulate and / or modulate kinases, particularly p70S6 and / or Akt kinases. Methods of using and preparing the compounds, and pharmaceutical compositions thereof, to treat kinase-dependent diseases and conditions are also an aspect of the invention.

Regulation of expression of programmed cell death, including senescence, in plants is achieved by integration of a gene or gene fragment encoding senescence-induced deoxyhypusine synthase, senescence-induced elF-5A or both into the plant genome in antisense orientation. Plant genes encoding senescence-induced deoxyhypusine synthase and senescence-induced elF-5A are identified and the nucleotide sequences of each, alone and in combination are used to modify senescence in transgenic plants.

The invention relates to BALB / c mice that are deficient in the programmed cell death-1 receptor (PD-1), a screening method for autoimmune disease medicine using these mice, an IgG self-reactive antibody that the mice produce, a protein that specifically reacts to the antibody and is produced in heart, and a diagnostic method for dilated cardiomyopathy using the protein. Because PD-1 deficient BALB / c mice spontaneously develop autoimmune disease, and specifically dilated cardiomyopathy, they are useful for screening for medicines against these diseases.

The present invention relates to novel chemical compounds, methods for their discovery, and their therapeutic use. In particular, the present invention provides benzodiazepine derivatives and related compounds and methods of using benzodiazepine derivatives and related compounds as therapeutic agents to treat a number of conditions associated with the faulty regulation of the processes of programmed cell death, autoimmunity, inflammation, hyperproliferation, and the like.

The present invention relates to novel chemical compounds, methods for their discovery, and their therapeutic use. In particular, the present invention provides benzodiazepine derivatives and methods of using benzodiazepine derivatives as therapeutic agents to treat a number of conditions associated with the faulty regulation of the processes of programmed cell death, autoimmunity, inflammation, and hyperproliferation, and the like.

The present invention relates to novel chemical compounds, methods for their discovery, and their therapeutic use. In particular, the present invention provides novel 1,4-benzodiazepine-2,5-dione compounds, and methods of using novel 1,4-benzodiazepine-2,5-dione compounds as therapeutic agents to treat a number of conditions associated with the faulty regulation of the processes of programmed cell death, autoimmunity, inflammation, hyperproliferation, and the like.

The present invention relates to novel chemical compounds, methods for their discovery, and their therapeutic use. In particular, the present invention provides benzodiazepine derivatives and related compounds and methods of using benzodiazepine derivatives and related compounds as therapeutic agents to treat a number of conditions associated with the faulty regulation of the processes of programmed cell death, autoimmunity, inflammation, hyperproliferation, and the like.

Compositions, systems and methods are provided for conferring disease resistance to plant pathogens that use proteases to target plant substrate proteins inside plant cells. Briefly, the compositions, systems and methods are based upon plant substrate proteins that are targeted by pathogen-specific proteases and that activate nucleotide binding site-leucine rich repeat (NB-LRR) disease resistance proteins when cleaved by the protease. These substrate proteins are modified such that the endogenous protease recognition sequence is replaced by a protease recognition sequence specific to a different pathogen protease (i.e., a heterologous protease recognition sequence). The modified plant substrate protein therefore can be used in connection with its corresponding NB-LRR protein to activate resistance in response to cleavage by the heterologous pathogen-specific protease. When activated by the plant pathogen-specific protease, the pair initiates host defense responses thereto, including programmed cell death.

The invention relates to polynucleotide agents targeting programmed cell death 1 ligand 1 (PD-L1) gene, and methods of using such polynucleotide agents to inhibit expression of PD-L1 and to treat subjects having a PD-L1-associated disorder.

The invention is directed to methods for identifying molecules that modulate paraptosis, a newly identified nonapoptotic form of programmed cell death. The invention also provides a method of inhibiting paraptosis by preventing association of caspase-9 and an endogenous paraptosis-mediating molecule. In one embodiment, the invention provides a method of inhibiting paraptosis by preventing association of caspase-9 and the Insulin-Like Growth Factor I Receptor (IGFIR). The invention further is directed to therapeutic methods for treatment of pathologies associated with aberrant levels of paraptosis such as neural cell death disorders and neoplastic disorders. Also provided by the present invention are methods of identifying endogenous paraptosis-mediating molecules.

This invention describes methods and pharmaceutical compositions for combinational cancer treatments that are capable of inducing JNK phosphorylation and induce programmed cell death. It also identified genes as target for anti-cancer drug development and enhancement of the chemotherapeutic drug effect for the treatment of cancer. This invention points to a novel method and principle for a new avenue of developing more efficient and low or non cytotoxic cancer treatment.

The present invention provides compounds for modulating protein kinase enzymatic activity for modulating cellular activities such as proliferation, differentiation, programmed cell death, migration and chemoinvasion. Even more specifically, the invention provides compounds for modulating c-Kit kinase activity and methods of treating diseases mediated by c-Kit activity utilizing the compounds and pharmaceutical compositions thereof.

The present invention relates generally to methods and compounds for regulating the release of nitric oxide in the vicinity of biofilm-forming microorganisms to regulate programmed cell death in the microorganisms and thereby promote dispersal of microorganism from biofilms and / or inhibit biofilm formation or development. More particularly, the invention relates to the use of compounds to provide spatial and temporal control over nitric oxide release.

This invention is concerned with clinical investigation of therapeutic effects of garlic extracts containing allicin, diallyl disulfide, and diallyl trisulfide. Because the intake of garlic or therapeutically active substance such as allicin from garlic, induces immunostimulation and possess strong antitumor effects concomitant with apoptosis of tumors that can in turn induces a programmed cell death of human prostatic and bladder tumor cells. This invention claims that garlic and / or garlic extracts possess very effective therapeutic substances not only to treat human prostate and bladder cancers to extend life span of patients, but also to suppress or prevent bladder and prostate gland cancers.

The invention discloses an engineering nucleic acid, which comprises nucleic acid of an antigen acceptor modified by gene engineering and can specifically binds an antigen from HPV; a nucleic acid ofan immune checkpoint acceptor for preventing tumor expression, wherein the nucleic acid can code one block protein; an engineering T cell, which comprises the above mentioned nucleic acid sequence; anapplication of the engineering T cell in the preparation of drugs for treating cancers; and a method for producing the engineering T cell. According to the method, a carrier is introduced into a T cell to obtain a TCR-T cell, then amplification is carried out to obtain the engineering T cell, and the carrier comprises the nucleic acid. The invention provides an engineering nucleic acid, a T cell,and an application and production method thereof. The obtained T cell can be used to recognize HPV E6 tumor antigen and can secrete a single chain antibody that blocks programmed cell death of protein PD-1. The engineering T cell has a strong antitumor function, the failure of T cell is reduced, and the nucleic acid and the T cell can be applied to immunological therapy of cancers of HPV E6 expression.

A pesticidal compound that regulates programmed cell death pathways via the topical application of double strand RNA is disclosed. The compound is constructed as a specific-target pesticide that is a biosafe nucleic acid pesticide for pest control.

The present invention relates to guanosine-rich oligonucleotides having the capacity to induce cell death, having characteristics of programmed cell death, in non-quiescent cells of higher eukaryotic organisms. The invention also relates to therapeutic methods involving the administration of these nucleic acid molecules to subjects suffering from, or being predisposed to, disorders involving abnormal cell proliferation and migration. The invention also concerns pharmaceutical compositions comprising the guanosine-rich nucleic acid molecules, in association with suitable carriers.

This invention provides a novel ratiometric bioluminescent sensor and methods of use thereof. The bioluminescent sensor comprises two luminescent proteins that exhibit different characteristics associated a biological condition, and thereby illuminates differently in response to the biological condition. A ratio between the luminescence of the two luminescent proteins indicates a change in the biological condition. The bioluminescent sensor of the invention can be used to image an oxidative stress or its associated conditions, including a programmed cell death.

The invention is based on the surprising finding that treatment with a chemotherapeutic agent such as 5-fluorouracil (5-FU) and an autophagy inducer effectively inhibit the continued growth of, and prevent the recovery following drug withdrawal, of cancer cells. In vivo, drug resistance from a failure to adequately engage in apoptotic programmed cell death leads to a recurrence of cancer and tumours can remain dormant for periods of time before re-emerging as drug resistant metastases. It has been hypothesised that autophagy (Type II cell death) may help cancer cells survive in response to growth limiting conditions, such as nutrient depletion, hypoxia, absence of growth factor, or presence of cytotoxic drug. LiCl is a known autophagy inducer and accelerates cell survival to autophagic programmed cell death.