71 results about "Apoptosis pathways" patented technology

A nutritional supplement composition for normalizing impaired or deteriorating neurological function in humans is composed of: at least one agent which promotes synthesis of ATP and/or creatine phosphate in the body, at least one antioxidant for scavenging free radicals in at least one pathway in the body; at least one agent for normalizing or maintaining membrane function and structure in the body; at least one agent for normalizing or maintaining normal neurotransmitter function in the body; at least one agent for down-regulating cortisol action; and at least one agent for suppressing activation of apoptotic pathways in the body. The composition may further contain one or more of: at least one agent for suppressing inflammation in the body; at least one agent for normalizing or maintaining vascular wall function and structure in the body; at least one agent for normalizing or maintaining function of nerve growth factors and/or neurotropic factors in the body; at least one agent for suppressing toxic metal ionic effects; at least one agent for normalizing or maintaining methyl metabolism in the body; at least one agent for normalizing or maintaining metabolism of insulin and glucose in the body; and at least one agent for up-regulating activity of heat shock proteins in the body. A method for normalizing impaired neurological function in humans modulating nutrient partitioning in a human involves administering the aforementioned composition to the human, preferably on a daily basis, for a therapeutically effective period of time. Preferably, the method further involves having the human follow a stress reduction program, and/or a cognitive retraining program, and/or a dietary program designed to maximize insulin and glucose metabolism.

This invention provides a non-radioactive assay to monitor and quantify the target-cell killing activities mediated by cytotoxic T lymphocytes (CTLs). This assay is predicated on the discovery that apoptosis pathway activation and, in particular, granzyme B activity, provides a measure of cytotoxic effector cell activity. In one embodiment, measurement of CTL-induced granzyme B activation in target cells is achieved through detection of the specific cleavage of fluorogenic granzyme B substrates. This assay reliably detects antigen-specific CTL killing of target cells, and provides a more sensitive, more informative and safer alternative to the standard ⁵¹Cr-release assay most often used to quantify CTL responses. The assay can be used to study CTL-mediated killing of primary host target cells of different cell lineages, and enables the study of antigen-specific cellular immune responses in real time at the single-cell level. As such, the assay can provide a valuable tool for studies of infectious disease pathogenesis and development of new vaccines and immunotherapies.

The invention relates to methods of treating cancer. The invention further relates to a method of treating cancer by exploiting apoptotic pathways. The invention particularly relates to regulation of apoptotic pathways in cancerous cells, to metastasis of cancer cells, and to methods of preventing cancer metastasis.

Disclosed is a method for preparing a citrinin-free Monascus biomass. Also disclosed are a pharmaceutical and a functional food comprising a preparation by the method. The Monascus biomass possesses anti-oxidation property, and shows anti-proliferation property on cancer cells via apoptosis pathway.

Described is a replication competent recombinant virus, being capable to replicate and having lytic capacity in target cells, the said cell being hampered in the p53 dependent apoptosis pathway, the virus including in the genome thereof, the coding sequence of at least one restoring factor functional in restoring the p53 apoptosis pathway in the said target cells, operably linked to one or more expression control sequences, functional in the said target cells, as well as the use thereof in the preparation of a medicament, in particular for suppressing uncontrolled cell growth.

The invention provides a multifunctional nano-biomaterial transfection reagent with an effect of treating parkinsonism by gene, as well as a preparation method and application thereof. According to the method, a nerve growth factor (NGF) is immobilized on the surface of a hydrogel coated ferroferric oxide nano-particle (Fe3O4-OA-NAPI-AA) by virtue of a photo-grafting method, and plasmid DNA (Deoxyribonucleic Acid) capable of interfering with alpha-synuclein synthesis is adsorbed. The nano-material transfection reagent acts on the cell of an MPP+ (1-methyl-4-phenylpyridinium) induced in-vitro parkinsonism model PC12, and cell apoptosis is remarkably inhibited, wherein expression of the nerve growth factor receptor (NGFR) is up-regulated, expression of alpha-synuclein is down-regulated, and classic apoptosis pathway of BAX, P53 and Bcl-2 is influenced so as to achieve the aim of treating parkinsonism. The nano-material transfection reagent is non-toxic and less in side effects, can smoothly carry a gene to enter cells, is remarkable in action, and is worthy of popularization and application of parkinsonism treatment.

The present invention is directed to methods and agents used for treating cancer or infectious diseases by providing toll-like receptors such as toll-like receptor 5 (TLR-5) in combination with providing a toll-like receptor agonists such as flagellin resulting in a cis and intrans effect that recruits cells involved in both the innate (cis effect) and adaptive (trans effect) immune response to specifically kill cancer cells and cells infected with a pathogen via the NF-κB apoptosis pathway.

A method for preventing UV-induced skin-cellular injury by using a green algae extract and a cosmetic composition containing the green algae extract are disclosed. An effective dose of the green algae extract is used to protect fibroblasts from UV-induced apoptosis. The mechanism of the disclosed method is using the green algae extract to inhibit interaction between apoptosis pathway molecules Fas/FasL so as to inhibit an adapter protein (FADD) in a death-inducing signaling complex (DISC) and in turn to inhibit caspase-3 activation and cleaved polymerase (PARP) such that irreparable damage to DNA can be prevented. The green algae extract can be mixed with a skin permeable cosmetic composition so that the cosmetic composition possesses the function of preventing skin from UV-induced injury.

The present invention, based on the discovery of a new biological phenomena, provides methods and compositions for use in identifying agents that modulate the phosphorylation of survivin, the interaction between survivin and p34^cdc2-cyclin B1 kinase complex, and the interaction between survivin and caspase-9. Related methods and compositions can be used to modulate survivin regulated apoptosis.

Despite initial sensitivity BAD-protein phosphorylation were evaluated in patient samples and cell lines as determinants of chemo-sensitivity and/or clinical outcome, and as therapeutic targets. Induced in-vitro OVCA cisplatin-resistance was associated with BAD-pathway expression. Expression of the pathway was also associated with resistance of 7 different cancers cell-types to 8 chemotherapeutic agents. Phosphorylation of the BAD-protein was associated with platinum-resistance in OVCA cells and primary OVCA specimens, and also overall patient survival. Targeted modulation of BAD-phosphorylation levels influenced cisplatin-sensitivity. A 47-gene BAD-pathway signature was associated in-vitro phospho-BAD levels and with survival of 838 patients with ovarian, breast, colon, and brain cancer. The survival advantage associated with both BAD-phosphorylation and also the BAD-pathway signature was independent of surgical cytoreductive status. The BAD apoptosis pathway influences human cancer chemo-sensitivity and overall survival. The pathway is useful as a biomarker of therapeutic response, patient survival, and therapeutic target.

This invention provides a non-radioactive assay to monitor and quantify the target-cell killing activities mediated by cytotoxic T lymphocytes (CTLs). This assay is predicated on the discovery that apoptosis pathway activation and, in particular, caspase activity, provides a measure of cytotoxic effector cell activity. In one embodiment, measurement of CTL-induced caspase activation in target cells is achieved through detection of the specific cleavage of fluorogenic caspase substrates. This assay reliably detects antigen-specific CTL killing of target cells, and provides a more sensitive, more informative and safer alternative to the standard ⁵¹Cr-release assay most often used to quantify CTL responses. The assay can be used to study CTL-mediated killing of primary host target cells of different cell lineages, and enables the study of antigen-specific cellular immune responses in real time at the single-cell level. As such, the assay can provide a valuable tool for studies of infectious disease pathogenesis and development of new vaccines and immunotherapies.

The invention provides a construction method and application of a DSC2 gene knockout mouse model, and particularly relates to application of the DSC2 gene knockout mouse model in preparation of a reagent and a medicine for preventing and treating right heart disease, monitoring right ventricular diastole and contraction, and preparing an apoptosis pathway regulation reagent and a medicine or preparing a fibrosis pathway regulation reagent and a medicine. A DSC2 deletion mutant mouse is constructed on the basis of a C57BL/6J mouse through a CRISPR-Cas9 technology, and the DSC2 knockout mouse can effectively induce right ventricular cardiomyopathy and can be used for a mouse model for right ventricular cardiomyopathy research; after the DSC2 gene is simply knocked out, along with the increase of the age of the mouse, the mouse has the expression of right ventricular cardiomyopathy such as right ventricular enlargement, right ventricular myocardial fibrosis and middle and advanced right ventricular heart failure, so that the mouse model can be used as an effective model in subsequent molecular mechanism research on the right ventricular cardiomyopathy.

The invention relates to application of triclabendazole in preparation of drugs for treating breast cancer. According to the application of the triclabendazole in the preparation of the drugs for treating the breast cancer, the drugs for treating the breast cancer are tablets, granules, pills or capsules. Application of a triclabendazole composition in the preparation of the drugs for treating thebreast cancer is also included. Cancer cells of the to-be-treated breast cancer are MCF-7 or MDA-MB-231. The application has the advantages that the triclabendazole can induce apoptotic pyroptosis invitro and in vivo, and GSDME is cut by activated caspase-3 to generate GSDME-NT that take effects and forms vacuoles; the discovery suggests that the triclabendazole plays a role in cancer treatmentby inducing apoptosis of the cancer cells, specifically inducing GSDME-dependent apoptosis through the activated caspase-3 and at least partially through enhanced ROS/JNK/bax mitochondrial apoptosis pathways.

The invention discloses application of a PCBP1 gene in preparing a radiotherapy sensitivity enhancing kit, and in particular relates to application of the PCBP1 gene in preparing a sensitivity enhancing kit for tumor radiotherapy utilizing ionizing radiation including heavy ion rays. The nucleotide sequence of the PCBP1 gene is as shown in SEQ ID NO.1 and the PCBP1 gene is established in eukaryotic expression plasmid. Together with heavy ion beams, the PCBP1 gene regulates and controls expression of the CD44v6 gene related to tumor metastasis and invasion, inhibits proliferation, migration and invasion of HeLa tumor cells, remarkably down-regulates the cell cycle regulatory protein Cyclin D1, prompts cells to generate G0/G1 retardation, enhances the radiotherapy sensitivity of HeLa cells, up-regulates pro-apoptotic protein Tap73 and expression of the mitochondria apoptosis pathway MCL, down-regulates the apoptosis inhibition DelNp73 protein, and induces apoptosis of many HeLa cells.

The present invention relates to a polypeptide binding with tumor necrosis factor (TNF-alpha), and applications thereof. According to the present invention, the polypeptide and TNF-alpha have high affinity, and the polypeptide can be bound with the excess TNF-alpha to make the apoptosis promoting protein Bid in the apoptosis-related mitochondrion apoptosis pathway be down-regulated while make the anti-apoptosis protein Bcl-2 be up-regulated in the apoptosis-related mitochondrion apoptosis pathway so as to inhibit the apoptosis caused by TNF-alpha, such that the polypeptide can be used for preparation of TNF-alpha-related disease treating drugs. The present invention further provides a method for screening at the molecular and cellular level and researching the influence of the polypeptide antagonist on the TNF-alpha physiological effect, and applications thereof so as to provide the effective method for development of the low-cost anti-TNF-alpha drug.

The invention provides application of evodiamine in the preparation of a preparation for resisting white spot syndromevirus. Evodiamine can act on the protein essential for the apoptosis pathway of prawns, so the small molecules can be utilized to prepare the preparation for resisting the white spot syndromevirus so as to greatly enhance the resistance of the prawns to the white spot syndromevirus (WSSV) and reduce the fatality rate. The advantages of the invention are mainly embodied in that: the evodiamine can effectively induce activation of the PjCaspase, greatly enhance the resistance of the prawns to the white spot syndromevirus (WSSV) and reduce the fatality rate; and because the evodiamine is the medicament which is widely used in human body for improving the immunity, the evodiamine has no toxicity to the human body, and the prawns using the evodiamine can be enjoyed with safety no matter whether the medicament is completely metabolized.

The chimeric Bcr-Abl oncoprotein is the molecular hallmark of chronic myelogenous leukemia (CML). In the cytoplasm, the protein transduces a growth signal that is responsible for overexpansion of cells. In the nucleus, the protein induces apoptosis. The invention is a method of treating cancer/killing Bcr-Abl expressing cells by inducing the translocation of Bcr-Abl to the nucleus to activate the apoptotic pathway in cancer cells.

The invention discloses a protein nano-drug for cancer targeted therapy and a preparation method thereof. The protein nano-drug is an exosome of humanized p53 protein transferred with covalent cross-linked triphenylphosphine (TPP). A protein nano-drug delivery system TPP/p53@Exos developed by the invention can recognize specific cancer cells in a targeted manner, efficiently inhibits the growth ofthe cancer cells by activating endogenous apoptosis pathways of the cells, has no toxic or side effect, and provides a new means for cancer treatment. The preparation method of the nano-drug deliverysystem has a high protein loading rate (about 75%), and can also be used for protection and targeted delivery of other protein drugs.

The invention discloses application of rhizoma polygonati in preparation of a medicine for preventing and treating low-dose or/and chronic uranium exposure, belongs to the technical field of medicines, and solves the technical problems that no low-toxicity and high-efficiency uranium detoxification medicine is available for being administered preventively and taken for a long time. The invention discloses application of rhizoma polygonati in preparation of the medicine for preventing and treating low-dose uranium exposure or/and chronic uranium exposure. The medicine has an inhibiting effect on a mitochondrial apoptosis pathway and has an activating effect on an endogenous antioxidant pathway. The medicine has good effects of preventing and treating low-dose uranium exposure and chronic uranium exposure. Experiments show that the polygonatum polysaccharide and the water extract can significantly improve the activity of HK-2 cells, reduce the apoptosis of the HK-2 cells and improve the mitochondrial function, and the polygonatum polysaccharide and the water extract inhibit the uranium-induced cytotoxic effect by inhibiting a mitochondrial apoptosis pathway and activating an endogenous antioxidant GSK-3beta/Fynin/Nrf2 pathway.

The invention relates to an anti-tumor medicament prepared for treating glioblastoma. The medicament refers to withaferin A, realizes the activity of resisting glioblastoma by inducing apoptosis, induces apoptosis of glioblastoma through a mitochondrial pathway, and activates the mitochondrial apoptosis pathway by upregulating the protein content of Bad and Bim.