82 results about "Inhibitory molecules" patented technology

Embodiments herein generally relate to methods, compositions and uses for enhancing tolerance of production of organic acids and alcohols by microorganisms. This application also relates generally to methods, compositions and uses of vectors having one or more genetic element to increase the tolerance of organic acids or alcohols by a microorganism. Certain embodiments relate to compositions and methods of enhancing the tolerance for production of 3-hydroxypropionic acid (3-HP) by bacteria. In some embodiments, compositions and methods relate to regulating the expression of an inhibitory molecule of an enhancing gene to increase production of organic acid by bacteria.

The present invention relates to isolated male tissue-preferred regulatory sequences from Ms45 gene. The invention also relates to the use of Ms45 gene male tissue-preferred regulatory sequences in mediating male fertility in a plant, and in producing hybrid seed. The Ms45 male tissue-preferred regulatory region can be operably linked to exogenous genes encoding cytotoxins or inhibitory molecules. The invention also relates to plant cells, plant tissue and plants that contain the MS45 gene regulatory sequences.

Benzoxazole and benzothiazole compounds and the stereoisomers, tautomers, solvates, oxides, esters, and prodrugs thereof and pharmaceutically acceptable salts thereof are disclosed. Compositions of the compounds, either alone or in combination with at least one additional therapeutic agent, with a pharmaceutically acceptable carrier, and uses of the compounds, either alone or in combination with at least one additional therapeutic agent are also disclosed. The embodiments are useful for inhibiting cellular proliferation, inhibiting the growth and / or metathesis of tumors, treating or preventing cancer, treating or preventing degenerating bone diseases such as rheumatoid arthritis, and / or inhibiting molecules such as CSF-1R.

We examined IQGAP1 copy gain and its relationship with clinicopathologic outcomes of thyroid cancer and investigated its role in cell invasion and molecules involved in the process. We found IQGAP1 copy number (CN) gain ?3 in 1 of 30 (3%) of benign thyroid tumor, 24 of 74 (32%) follicular variant papillary thyroid cancer (FVPTC), 44 of 107 (41%) follicular thyroid cancer (FTC), 8 of 16 (50%) tall cell papillary thyroid cancer (PTC), and 27 of 41 (66%) anaplastic thyroid cancer, in increasing order of invasiveness of these tumors. A similar tumor distribution trend of CN ?4 was also seen. IQGAP1 copy gain was positively correlated with IQGAP1 protein expression. It was significantly associated with extrathyroidal and vascular invasion of FVPTC and FTC and, remarkably, a 50%-60% rate of multifocality and recurrence of BRAF mutation-positive PTC (P=0.01 and 0.02, respectively). The siRNA knock-down of IQGAP1 dramatically inhibited thyroid cancer cell invasion and colony formation. Co-immunoprecipitation assay showed direct interaction of IQGAP1 with E-cadherin, a known invasion-suppressing molecule, which was upregulated when IQGAP1 was knocked down. IQGAP1, through genetic copy gain, plays an important role in the invasiveness of thyroid cancer and represents a useful prognostic marker and therapeutic target for this and other cancers.

Provided herein are methods for inhibiting tumor angiogenesis in a cancer patient, the method comprising administering to the subject an effective amount of a first isolated binding molecule which specifically binds to semaphorin-4D (SEMA4D) and an effective amount of a second isolated binding molecule which specifically binds to VEGF.

Disclosed herein are compounds and their oxides, esters, prodrugs, solvates, and pharmaceutically acceptable salts thereof, compositions of the compounds, either alone or in combination with at least one additional therapeutic agent, with a pharmaceutically acceptable carrier, and uses of the compounds, either alone or in combination with at least one additional therapeutic agent. The embodiments are useful for inhibiting cellular proliferation, inhibiting the growth and / or metathesis of tumors, treating or preventing cancer, treating or preventing degenerating bone diseases such as rheumatoid arthritis, and / or inhibiting molecules such as CSF-1R.

Demineralized bone matric (DBM) and native bone morphogenetic protein (nBMP) are complex mixtures of non-collagenous bone proteins. These mixtures contain many of the BMPs that are available as recombinant molecules. Information regarding the presence in these materials of molecules that may affect the availability and activity of the BMPs is very limited. A chemical extraction of DBM, such as using alkali-urea produces a water soluble extractate which inhibits the osteogenic activity of DBM. Noggin, an extracellular BMP ligand antagonist is found in the water soluble extractate from DBM. Differential chemical extraction is a useful means of removing non-osteogenic, or osteogenic inhibitory molecules from DBM and nBMP.

Provided herein are methods for inhibiting tumor angiogenesis in a cancer patient, the method comprising administering to the subject an effective amount of a first isolated binding molecule which specifically binds to semaphorin-4D (SEMA4D) and an effective amount of a second isolated binding molecule which specifically binds to VEGF.

Inhibitors of mammalian protein kinase C isoforms that comprise an inhibitor moiety, which is capable of inhibiting protein kinase activity, operatively associated with a peptide recognition element (PRE), which has an affinity for one or more PKC isoforms are provided. The targeted inhibitory molecules (TIMs) of the present invention are capable of inhibiting one or more PKC isoforms. The TIMs can be designed to target a specific PKC isoform by selection of a PRE component that is shown to preferentially target that PKC isoform. The TIMs are useful as therapeutic agents in the treatment of PKC-related diseases and disorders, such as cancer, psoriasis, angiogenesis, restenosis, atherosclerosis, cardiovascular disease, hypertension, diabetes, neurological disorders, rheumatoid arthritis, kidney disorders, inflammatory disorders and autoimmune disorders.

The present invention provides a gene delivery system containing nanoparticles. In more detail, the present invention provides a gene delivery system containing (a) a nanomaterial; (b) an oligonucleotide as an universal binding partner covalently linked to the surface of the nanomaterial; and (c) a cargo comprising (i) a complementary oligonucleotide containing a nucleotide sequence complementary to the universal binding partner as a binding counter-partner, and (ii) an inhibitory molecule having a nucleotide sequence complementary to a target gene of interest to be inhibited or an inducible molecule having a nucleotide sequence of a target gene of interest to be expressed. The present invention is a gene delivery system capable of feasibly deliver aptamer, siRNA, shRNA, miRNA, ribozyme, DNAzyme, PNA or gene as well as antisense oligonucleotide into the cells. In addition, the present invention is more efficient than the commercially available gene transfer reagent in respect to the degree of knockdown of target protein expression.

The invention discloses a preparation method of a high-efficiency killer cell preparation adopting an immunodetection point dual-block CTL (cytotoxic lymphocyte). The preparation method comprises steps as follows: step 1), collecting mononuclear cells in peripheral blood; step 2), performing DC (dendritic cell) separation and T cell separation on the separated mononuclear cells with an adherence method; step 3), adding adhering DCs to a serum-free culture medium containing GM-CSF (granulocyte-macrophage colony-stimulating factor) and IL-4 (interleukin-4) for preparation of a DC vaccine; step 4), adding suspending T cells to CD3 and IL-2 for T cell culture and amplification; step 5), adding antigen-supported DCs to the amplified T cells for preparation of the CTL, and adding PD-1 (Programmed death 1) and CTLA-4 (cytotoxic t lymphocyte associated antigen-4) antibodies for preparation of the cell preparation with the dual-block CTL effect. According to the novel technology and the novel method provided by the invention, an immune brake effect is effectively regulated and T cell depletion is retarded by blocking inhibitory molecules on the tumor specific CTL surfaces, so that the tumor cytotoxicity of CTL effector cells is substantially improved.

The invention provides a method for rapidly screening a bacterial quorum sensing inhibitor (QSI) by utilizing a suicide gene. The method is characterized in that under natural light, bacteria not infected with a phage do not turn blue and bacteria infected with the phage turn blue; induced by an added lethal condition inducer, a specific polypeptide with the function of inhibiting QS does not start expression of the suicide gene because of inhibiting the activities of QS molecules, so the bacteria survive; a non-specific polypeptide can not inhibit the QS molecules, so the suicide gene starts lethal; then survival candidate clones are picked out, functional verification is further carried out and finally a DNA (deoxyribonucleic acid) sequence corresponding to a specific polypeptide sequence is obtained by a method of DNA sequencing, thus obtaining an efficient and specific QSI polypeptide. The method is simple in steps, and multiple QSI candidate polypeptides can be obtained only within three days to about one weak, so that the method has very obvious advantages.

The present invention relates to the diagnosis and treatment of cancer, and in particular breast cancer. Specifically, in some embodiments the invention relates to methods of diagnosing cancer, and in particular breast cancer, using an antibody specific for a gene product that localizes selectively to the endoplasmic reticulum of the cancer cell(s). In some embodiments, the invention relates to methods of treating cancer, and in particular breast cancer, by administering a composition comprising an RNA interference sequence (e.g., shRNA, RNAi and / or siRNA molecule) characterized by an ability to inhibit an mRNA molecule, which mRNA molecule is encoded by the C43 gene (SEQ ID NO: 1). The invention additionally relates to methods for detecting cancer cells by detecting reduced methylation of the C43 promoter, and methods for reducing cancer metastasis by using demethylation inhibitors that result in increased methylation of the C43 promoter. The invention additionally relates to an in vitro 3-dimensional assay for detecting migrating cells, identifying test agents and / or nucleotide sequences that alter cell migration.

The present invention provides a composition of matter, comprising: DNA encoding a viral Vpx protein fused to DNA encoding a protein. In another embodiment of the present invention, there is provided a composition of matter, comprising: DNA encoding a viral Vpr protein fused to DNA encoding a protein. The present invention further provides DNA, vectors and methods for expressing a lentiviral pol gene in trans, independent of the lentiviral gag-pol. A gene transduction element is optionally delivered to a lentiviral vector according to the present invention. Also provided are various methods of delivering a virus inhibitory molecule to a target in an animal. Further provided is a pharmaceutical composition.

The present invention provides RNA purification and / or analysis methods that use ammonium sulfate to mitigate or neutralize inhibitory effects of certain molecules. Exemplary inhibitory molecules that interfere with RNA function or analysis are those that bind to or cleave RNA, or stabilize RNA secondary structures.

The invention discloses a double-modified collagen scaffold and an application of the double-modified collagen scaffold in a product for repairing of spinal cord injury. The double-modified collagen scaffold comprises a collagen scaffold material, and an EGFR antibody and microtubule stabilizing molecules modified on the collagen scaffold material. The EGFR antibody cetuximab and the microtubule stabilizing molecule paclitaxel are combined to modify the linear ordered collagen scaffold material, which can effectively antagonize the inhibitory effect of myelin-related inhibitory molecules on nerve regeneration by blocking the activation of an EGFR signaling pathway, the collagen scaffold promotes the generation of more neurons in the spinal cord injury position, is beneficial to the myelination of nerve fibers, and can also promote the regeneration of axons by stabilizing the structure of microtubules, reduces the deposition of inhibitory scar components in a injured area, blocks the formation of inhibitory scars, and reconstructs the spinal cord neural circuit, and ultimately achieves better behavioral recovery after spinal cord injury.

Demineralized bone matric (DBM) and native bone morphogenetic protein (nBMP) are complex mixtures of non-collagenous bone proteins. These mixtures contain many of the BMPs that are available as recombinant molecules. Information regarding the presence in these materials of molecules that may affect the availability and activity of the BMPs is very limited. A chemical extraction of DBM, such as using alkali-urea produces a water soluble extractate which inhibits the osteogenic activity of DBM. Noggin, an extracellular BMP ligand antagonist is found in the water soluble extractate from DBM. Differential chemical extraction is a useful means of removing non-osteogenic, or osteogenic inhibitory molecules from DBM and nBMP.

The invention provides application of akkermansia muciniphila or prevotella copri to preparation of drugs for enhancing the anti-tumor immune function of CD4+T cells and / or CD8+T cells and / or for enhancing the anti-tumor immune function of CD8+T cells in the tumor microenvironment. The akkermansia muciniphila or the prevotella copri can significantly inhibit PD-1 expressed by systematic CD4+T cells and / or CD8+T cells, can also promote infiltrating and / or accumulating of the CD8+T cells in the tumor microenvironment, inhibits expression of PD-1 molecules, and significantly inhibits tumor growth.

The invention provides a thermal activation delayed fluorescence material and an application thereof. The thermal activation delayed fluorescence material has the following structure: a compound taking tris([1, 2, 4] triazole)[4, 3-a: 4', 3'-c: 4'', 3''-e][1, 3, 5] triazine as a receptor core has the property of thermally activated delayed fluorescence, and the receptor has a rigid planar structure, so that the thermal stability of the material is effectively improved; a large torsion angle between a donor unit and an acceptor unit can inhibit intermolecular accumulation; the solubility and the film-forming property are improved; meanwhile, the larger torsion angle can reduce overlapping of molecular front line orbits, so that the lowest excited singlet state-triplet state energy level difference is reduced, triplet state excitons can return to the singlet state through reverse intersystem crossing and finally return to the ground state in a radiation transition mode to emit fluorescence, the exciton utilization rate is increased, and finally the purpose of improving the device efficiency is achieved.

The present invention relates to an isolated nucleic acid sequence encoding the Ms45 male tissue-preferred regulatory region. In one aspect this invention relates the use of this male tissue-preferred regulatory region in mediating fertility. An example of such use is the production of hybrid seed such as in a male sterility system. The Ms45 male tissue-preferred regulatory region can be operably linked with exogenous genes, such as those encoding cytotoxins, complementary nucleotidic units and inhibitory molecules. This invention also relates to plant cells, plant tissue and differentiated plants which contain the regulatory region in this invention.

The invention discloses microRNA (micro ribonucleic acid) for regulating gene expression of B7-H3 (a molecule of the B7 family). The microRNA is nucleic acid, functional segment or variant including a sequence of 5'-UGAGAUGAAGCACUGUAGCUC-3'. The microRNA is miR-143. Performed in-vitro biological function tests show that hsa-miR-143 is capable of inhibiting molecular expression of the B7-H3 by bonding with 3'-UTR (untranslated regions) of the B7-H3 gene, and antitumor effect is achieved by regulating a signal path of the B7-H3 and / or expression and functions of the miR-143.

The invention provides a gene HDAC11 interfered chimeric antigen receptor T-cell and application thereof. Particularly, the invention provides an engineering immune cell. The engineering immune cell comprises (a) a chimeric antigen receptor CAR, wherein the chimeric antigen receptor CAR comprises an antigen bonded structural domain, a transmembrane structural domain and an intracellular structuraldomain, and the antigen bonded structural domain is specifically bonded to a surface antigen of a tumor cell; and (b) an inhibiting molecule for lowering or inhibiting expression activity of an HDAC11 protein. The engineering immune cell provided by the invention has a good tumor killing effect.

The invention provides a transgenic lymphocyte, a construct, and a therapeutic composition for treating cancer. The cellular immune checkpoint of the transgenic lymphocyte is silenced, and the transgenic lymphocyte expresses a chimeric antigen receptor. The chimeric antigen receptor comprises an extracellular region, which comprises the heavy-chain variable region and the light-chain variable region of a single-chain antibody that specifically recognizes the antigen MSLN; a transmembrane region, which is connected with the extracellular region and embedded into the cell membrane of a T lymphocyte; and an intracellular region, which is connected with the transmembrane region and comprises the intracellular segment of CD28 and a CD3 zeta chain. The transgenic lymphocyte has the characteristic of resisting tumor cell-mediated immunosuppression, is substantially strengthened in the ability of killing tumor cells, and particularly has remarkable directional killing effect on tumors with high expression of MSLN.

The invention provides an organic compound, an organic light-emitting display panel and application thereof. The organic compound has a structure as shown in a formula I. Nitrogen atoms of pyrimidine in a receptor and hydrogen atoms in a donor form intramolecular hydrogen bonds, the torsion angle between D and A is adjusted, proper HOMO and LUMO distribution is obtained, the oscillator strength is improved, meanwhile, the molecular rigidity is enhanced, and non-radiative transition of molecules is inhibited; according to the organic compound provided by the invention, carbonyl, pyrimidine and donor groups in molecules are linearly arranged due to para-position substitution, the horizontal orientation degree of the molecules is improved, the optical coupling efficiency is favorably improved, and the device efficiency is improved.

Compositions and method for stimulating and controlling arteriogenesis and lymphatic vasculature by preventing and / or reducing the cellular interaction between RAF1 and AKT have been developed. The compositions include molecules that increase the bioavailability of non-phosphorylated RAF1, for example, the RAF1 Ser259 to Ala259 mutant in (RAF1 S259A), and AKT1 inhibitory molecules. Defects, disorders or diseases of insufficient blood or lymphatic vasculature are treated by administering to a patient in need thereof, a pharmaceutical composition comprising a molecule specifically blocking RAF1-AKT crosstalk in a pharmaceutically acceptable carrier or excipient in an amount effective to enhance the growth of blood or lymphatic vasculature in the patient. Compositions can be administered by injection or by controlled or sustained release devices, coating on devices or implants, microparticles, bulking agents or depots, or other techniques providing controlled or sustain release over a period of time effective to induce blood or lymphatic vasculature growth as desired.

The invention provides a non-natural amino acid modified protein drug combined with immunosuppressive molecule PD-L1. The protein drug is integrated into a covalent protein drug through non-natural amino acid with potential biological activity, and is combined with a target protein through an accessible reaction, and the non-natural amino acid can be covalently combined with a target protein aminoacid residue. The non-natural amino acid modified PD-1 enhances the binding capacity with PD-L1, has the effect of inhibiting cancer cells, and has the effect of treating tumors.

The invention discloses MicroRNA (micro ribonucleic acid) for regulating gene expression of B7-H4 (a molecule of the B7 family). The microRNA is nucleic acid, functional segment or variant including a sequence of 5'-UGAGAUGAAGCACUGUAGCUC-3'. The microRNA is miR-143. Performed in-vitro biological function tests show that hsa-miR-143 is capable of inhibiting molecular expression of the B7-H4 by bonding with 3'-UTR (untranslated regions) of the B7-H4 gene, and antitumor effect is achieved by regulating a signal path of the B7-H4 and / or expression and functions of the miR-143.

Isolated nucleotides encoding polypeptides with mutations leading to amino acid substitutions linked to hereditary kidney disease or malformation of the urinary tract are provided herein. Constructs, cells, probes and inhibitory molecules comprising these mutations are also provided and may be used in screening assays for candidate agents to treat or reverse these diseases or alternatively to provide diagnostic tests. Methods of diagnosing subjects likely to develop these diseases or to be carriers of these diseases are also provided.