100 results about "Signaling proteins" patented technology

The invention provides a natural killer cell, NK-92, modified to express an Fc receptor on the surface of the cell, such as CD16 (FcγRIII-A), or other Fcγ or Fc receptors. The modified NK-92 cell can be further modified to concurrently express an associated accessory signaling protein, such as FcεRI-γ, TCR-ζ, or to concurrently express interleukin-2 (IL-2) or other cytokines. Additional methods are disclosed for various assays, assessments, and therapeutic treatments with the modified NK-92 cells.

Superantibodies having enhanced autophilic, catalytic, and/or membrane-penetrating properties are prepared by affinity-based conjugation of a photoactivatable organic molecule to a target immunoglobulin. The photoactivatable organic molecule bears a chromophoric aromatic hydrocarbon moiety, which has affinity for the immunoglobulin. Upon photolysis, the organic molecule is covalently linked to the immunoglobulin. A preferred organic molecule is a peptide and a preferred aromatic hydrocarbon moiety is a tryptophan residue. The photoactivatable organic molecule need not bear a purine, pyrimidine or azido group to effect binding to the immunoglobulin and/or photoactivation. The superantibodies can enhance the potency and expand the targeting range of target antibodies. Autophilic superantibodies can promote apoptosis of target cells and/or enhance therapeutic efficacies in the treatment of patients with diseases or disorders responsive to antibody therapy. Exemplary of such diseases are atherosclerosis and cardiovascular disease. Membrane-penetrating superantibodies can prevent apoptosis by binding to intracellular anti-caspase signal proteins. Compositions containing the superantibodies, as well as methods of making and using them, are disclosed.

Disclosed is a system for detecting a protease inside a cell. In one embodiment, the system includes a chimeric protein that comprises as covalently linked components: 1) at least one optionally masked signal protein; 2) at least one protease-specific cleavage site; and 3) at least one detectable amino acid sequence. The invention has a wide spectrum of applications including use in the detection of novel protease inhibitors inside cells and tissue.

The invention provides a compound for targeted ubiquitinated degradation of Smad3. The compound for targeted ubiquitinated degradation of Smad3 is formed by connecting a compound shown in a formula (I) and an ubiquitin ligase E3 identifying ligand shown in a formula (II) through a Linker shown in a formula (III) for connecting the two. The invention constructs a compound which can be specifically combined with Smad3 to degrade Smad3 proteins in a targeted manner through ubiquitination by jointly applying computer virtual screening and a technology of target ubiquitinated degradation of proteins, and the compound is verified to be capable of degrading Smad3 in a targeted ubiquitinated manner. As Smad3 is the major known fibrosis-inducing signaling protein, the Protac theoretically has an anti-fibrosis effect. Moreover, the molecular weight of the compound is small, so that the Protac can get into or out of cells freely, and therefore, the compound is likely to become a novel drug for treating fibrosis. The compound not only has scientific value, but also has important social value.

Disclosed are materials and methods relevant to taste transduction. Also disclosed are human gastrointestinal cells that comprise or are capable expressing endogenous taste signaling proteins. Also disclosed are human gastrointestinal cells that comprise or are capable of expressing endogenous taste signaling proteins as well as hormones, neurotransmitters or soluble mediators of the gastrointestinal tract that are involved in or affect metabolism, digestion and appetite. Also disclosed are the uses of these human cells or their membranes to study how compounds affect taste transduction and/or metabolism, digestion and appetite, including effects on satiety, emesis and diabetes.

Disclosed herein is a completely synthetic cell-free therapy based on peptide amphiphile nanostructures designed to mimic the activity of vascular endothelial growth factor (VEGF), one of the most potent angiogenic signaling proteins. The VEGF-mimetic filaments disclosed herein were found to induce phosphorylation of VEGF receptors and induce pro-angiogenic behavior in endothelial cells, indicated by an enhancement in proliferation, survival and migration in vitro.

The present disclosure relates to compositions and methods for using cells having chemically-induced fusion protein complexes to spatially and temporally control immune cell signal initiation and downstream responses for treating disease.

The present invention relates to methods for laser surgery and growth factor stimulation for ultra-precision surgery with healing. The method is achieved by cutting biological tissue using an ultrafast laser, which produces laser pulses less than 10 picosecond in duration, to induce a cold ablation process in order to avoid the formation of carbonaceous or other materials that cannot be removed efficiently or completely from the wounded area through natural healing mechanisms. By use of femtosecond lasers, a negligible amount of debris is generated and an outer layer of intact but non viable cells are created principally through shock wave induce damage and ionizing radiation effects induced by multiphoton absorption of ultrashort laser pulses. The normal healing process is blocked by this outer layer of cells as all cell contacts are still intact. Therefore the healing process must be stimulated. The healing may be triggered or accelerated, or both, by application of growth factor molecules and/or signal proteins to the effectively undamaged cells causing the damaged cells to be replaced and the wound to close. The combination of very precise laser cutting used in combination with growth factors is the key to this unique tool.

The invention is related to methods of producing rod-derived cone viability factor (RdCVF). This invention also relates to the treatment of an ocular disease in a mammal using RdCVF. Also provided are expression vectors for high secreted expression of RdCVF of using nucleotide sequences encoding heterologous signal proteins and optionally markers for furin cleavage.

The invention relates to a method for cell-free expression of signal protein and an expression system. The method includes joining a target gene of the signal protein on a pIX3.0 vector to obtain expression plasmids; extracting escherichia coli Rosetta (DE3) by S30 buffer solution to obtain escherichia coli extract; preparing an energy supply system comprising PEP (phosphoenolpyruvic acid)/PK (pyruvate kinase), CP (phosphocreatine)/CK (creatine kinase) and glucose; preparing an amino acid mixture and a saline solution; preparing lecithin/cholesterol liposome; adding the expression plasmids into a cell-free protein expression system comprising the escherichia coli extract, the energy supply system, the amino acid mixture, the saline solution and the lecithin/cholesterol liposome for expression. The method is capable of solving the problem of small signal protein expression quantity.

The present invention includes compositions and methods for the identification, characterization and use of a novel anti-viral protein that includes a mitochondrial anti-viral signaling protein.

The invention relates to a combined medium and method for testing snail fever. It has the following characters: the medium contains recombination antigen mixture and recombination snail signal protein (rSj14-3-3) monoclonal antibody, and recombination antigen is mixed as recombination snail signal protein (rSj14-3-3) and recombination snail glutathione-s-transferase (rSjGST). The test operation is separately according to indirect enzyme immunosorbent test and double antibody bedded texture method. The invention adopts the two advantage diagnosis antigen molecule and its corresponding monoclonal antigen to form combined testing medium box.

The present invention relates to novel therapies for treatment and new biomarkers for earlier detection of pancreatic and other cancers. In particular, the present invention identifies Reg1α and Reg3α, and other members of the Reg protein family, as signaling proteins for a receptor on the surface of human cancer cells, Megi, and the downstream pathways activated through this receptor in pancreatic and other tumor cells. These signaling proteins may be targeted by means known in the art to disrupt the downstream signaling pathway that catalyzes tumorigenesis, by the usage of antibodies, antisense, RNA interference, small molecule inhibitors and vaccines.

Methods are provided in which a sterol-depleting agent such as β-cyclodextrin (βCD), is used to modulate signaling by a differentiation signaling protein such as Hedgehog protein or a BMP in vitro. As illustrated herein, the use of βCD in conjunction with Sonic Hedgehog N-terminal peptide (ShhN) causes substantially all of the cells in neural plate explants to differentiate as neurons, such as motor neurons. Also provided are cell therapy methods and screening methods that rely on the modulation of signaling of a differentiation signaling protein such as Hedgehog, by a sterol-depleting agent such as βCD.

The invention discloses 214 novel phosphorylation sites identified in signal transduction proteins and pathways underlying human carcinoma, and provides phosphorylation-site specific antibodies and heavy-isotope labeled peptides (AQUA peptides) for the selective detection and quantification of these phosphorylated sites/proteins, as well as methods of using the reagents for such purpose. Among the phosphorylation sites identified are sites occurring in the following protein types: Adaptor/Scaffold proteins, Cytoskeleton proteins, GTP Signaling proteins, Kinases, Metabolism proteins, Phosphatases/Phospho-diesterases/Proteases, Receptor proteins, RNA Processing proteins, Transcription proteins, Translation proteins, Transporter proteins, and Ubitquitin proteins, as well as other protein types.

The present disclosure provides a method of deriving and maintaining a midbrain-like organoid in culture, comprising (a) culturing pluripotent stem cells to obtain neuronal lineage embryoid bodies; (b) culturing the neuronal lineage embryoid bodies from (a) to obtain midbrain regionalized tissues; (c) embedding and culturing the midbrain regionalized tissues from (b) in an extracellular matrix to obtain neuroepithelial tissues; and (c) culturing the neuroepithelial tissues from (c) to obtain a midbrain-like organoid. Also disclosed herein are culture media suitable for deriving and maintaining neuronal lineage embryoid bodies comprising (a) TGF-β Inhibitor and/or SMAD2/3 inhibitors; and (b) WNT-signaling activator; culture media suitable for deriving and maintaining midbrain regionalized tissues comprising (a) TGF-β Inhibitor and/or SMAD2/3 inhibitors; (b) WNT-signaling activator; (c) hedgehog signaling protein; and (d) fibroblast growth factor; culture media suitable for deriving and maintaining neuroepithelial tissues comprising (a) hedgehog signaling protein; and (b) fibroblast growth factor and culture media suitable for deriving and maintaining a midbrain-like organoid comprising (a) neurotrophin factor; (b) ascorbic acid; and (c) activator of cAMP-dependent pathway.

The invention relates to a series of peptide compounds containing integrin conserved sequences and having a function of inhibiting in vitro and vivo neovascularization. The functional peptide compounds have amino acid sequences shown as the first item of claims. The micromolecular peptide compounds can be coupled to cell-penetrating peptides to enter cells and then be combined with common signaling protein molecules to inhibit neovascularization and to achieve the effect of inhibiting in vivo solid tumor growth of tested mice. The peptide compounds belong to the field of biomedicine. The functional micromolecular peptide compounds and the effect protein molecules of the functional micromolecular peptide compounds can inhibit in vitro human umbilical vein endothelial cells from forming vascular structures, inhibit vascularization in subcutaneous vaccination matrix gels of nude mice and inhibit growth of subcutaneous vaccination solid tumors of the nude mice. The invention not only provides a number of leading compounds capable of inhibiting neovascularization, but also discloses a new neovascularization regulating mechanism, thereby providing new target sites for developing a new generation of neovascularization inhibiting and antineoplastic drugs.