39 results about "Docking (molecular)" patented technology

The invention provides a method for screening pharmaceutically active compounds from traditional Chinese medicines and an acting agent. The method comprises the following steps: determining a key signal pathway related to diseases, enabling different traditional Chinese medicine extracts to act on cell lines related to the diseases, and quantitatively analyzing the change condition of a transcription spectrum in cells based on a characteristic gene expression profile, so as to determine the adjusting effect of the different traditional Chinese medicine extracts on the key signal pathway, and selecting traditional Chinese medicines which have effects on the key signal pathway related to the diseases; collecting component compounds of the traditional Chinese medicines from different traditional Chinese medicine databases, and screening potential active compounds from the component compounds according to oral bioavailability and medicine similarity; screening a medicine target which can be used as a medicine effect in the key signal pathway; and further screening the potential active compounds by utilizing the medicine target to obtain the pharmaceutically active compounds. The methodprovided by the invention is a method for screening medicines or small molecular compounds on a large scale on a transcription level by combining a high-throughput medicine screening platform and a second-generation sequencing technology with molecular docking and molecular dynamics simulation, is high in screening efficiency, and provides a new idea for medicine screening.

Systems and methods for molecular simulation in accordance with embodiments of the invention are illustrated. One embodiment includes a method for predicting a relationship between a ligand and a receptor. The method includes steps for identifying a plurality of conformations of a receptor, computing docking scores for each of the plurality of conformations and a set of one or more ligands, and predicting a relationship between the set of one or more ligands and the plurality of conformations of the receptor.

Disclosed is a differential evolution-based protein ATP docking method. First, an ATPbind server is used to predict protein-ATP binding residue information, which improves the prediction accuracy of acomplex molecular spatial structure. Then, the original protein-ATP structure prediction problem is transformed into an optimal problem of searching for the optimal individual through the design of the individual population, which reduces the computational cost. Finally, by the differential evolution algorithm is used to search for the optimal individual, which improves the prediction accuracy ofthe protein-ATP complex structure. The invention provides a differential evolution-based protein ATP docking method with low computational cost and high search efficiency.

The invention relates to an ssDNA aptamer capable of specifically recognizing N-acetylneuraminic acid and application thereof. According to the invention, 4 ssDNA aptamer sequences capable of being highly specifically combined with Neu5Ac are obtained through screening of a magnetic bead-SELEX (systematic evolution of ligands by exponential enrichment) technology, and sequence ap1 has the highest affinity and specificity; and moreover, sequence ap1 is stable in structure. On the basis of sequence ap1, the sequence is truncated according to a secondary structure and a molecular simulation docking result to obtain one aptamer ap2 with the sequence length of 21nt, and the affinity is improved compared with that before truncation. The ssDNA aptamer disclosed by the invention is relatively high in binding specificity and affinity with Neu5Ac, and is high in sensitivity when being applied to Neu5Ac detection.

The invention relates to a drug virtual screening method and system based on receptors and ligands. The method comprises the following steps: (1) obtaining activity data of a target receptor, the activity data of the receptor being used for molecular docking; (2) obtaining ligands of the target receptor and activity data of the ligands to construct a ligand structure library; (3) processing the activity data of the ligands in the ligand structure library to obtain molecular fingerprints of the ligands; (4) carrying out molecular docking on the target receptor and ligands in the ligand structure library, then carrying out molecular dynamics simulation, and then carrying out energy decomposition to obtain an energy decomposition value; (5) selecting the molecular fingerprints and the energy decomposition values in proportion for feature fusion, and establishing a model according to a machine learning algorithm; and (6) performing virtual drug screening by using the model. The drug screening method and system are low in cost and high in efficiency, and have wide application prospects in the fields of drug activity prediction, structure optimization and design.

The invention provides a method for screening chitinase OfCht I inhibitors. Firstly, according to the pesticide-like rules, qualified small molecular compounds are screened out in the SPECS library, and a database 1 is established; and OfCht I is obtained from the Protein Data Bank. The three-dimensional structure of the co-crystal with the ligand is compared and analyzed to determine the active pocket; then according to the interaction analysis, the pharmacophore model based on the receptor is established, and the database 1 is screened to establish the database 2; then, using the molecular docking program, Docking and scoring the small molecule compounds in database 2 to establish database 3; finally, using the skeleton analysis module in the software, the compounds in database 3 were classified into skeletons to obtain the chitinase OfCht I inhibitor with the structure of formula (I) The research shows that the chitinase OfCht I inhibitor has better inhibitory activity for chitinase OfCht I.

The invention relates to an application of anthocyanin screened based on the molecular simulation technology in inhibiting malignant biological behaviors of colon cancer cells. On the basis of computer simulation, a large amount of anthocyanin with an outstanding docking effect is screened, cancer cells are taken as a model, and the influence of anthocyanin on malignant biological behaviors of thecancer cells is inspected, so that the anthocyanin is proved to have the capacity of promoting cancer cell apoptosis and can be applied to anti-cancer treatment research.

The invention discloses a construction method for distinguishing a model of the activity effect of PBDEs derivatives on enoyl-ACP reductase. The construction method comprises the steps of receptor andligand modeling, molecular docking and molecular dynamics simulation. The calculation result of the model is consistent with the result of an in-vitro binding activity determination experiment, and the result shows that the construction method of the model can accurately calculate the activity effect of the PBDEs derivatives on the enoyl-ACP reductase.

The invention belongs to the technical field of bioengineering, and particularly discloses a ribosome inactivated protein attenuated transformation method for blocking receptor binding, which comprises the following steps of: A, predicting a binding site, namely predicting a part where ribosome inactivated protein is bound with a receptor and the binding site by using molecular docking software; b, performing mutation transformation on the amino acid residues of the binding sites according to the prediction result in the step A; c, performing codon optimization according to the mutant gene obtained in the step B; d, synthesizing the whole gene of the target mutant optimized in the step C, and constructing an expression vector; and E, detection: detecting the target mutant gene protein constructed in the step D, detecting whether the target mutant gene protein enters cells or not through a toxicity test and a fluorescence test, and detecting whether the target mutant gene protein is expressed or not. The structural modification mode of the mutation binding site amino acid residues created by the scheme can significantly block alpha-MMC from entering cells and causing cytotoxicity thereof, thereby achieving a significant attenuation effect.

The invention provides a nucleic acid adapter computer-aided screening method based on a high-performance calculating platform, wherein the method relates to the field of molecular biology detecting technology. According to a matching principle, whether a protein structure which matches a target protein exists in a database system which is integrated in a screening platform is determined through searching; if yes, the protein structure is used as an acceptor template; and otherwise, homologous construction is performed. A primary selected nucleic acid adaptor is obtained through modular dynamics simulation and molecular docking screening as a nucleic acid adaptor candidate. The method and the nucleic acid adapter have advantages of high efficiency, high speed and high accuracy. The screening method can be combined with wet-method experiments, thereby reducing the number of the wet-method experiments, saving experiment cost and improving screening success rate. Through computer-aided simulation analysis, information such as chemical reaction mechanism between the protein and nucleic acid molecule in an adaption process is obtained. Furthermore the data are displayed on a terminal. Furthermore a data support is supplied at an aspect of disclosing a possible interaction mechanism between a corresponding biomaterial and the nucleic acid molecule. Therefore the method and the nucleic acid adapter have an important researching meaning and high use value.

The invention provides a computer-aided screening method for small molecule target nucleic acid aptamers based on a high-performance computing platform, and relates to the technical field of molecular biology. Firstly, analyze the structure of the small molecule target, and then screen in the small molecule compound library. If the matching principle is met, it will be used as the target small molecule target for molecular docking with nucleic acid molecules. If the matching principle is not met, the molecular structure can be constructed. , the small molecule target after molecular structure construction is used as the target small molecule target, and molecular docking is carried out with the nucleic acid molecule. If the docking is successful, the nucleic acid molecule is the primary nucleic acid aptamer, which solves the binding site between the small molecule target and the nucleic acid molecule Small molecular weight, weak affinity, difficulty in grasping nucleic acid molecules, many consumables, small differences in size, mass, and charge properties between the complex formed by the small molecule target and the nucleic acid itself, and the difficulty in separating the two.

A differential evolution-based protein ATP docking method. First, the ATPbind server is used to predict the protein-ATP binding residue information, which improves the prediction accuracy of the molecular spatial structure of the complex; then, the original protein-ATP is designed by population individuals. The ATP structure prediction problem is transformed into an optimization problem of searching for the optimal individual, which reduces the computational cost. Finally, by using the differential evolution algorithm to search for the optimal individual, the prediction accuracy of the protein-ATP complex structure is improved. The invention provides a protein ATP docking method based on differential evolution with low computational cost and high search efficiency.

The rational design method of the present invention to transform prolyl endopeptidase to improve its catalytic efficiency is mainly to obtain Sphaerobacter thermophiles prolyl endopeptidase through homology modeling, and obtain enzyme-substrate complex by molecular docking Structure, MD simulation stabilizes the structure, virtual saturation mutation of enzyme residues near the substrate, constrained MD simulation puts the enzyme in a perfect catalytic "near-offensive" conformation, uses MM / GBSA method to calculate binding free energy for virtual screening Mutant enzymes with improved potential catalytic efficiency were obtained. The enzyme was expressed by an Escherichia coli expression system, purified by a nickel column, and the enzyme activity and kinetic parameters of the recombinant enzyme for the nonapeptide substrate were determined by HPLC. The results show that the molecular transformation design method of the present invention can rapidly and effectively improve the catalytic activity of prolyl endopeptidase, which shows that the enzyme transformation method of the present invention is reliable.

The invention discloses a method for distinguishing the activities of peroxidase-activated proliferation receptor gamma full agonists, partial agonists and antagonists, including receptor and ligand modeling; molecular docking; traditional molecular dynamics simulation; Well-Tempered Meta ‑dynamic molecular dynamics simulation; pharmacophore construction. The method of the present invention can quickly distinguish the PPARγ activity of compounds with different structures, greatly reduces the use of chemicals and cells in the traditional toxicology experiment process in the laboratory, reduces the workload of the laboratory, and saves laboratory funds; thereby distinguishing compounds before QSAR modeling The activity of PPARγ makes the results of QSAR model closer to reality, so that traditional QSAR can be more widely used.

The invention discloses a rational design method for modifying prolyl endopeptidase to improve the catalytic efficiency of the prolyl endopeptidase. The rational design method mainly comprises the following steps: obtaining the prolyl endopeptidase of Spharobacter thermophiles through homologous modeling; carrying out molecular docking to obtain an enzyme-substrate compound structure, wherein mD simulation makes the structure stable; performing virtual saturated mutation on enzyme residues near a substrate, wherein constraint MD simulation enables the enzyme to be in a perfect catalytic near-attack-state conformation; utilizing an MM / GBSA method to calculate and combine free energy so as to virtually screen out mutant enzyme with potential catalytic efficiency improved. Enzyme expression and nickel column purification are carried out through an escherichia coli expression system, and HPLC is used for determining enzyme activity and kinetic parameters of the recombinase on a nonapeptidesubstrate. Results show that the molecular modification design method can rapidly and effectively improve the catalytic activity of the prolyl endopeptidase, which shows that the enzyme modificationmethod is reliable.