51 results about "Competitive binding" patented technology

The invention discloses an antibody for detecting indol sulfate, a detection kit and application of the antibody, and the antibody can be specifically combined with indol sulfate and has high combination activity. The detection kit detects the content of indoxyl sulfate in a to-be-detected sample through a competitive binding reaction of an immunomagnetic bead coated indoxyl sulfate antibody, an antigen in the sample and an alkaline phosphatase labeled indoxyl sulfate antigen, and has important economic value and social significance.

The invention provides a method for analyzing interaction between procambarus clarkia arginine kinase and shark source nano antibody. The method comprises the following steps: performing three-dimensional structure prediction on a VNAR sequence, and screening a high-confidence VNAR model by using a Laplace map; docking an amino acid sequence corresponding to the VNAR model with an arginine kinase sequence to obtain an optimal compound model, and analyzing an interaction site of an arginine kinase epitope region and a nanometer antibody complementary determining region CDR3; performing molecular dynamics simulation on the compound model, calculating conformational change indexes and binding free energy through energy optimization, system balance and extended simulation sampling, and outputting a binding stability sequence of the nano antibody and arginine kinase; the method comprises the following steps: screening out a high-stability nano antibody, pre-incubating a fusion protein of the high-stability nano antibody and immobilized arginine kinase to form a compound, adding serum of an allergic patient for competitive binding, quantifying the binding activity of residual IgE through an immunodetection technology, and verifying the inhibition effect of the shark source nano antibody on the sensitization effect of arginine kinase.

The invention relates to the fields of pharmacology and molecular biology, and discloses an autophagy inhibitory polypeptide competitively combined with an LIR docking site of an autophagy-related protein LC3 and application of the autophagy inhibitory polypeptide. Through molecular docking simulation, through LIR docking sites of targeted LC3 protein, 794 bioactive polypeptides which can be combined are screened out. Functional result analysis shows that peptide 3 #, peptide 4 # and peptide 5 # are competitively combined with LIR docking sites of the LC3 protein, so that formation of autophagy vesicles is inhibited in a targeted manner, and proliferation and survival of autophagy-dependent pancreatic cancer cells are effectively inhibited; the strategy is combined with chemotherapeutic drugs to show a synergistic effect, and the pancreatic cancer resisting curative effect is remarkably enhanced.

The invention discloses application of inhibiting combination of Hic-5 and SMAD7 and / or inhibiting Hic-5 in treatment of pulmonary arterial hypertension, and finds that PLEKHH2 and SMAD7 have competitive combination with Hic-5 protein in lung tissue, more SMAD7 can be released into cytoplasm by preventing combination of Hic-5 and SMAD7, and SMAD2 / 3 phosphorylation is inhibited for the first time, so that the purpose of treating the pulmonary arterial hypertension is achieved. The invention provides a new research and development direction for the development of pulmonary arterial hypertension treatment medicines.

This invention provides a monoclonal antibody 6D11 and its applications. The CDR amino acid sequence of the heavy chain of the anti-monoclonal antibody 6D11 is shown in SEQ ID No. 1, and the CDR amino acid sequence of the light chain is shown in SEQ ID No. 2. This invention also provides the application of monoclonal antibody 6D11 in the preparation of drugs for treating dengue virus infection. The monoclonal antibody 6D11 of this invention has advantages such as competitive binding to DENV1-4NS1 protein, inhibition of vascular leakage symptoms, and protection against lethal damage from DENV infection in vivo, and has significant potential therapeutic value against dengue virus.

The application discloses a preparation method and application of an amphiphilic tyrosinase copper competitive binding agent. Two new compounds P4TA or P2TA are synthesized by coupling tyramine TA with 4,4',4'',4'''-(porphyrin-5,10,15,20-tetrayl) tetrakisbenzoic acid TCPP or 3,7,12,17-tetramethyl-8,13-diethyl-2,18-porphyrin dipropionic acid PPIX. An optimal synthesis process of P4TA and P2TA is provided, and an experience is provided for related synthesis. The obtained P4TA and P2TA can recognize tyrosinase and are good copper ion binding reagents, and the two compounds exhibit a significant inhibitory effect on TYR. The application can be used for tyrosinase targeted inhibition and copper ion metabolism intervention in biological medicines and food.

The invention discloses a compound and application thereof. The invention provides a series of novel compounds with chemical structures reported for the first time. An activity research result shows that the series of novel compounds can competitively inhibit the combination of a natural substrate simulant of an SH2 substructural domain in a Cbl-b TKB structural domain and the SH2 substructural domain in the Cbl-b TKB structural domain. The competitive inhibition effect of the series of novel compounds can reduce the function of the Cbl-b protein, so that the continuous activation of T cells can be caused, and the tumor removal capability mediated by the T cells can be enhanced. Therefore, the series of novel compounds have the prospect of being developed into antitumor drugs. In addition, the series of novel compounds can also be developed into a reagent which is competitively combined with the SH2 substructural domain in the Cbl-b TKB structural domain, and the effect of the reagent includes but is not limited to a competitive inhibitor reference substance of the SH2 substructural domain in the Cbl-b TKB structural domain.

The application discloses a ricin toxin detection sensor based on competitive binding of ricin to mitochondrial adenine nucleotide translocator (ANT) and a detection method, which comprises ANT protein, hollow dialysis fiber, chemical cross-linking agent and fluorescently labeled ATP. When in use, the ANT is first fixed on the inner wall of the hollow fiber dialysis membrane and the fluorescently labeled ATP (cy5-12-ATP or cy3-12-ATP or DEPC-12-ATP) is added; then, it is placed in the to-be-detected solution for 30-60 seconds, and then is placed under a fluorescence detection instrument (such as a fluorescence microscope) for observation, so that the presence or absence of the ricin toxin and the approximate concentration of the toxin are determined; then, the relative intensity of the fluorescence of the to-be-detected solution is determined; a standard curve of the corresponding relationship between the concentration of the fluorescent group and the concentration of the toxin is established; and the concentration of the ricin toxin in the to-be-detected solution is obtained by substituting the concentration of the fluorescent group of the to-be-detected solution into the above standard curve and performing calculation. The application can effectively improve the detection efficiency, simplify the detection method and be widely applied in the society.

The invention discloses an application of long-chain non-coding RNA (Ribonucleic Acid) Cslnc256 in regulating and controlling an anti-colletotrichum gloeosporioides posttranscriptional mechanism of a tea tree. According to the application of the long-chain non-coding RNA Cslnc256 in regulating and controlling the colletotrichum gloeosporioides resisting post-transcription mechanism of the tea tree, the long-chain non-coding RNA Cslnc256 can accurately act on Cslnc256-CsmiR395-CsSultr2 in the tea tree body; therefore, the defense mechanism of the plant is efficiently activated. When the expression of the Cslnc256 is inhibited, the competitive binding capacity of the Cslnc256 and the CsmiR395 is reduced, so that the concentration of the free CsmiR395 is increased, and further, the activity of the Cslnc256 on the target gene CsSultr2; 1 is an inhibitory effect. The regulation and control process can reduce the activity of sulfate transporter protein in the tea tree body, so that sulfate ions are accumulated in leaves, and the sulfate ions serving as important defense signal molecules can effectively improve the resistance of the tea tree to colletotrichum gloeosporioides and relieve scab expansion and tissue damage caused by pathogenic bacterium infection.

The present invention relates to a bispecific fusion protein targeting TNF-α and IL-17A, a polynucleotide encoding the same, a method for preparing the same, and uses thereof. The bispecific fusion protein targeting TNF-α and IL-17A is a dimer with a symmetric structure and contains, from the N-terminus to the C-terminus, three structural functional regions: a soluble TNF receptor or a portion thereof, a human IgG Fc fragment, and a functional domain that competitively binds to IL-17A or an anti-IL-17A domain. The fusion protein can effectively bind to both TNF-α and IL-17A and has the effect of blocking their signaling pathways. The fusion protein has good stability, specificity, and biological activity.

The invention discloses a DNA (Deoxyribose Nucleic Acid) probe ATP-3 and application thereof. The DNA (Deoxyribose Nucleic Acid) probe ATP-3 disclosed by the invention comprises DOX-3 and DOX-3-CP (Chlorinated Drug detection can be realized by using the DNA probe ATP-3 based on a non-label method DNA biosensor. Based on a double-strand competitive binding mechanism (DOX-3 and DOX specific binding leads to double-strand dissociation) of a DNA probe ATP-3, and in combination with a fluorescence switching characteristic (fluorescence enhancement during double-strand binding and quenching during dissociation) of an embedded fluorescent agent DAPI, trace detection of drugs is realized. By using a fluorospectro photometer as a detection auxiliary instrument, the method has the advantages of sensitive result, simplicity in operation, lower cost and the like.

The invention relates to the technical field of pharmaceutical preparations, and discloses a doxorubicin and cyclophosphamide liposome compound injection which is prepared from doxorubicin hydrochloride, cyclophosphamide, hydrogenated soybean phosphatidylcholine, cholesterol, polyethylene glycol derivative phospholipid, anhydrous magnesium sulfate, L-arginine and a sucrose octasulfate ammonium solution. Magnesium ions introduced into an inner water phase participate in competitive binding, doxorubicin and sucrose octasulfate are induced to form a loose co-precipitation structure with lattice defects, hydrophilic cyclophosphamide is physically filled and cured by using micro gaps, and efficient encapsulation of non-gradient dependent drugs is realized. Meanwhile, an in-situ pH buffer system is constructed by using L-arginine, protons generated in a drug loading process are neutralized, an internal water phase is maintained in a neutral environment, and acid-catalyzed hydrolysis of cyclophosphamide is effectively inhibited. According to the invention, the double-drug encapsulation efficiency and storage stability of the compound liposome are obviously improved.

The invention provides a small peptide for preventing and treating colon cancer and application thereof, and belongs to the technical field of biological medicine. Through structural simulation and functional verification, a polypeptide capable of specifically inhibiting G3BP1 lactylation in colon cancer cells in a targeted manner is screened out. The polypeptide inhibits the lactic acid modification level of G3BP1 by simulating a G3BP1 lactic acid recognition site and competitively combining with lactic acid enzyme, so that the G3BP1 mediated autophagy process is blocked, and finally proliferation and migration of colon cancer cells are inhibited. In-vitro cell experiments (including cell proliferation, migration and autophagy level analysis) and in-vivo transplantation tumor animal experiments prove that the oligopeptide can significantly inhibit growth and tumor formation of colon cancer cells. The discovery provides a new strategy and candidate drug molecules for molecular targeted therapy of colon cancer.

The application discloses a method for screening multifunctional peptides of perilla albumin source for treating diabetes and hypertension, which comprises the following steps: obtaining perilla albumin sequence, predicting the potential of perilla albumin as DPP-Ⅳ and ACE inhibitory peptide source, performing computer simulation digestion, and screening DPP-Ⅳ and ACE inhibitory peptides. Through the bioactive peptide database BIOPEP-UWM, 40 perilla albumin sequences are predicted for active fragments, and it is found that perilla albumin is rich in a large number of fragments with DPP-Ⅳ and ACE inhibitory activity. Perilla albumin is subjected to computer simulation digestion, polypeptides capable of resisting gastrointestinal digestion are obtained, and perilla albumin source multifunctional peptides with DPP-Ⅳ and ACE inhibitory activity are screened through related activity prediction and molecular docking. The practicability of the multifunctional peptides is predicted, and two multifunctional peptides without toxicity, allergenicity, bitterness and hemolytic activity, namely CDAF and CCAL, are screened. The two multifunctional peptides inhibit the catalytic activity of DPP-Ⅳ and ACE by competitively combining with the active centers of DPP-Ⅳ and ACE, so as to play the roles of reducing blood sugar and blood pressure.

The present invention provides antibodies that specifically bind to FGFR3, as well as methods for treating or preventing cancer, such as bladder cancer. Also provided herein are isolated antibodies or antigen-binding fragments thereof that specifically bind to FGFR3 or its antigen-binding fragments, which bind to the same FGFR3 epitope as the antibodies or antigen-binding fragments described herein or compete for binding to FGFR3. The present invention also provides complexes comprising such antibodies or antigen-binding fragments bound to FGFR3 or its antigen-binding fragments, which are also part of the present invention.

A computer-implemented framework for designing high-efficiency and high-specificity nucleic acid molecules targeting transfer RNA (tRNA) and its derivatives (tDRs). The framework comprises two primary algorithms. The first, tBOND-G, designs guide RNAs (gRNAs) for Cas13-mediated tRNA cleavage by calculating physical parameters, including target site accessibility and binding energy, and processing them through a Support Vector Machine (SVM) model to predict cleavage efficiency. The second algorithm, tBOND-L, designs therapeutic Locked Nucleic Acid-modified antisense oligonucleotides (LNA-ASOs) that specifically target a tDR without binding to its parent tRNA. This method utilizes a processor to derive an efficiency score based on relative binding affinity and a specificity score based on simulated competitive binding environments.

The invention relates to a radiolabeled Exendin-4 polypeptide probe precursor and application thereof, and belongs to the technical field of radiopharmaceutical chemistry and nuclear medicine diagnosis and treatment. The radioactive labeled Exendin-4 polypeptide probe precursor is R-HBED-CC-PEGn-Exendin-4, the general formula structure of the radioactive labeled Exendin-4 polypeptide probe precursor is shown in the specification, and n is equal to 3, 6 or 12; r is-OH or PEG chains with different lengths are introduced into R-HBED-CC-Exendin-4 to modify the medicine, so that the pharmacokinetics of the medicine is changed. Through a radionuclide labeling experiment, an in-vitro cell uptake experiment, an in-vitro receptor competitive binding experiment, biological distribution, model mouse imaging and other experiments, the targeting and in-vivo metabolism level of the novel probe are explored. And a novel targeted GLP-1R diagnosis and treatment drug with a clinical application prospect is screened out.

The invention provides an aptamer colorimetric sensor based on Au (at) Ce MOF and a preparation method and application thereof, the aptamer colorimetric sensor comprises a signal probe and a capture probe, the signal probe is obtained by mixed incubation of activated cDNA and Au (at) Ce MOF, and the capture probe is obtained by co-incubation of streptavidin modified magnetic beads and an aptamer. According to the aptamer colorimetric sensor based on Au-Ce MOF, Au-Ce MOF with high oxidase-like activity is synthesized on Ce MOF through a chemical reduction method, a rapid colorimetric aptamer sensor is developed on the basis of the competitive binding principle of MB-Apt, and the aptamer sensor is used for efficiently detecting DON and Au-Ce MOF-cDNA and target specificity, so that the aptamer colorimetric sensor has the advantages of high recovery rate, low detection limit and excellent anti-interference capability, and the sensor can be used for detecting DON and Au-Ce MOF-cDNA and target specificity. The huge practical application potential is realized in the aspect of detecting DON pollution in a food matrix.

Provided are systems / kits and methods for the preparation of cDNA from a sample of total RNA, in which excess RNA species such as rRNA and tRNA are depleted from the cDNA products via prevention of reverse transcription through competitive binding of DNA oligonucleotide probes that prevent binding and / or extension of randomer reverse primers. This process allows downstream high-throughput sequencing on a library prepared from the cDNA to efficiently profile RNA expression without significant loss of accuracy due to excess RNA species occupying too many reads. Compared to other approaches for excess RNA depletion, such as those based on RNAse H systems, the systems and methods provided herein neither require additional enzymes beyond reverse transcriptase, nor extra purification before reverse transcription.

This invention belongs to the field of biomedicine and discloses the application of palmitoyltransferase ZDHHC21 in the preparation of drugs for treating breast cancer. This invention demonstrates that ZDHHC21 knockdown upregulates RIPK1 expression, which is related to signal feedback induced by CD82 palmitoylation deficiency. Depalmitoylated CD82 competitively binds to RIPK1 inhibitory molecules, thereby releasing the regulation of RIPK1, promoting the interaction and phosphorylation activation of RIPK1 and RIPK3, and subsequently upregulating MLKL expression and inducing its activation. Downstream activation of Caspase-3 ultimately initiates necroptosis. A specific regulatory axis of "ZDHHC21–CD82–pan-apoptosis" is established. This provides a potential novel therapeutic target for triple-negative breast cancer and offers a theoretical and experimental basis for therapeutic strategies targeting tumor cell death. Further research can explore the role of this regulatory axis in vivo, providing support for clinical translation.

The invention relates to the technical field of medicines, and in particular discloses a novel application of RDV (Registevir, RDV) in preparation of a medicine for treating NUDT1 (NUDT1, also known as MTH1) high-expression cancer, in particular to a novel application of RDV in preparation of a medicine for treating NUDT1 (NUDT1, also known as MTH1) high-expression cancer. According to the application disclosed by the invention, various means such as an ATP competitive binding experiment, a molecular docking experiment, a thermal shift assay (TSA) experiment, a Western blot experiment, a long-chain PCR (Polymerase Chain Reaction) experiment and a cell proliferation experiment are used for verifying that the redefovir can be combined with an ATP binding site of NUDT1 protein, the protein stability is reduced, and the degradation of the NUDT1 protein is promoted, so that the level of 8-oxoguanine (8-oxoG) in DNA (Deoxyribonucleic Acid) under oxidative stress is increased, and the proliferation of cancer cells is obviously inhibited. According to the application, the potential of the ridecevir as the NUDT1 inhibitor is disclosed for the first time, high expression of the NUDT1 is used as an accompanying diagnosis index of treatment by using the ridecevir, and a brand-new scheme is provided for realizing accurate anti-cancer treatment. The application is essentially different from known antiviral effects and mechanisms of the ridecevir.

Provided are polypeptides capable of inhibiting MERS-like coronavirus infection and applications thereof. Based on the membrane fusion invasion characteristics of the S2 subunit of the MjHKU4r-CoV coronavirus S protein, the inventors take the HR1 functional domain as a target, and invent a group of polypeptides capable of efficiently inhibiting the membrane fusion invasion process of the MjHKU4r-CoV coronavirus. These polypeptides can inhibit the formation of the 6-HB six-helix fusion core by competitively binding to the HR1 functional domain of the virus, thereby efficiently blocking the process of the MjHKU4r-CoV coronavirus invading target cells. The present application can provide efficient preventive and therapeutic candidate drugs for the prevention and treatment of the MjHKU4r-CoV coronavirus with potential high pathogenicity and cross-species transmission.

The present invention relates to a bispecific fusion protein targeting TNF-α and IL-17A, a polynucleotide encoding same, a preparation method therefor, the use thereof, etc. The bispecific fusion protein targeting TNF-α and IL-17A is a dimer which has a bilaterally symmetrical structure, and comprises, in the order from N-terminal to C-terminal, three structural functional regions: a soluble TNF receptor or a portion thereof, a human IgG Fc fragment, and a functional domain competitively binding to IL-17A or against IL-17A. The fusion protein can effectively bind to both TNF-α and IL-17A, and has the effect of blocking the signal pathway thereof. The fusion protein has a good stability, specificity and biological activity.

Provided are a polypeptide capable of inhibiting a MERS-like coronavirus infection, and a use thereof. On the basis of a membrane fusion invasion feature mediated by an S2 subunit of a MjHKU4r-CoV coronavirus S protein, a group of polypeptides are invented by using the HR1 functional domain of the protein as a target. The polypeptides can efficiently inhibit the membrane fusion invasion process of a MERS-like coronavirus MjHKU4r-CoV. By competitively binding to a viral HR1 functional domain, these polypeptides inhibit the formation of a viral 6-helix bundle (6-HB) fusion core, thereby efficiently blocking the process of the coronavirus MjHKU4r-CoV invading a target cell. The present invention can provide an efficient preventive and therapeutic candidate drug for prevention and treatment of the MERS-like coronavirus MjHKU4r-CoV having potential high pathogenicity and cross-species transmission.

The invention discloses application of polypeptide for inhibiting expression of inflammasome NLRP3 in preparation of pneumonia treatment drugs, and belongs to the technical field of biological medicines. Derived peptide is obtained based on a DTX4 protein functional domain, the peptide fragment is derived from an interaction region of DTX4 and RNA binding protein HuR, and the action mechanism of the peptide fragment is competitive binding with the HuR, so that the stabilizing effect of the HuR on mRNA of various inflammatory factors is blocked, the mRNA is promoted to be degraded, and expression and secretion of the inflammatory factors are inhibited from the level after transcription. The polypeptide disclosed by the invention has the potential of being developed into a novel anti-infectious pneumonia treatment medicine, and a brand new strategy is provided for treating bacterial infectious pneumonia.

The invention discloses a DNA enhancer of ADAR1, a SELEX-HTCFQ platform screened by the DNA enhancer and application of the DNA enhancer of the ADAR1, the activity of the ADAR1 is enhanced through allosteric regulation, so that the inhibition effect of the ADAR1 on ZBP1 is enhanced, excessive inflammatory response is effectively relieved, and meanwhile subtle balance of an immune system is maintained. According to the SELEX-HTCFQ screening method, exponential enrichment system evolution and high-throughput competitive fluorescence quenching are combined, and the SELEX-HTCFQ screening method is used for screening the ADAR1 specific enhancer. Based on a mechanism that ADAR1 is competitively combined with Z-nucleic acid to naturally inhibit ZBP1, the SELEX-HTCFQ screening method performs affinity and selectivity dual evaluation, the aptamer A4 is successfully identified, and the ADAR1 selectivity of the aptamer A4 is 40 times that of ZBP1.

The application belongs to the technical field of short peptide medicine, and specifically discloses a Maged1 competitive short peptide and application thereof.The Maged1 competitive short peptide is short peptide MP1 or short peptide MP2, and the amino acid sequence is shown as SEQ ID No.1 or SEQ ID No.2.Experiments prove that the Maged1 competitive short peptide can compete with Maged1 to combine with P2X3 receptors, thereby inhibiting the activation of Maged1 on P2X3 receptors, and has a good clinical application prospect in the treatment of chronic pain.

The application provides a small peptide for preventing and treating colon cancer and an application thereof, and belongs to the technical field of biological medicine. Through structure simulation and function verification, a polypeptide capable of specifically targeting and inhibiting G3BP1 lactylation in colon cancer cells is screened. The polypeptide competitively binds to lactylase by simulating the G3BP1 lactylation recognition site, thereby inhibiting the lactylation modification level of G3BP1, blocking the autophagy process mediated by G3BP1, and finally inhibiting the proliferation and migration of colon cancer cells. Through in vitro cell experiments (including cell proliferation, migration and autophagy level analysis) and in vivo tumor transplantation animal experiments, it is proved that the short peptide can significantly inhibit the growth and tumor formation of colon cancer cells. This finding provides a new strategy and candidate drug molecule for the molecular targeted treatment of colon cancer.

This invention discloses a highly sensitive LCN2 detection kit and its preparation method for assessing the prognostic risk of patients with stress-induced cardiomyopathy. The kit contains a signal probe composed of rare-earth-doped upconversion nanoparticles and an LCN2-specific DNA aptamer, as well as a complementary oligonucleotide quenching probe with a quenching group. Its core principle is based on fluorescence resonance energy transfer regulated by competitive binding: when the target protein LCN2 is absent, the binding of the two probes leads to luminescence quenching; when LCN2 is present, they competitively bind to the aptamer and dissociate the quenching probe, thereby restoring upconversion luminescence. This homogeneous detection method effectively avoids the interference of autofluorescence in biological samples by utilizing near-infrared excitation. Combined with the high stability and specificity of the aptamer, it achieves a simple, rapid, highly specific, and ultra-sensitive quantitative detection of LCN2 protein in serum, providing a reliable tool for clinical prognostic assessment.

This invention discloses the use of oligomycin A in the preparation of a drug for competitively inhibiting EphB3 to reverse lorlatinib resistance, belonging to the field of biomedical technology. This invention experimentally discovered that EphB3 is a key factor mediating lorlatinib resistance in lung cancer, and that existing oligomycin A can effectively reverse EphB3-mediated resistance by competitively binding to EphB3. Based on this, this invention protects the use of oligomycin A in the preparation of a drug for reversing lorlatinib resistance in tumors (especially ALK-positive non-small cell lung cancer). Simultaneously, this invention also protects a therapeutically effective pharmaceutical composition comprising oligomycin A and lorlatinib, and a non-therapeutic method for reversing cellular resistance to lorlatinib in vitro. This invention provides a novel and effective solution for overcoming lorlatinib resistance in clinical practice.