116 results about "Cadherin" patented technology

The invention provides an antibody specifically combined with CDH6 (cadherin 6) and application thereof, and particularly discloses mouse and humanized antibodies combined with CDH6 as well as a preparation method and application thereof, and the mouse and humanized antibodies have better affinity with CDH6 protein and better endocytosis activity, so that the mouse and humanized antibodies can be applied to preparation of medicines for treating tumors and the like.

The invention provides application of G3BP1 in preparation of a medicine for protecting barrier function integrity of vascular endothelial cells, and belongs to the technical field of biological medicine manufacturing. The invention provides application of G3BP1 in preparation of a medicine for protecting barrier function integrity of vascular endothelial cells. The present invention relates to G3BP1 that ensures the sustained expression of key adherent junction proteins (VE-cadherin, p120) by directly binding to and stabilizing the mRNA of these proteins; meanwhile, the G3BP1 is combined with the MYD88mRNA to promote the degradation of the MYD88mRNA, so that a permeability-promoting MYD88-ARNO-ARF6 signal channel is inhibited, especially under the condition of an inflammation period. Therefore, the G3BP1 regulates and maintains the integrity of the vascular barrier through double transcription, and a new treatment strategy is provided for damage repair of the functional integrity of the vascular endothelial cell barrier.

The invention discloses application of 2-aminoethoxy diphenyl borate (2-APB) in preparation of a medicine for improving endometrial receptivity and treating diseases related to the endometrial receptivity, and belongs to the technical field of biological medicine. A large number of experiments prove that 2-APB specifically activates a TRPM6 channel, enhances calcium ion influx and activates a calcium-dependent CaM-CaMKII-Ecadherin signal axis, so that expression of receptivity markers (such as E-cadherin and ICAM-1) is up-regulated, and endometrial receptivity is improved. The problems of poor targeting property and high toxicity of the traditional calcium ion carrier are solved, and a safe and effective treatment strategy is provided for a patient suffering from repeated implantation failure (RIF).

The present invention relates to anti-CD 103 antibodies, as well as use of these antibodies in diagnosis, prognosis, monitoring, and treatment of diseases. Also disclosed is an imaging agent comprising the anti-CD 103 antibody and a detectable label, wherein the antibody either does not block CD 103 binding to E-cadherin or at least partially blocks CD 103 binding to E-cadherin. The methods of treatment involve administering the anti CD 103 antibody which may be optionally coupled to a cytotoxic agent. Diseases to be treated include e.g. Hairy Cell leukemia, HCLv, intestinal and extraintestinal lymphomas, enteropathy-associated T-cell lymphoma (EATL), T-lymphoblastic leukemia / lymphoma (T-ALL), T-cell prolymphocytic leukemia (T-PLL), adult T cell leukemia / lymphoma (ATLL), mycosis fungoides (ME), anaplastic large cell lymphoma ALCL, cutaneous T-cell lymphoma (CTCL), Sezary Syndrome (SS), Alzheimer's disease, Parkinson's disease or multiple sclerosis.

The present invention provides a kind of radix schizonepetae extract for treating ulcerative colitis and its preparation method and application, and relates to the field of biomedicine technology. The preparation method of the radix schizonepetae extract of the present invention comprises: soaking radix schizonepetae in water, heating and boiling, condensing and refluxing, filtering, and collecting the filtrate, which is the radix schizonepetae extract. The radix schizonepetae extract of the present invention can reduce collagen deposition and intestinal epithelial cell apoptosis in the colon epithelium of ulcerative colitis, has the effect of downregulating the abnormally high expression of genes and proteins such as N-cadherin, IntegrinA1, Vinculin, TGF-β2, Srcin, etc. in the colon tissue of ulcerative colitis, reduces colon fibrosis and inflammatory damage, protects the barrier function of the colon epithelium, and has the effect of inhibiting the overexpression of Wnt 5A / B and β-Catenin proteins caused by DSS, and alleviates colon fibrosis, thereby achieving the effect of treating ulcerative colitis and alleviating colon fibrosis.

The present invention relates to methods, uses, and compositions for the treatment of cancer (e.g., a breast cancer or a pancreatic cancer). More specifically, the invention concerns the treatment of patients having cancer for the therapeutic inhibition of cancer cell growth and metastasis with an anti-Cadherin 11 monoclonal antibody with specific monoclonal antibody clones 23C6 or 3H10.

The invention provides a method for promoting differentiation of induced pluripotent stem cells to trigerm layers and application of the method in differentiation potential detection, and relates to the technical field of biologication.The method comprises the steps that the induced pluripotent stem cells are inoculated into a culture medium containing 5-20 [mu] M of E-cadherin activator 1, shaking culture is conducted to form embryoid bodies, the embryoid bodies are added into a differentiation culture medium for differentiation culture, and the embryoid bodies are obtained. Obtaining an embryoid body for activating three-germ-layer differentiation potential; inoculating the embryoid body which activates the differentiation potential of the three-germ layer into a container coated with a cell adhesion matrix, adding a differentiation culture medium, continuing differentiation culture, and performing induced differentiation to form the three-germ layer cells. The technical problems that in the prior art, when iPSC is induced to be differentiated to three germ layers through an embryoid body path, the embryoid body forming capacity is poor, the embryoid body state is poor, the long-term maintaining capacity is poor, and the endoderm differentiation and climbing-out capacity is poor due to the fact that the embryoid body is poor in wall attaching capacity after plate rotation are solved.

The invention relates to the technical field of biomedicine detection, and discloses a tumor cell marker detection system for predicting the activation state of intracellular protein kinase. Comprising a marker detection module used for qualitatively detecting epithelial cell markers, mesenchymal cell markers, cell polarity markers and extracellular matrix related markers in tumor cells; the data processing module is used for performing cross validation on an epithelial cell marker, a mesenchymal cell marker, a cell polarity marker and an extracellular matrix related marker; the dynamic weighting module is used for performing dynamic weighting on different markers based on a complex system theory, and endowing epithelial cadherin with a higher weight; and the judgment module is used for determining whether epithelial intercellular substance transformation occurs or not according to the dynamically weighted marker data, and predicting the activation state of intracellular phosphoinositide 3-kinase alpha and the invasiveness of tumor cells based on the determination result of the epithelial intercellular substance transformation.

The present invention discloses the preparation of patchouli flavonoid nanoliposomes and their application in inhalation treatment of acute lung injury, and relates to the field of medical technology. The patchouli flavonoid nanoliposomes provided by the present invention prepare patchouli flavonoids into a liposome dosage form, which has good stability and biocompatibility. The drug is administered to mice with acute lung injury, so that patchouli flavonoids can act on the mouse lungs in a targeted manner, reduce the expression of inflammatory factors such as IL-6, IL-1β and TNF-α in the mouse lungs to relieve inflammation, improve pulmonary edema, and reduce lung tissue damage, while increasing the levels of tight junction factors such as ZO-1, VE-Cadherin, E-Cadherin and Claudin5 to repair lung barrier damage. The present invention is expected to provide an effective strategy for the treatment of acute lung injury.

Peptides for use in systems that prevent the interaction of the FadA protein released from the Fusobacterium nucleatum (F. nucleatum) bacterium with E-cadherin, which has a carcinogenic effect, or the inhibition of the microorganism with antimicrobial agents and that will inhibit the carcinogenesis mechanisms of F. nucleatum infection and enable the development of therapeutic systems against infections that may occur due to the decreased immunity of patients undergoing cancer treatment with the use of peptides with anti-cancer and antimicrobial properties by developing ten peptides with FadA protein binding energy greater than −11.6 kcal / mol. Peptides with anticancer and antimicrobial properties allow the development of therapeutic systems to prevent F. nucleatum infection, to prevent cancer development after F. nucleatum infection, or to develop therapeutic systems against infections that occur due to the decreased immunity of cancer patients due to cancer treatment.

The invention discloses application of a lactic acid modified gene ENO1 inhibitor in preparation of a medicine for treating nasopharynx cancer, and relates to the technical field of biological medicines. A head and neck squamous cell carcinoma prognosis model containing seven lactylation related genes is constructed by analyzing a TCGA database, the model can effectively distinguish patient risks, the total lifetime of a high-risk group is remarkably shortened, and a risk score is an independent prognosis factor; the functions of the key gene ENO1 are deeply studied through in-vitro experiments, and experimental results show that silencing of the ENO1 gene in nasopharynx cancer 5-8F cells causes up-regulation of cell pan-lactylation level, up-regulation of MMP2 expression and down-regulation of E-cadherin expression, and migration and invasion ability of tumor cells is significantly enhanced. The prognosis model provided by the invention has an important clinical prediction value, inhibition of ENO1 can promote tumor progression through abnormal lactylation, and a new thought is provided for taking ENO1 as a treatment target.

The invention provides modRNA (Ribonucleic Acid) for treating obliterated bronchitis, and belongs to the technical field of bioengineering. The modRNA for treating obliterated bronchitis provided by the invention is composed of an IL-10 modRNA (Interleukin-10) and an IFN (Interferon)-alpha modRNA (Interferon-alpha) modRNA. The BO treatment effect is achieved by inhibiting bronchial epithelial cell epithelial-mesenchymal transition (EMT), the expression of alpha-SMA and Vimentin in lung tissue can be remarkably reduced, the expression of E-cadherin and Cytokeratin 5 can be up-regulated, microbronchial epithelial injury is repaired, collagen deposition is reduced, and the lung function is improved. The synergistic effect of the two is better than that of single gene therapy, the safety is high, and the controllability is strong.

The present invention relates to humanized nanobodies targeting cadherin 17 and their applications, and to the technical fields of immunology and molecular biology. The complementary determining region of the humanized nanobody includes a CDR1 with an amino acid sequence as shown in SEQ ID NO: 2, a CDR2 with an amino acid sequence as shown in SEQ ID NO: 4, and a CDR3 with an amino acid sequence as shown in SEQ ID NO: 6; the framework region of the humanized nanobody includes a FR1 with an amino acid sequence as shown in any one of SEQ ID NO: 1 and SEQ ID NO: 8, an FR2 with an amino acid sequence as shown in any one of SEQ ID NO: 3, SEQ ID NO: 9, and SEQ ID NO: 11, an FR3 with an amino acid sequence as shown in any one of SEQ ID NO: 5 and SEQ ID NO: 10, and an FR4 with an amino acid sequence as shown in SEQ ID NO: 7. The humanized nanobody of the present invention reduces the immunogenicity of the nanobody, improves the target binding activity and killing activity, and can be used to develop immune detection reagents, CAR-T / NK cell drugs, and antibody drugs.

Described herein is an antigen binding polypeptide that specifically binds cadherin 17 (CDH17). Also described herein is a chimeric antigen receptor (CAR) comprising the antigen binding polypeptide as the antigen binding domain, a CAR-T cell expressing the CAR, as well as a method of treating diseases or disorders caused by or involving CDH17-positive cells, such as CDH17-positive cancers, using the antigen binding polypeptide or the CAR-T cell.

An aptamer composition is disclosed which has one or more oligonucleotides that include at least one of deoxyribonucleotides, ribonucleotides, derivatives of deoxyribonucleotides, derivatives of ribonucleotides, or mixtures thereof. The aptamer composition has a binding affinity for one or more cellular membrane glycoproteins selected from the group consisting of: intercellular adhesion molecule 1 (ICAM-1), low-density lipoprotein receptor (LDLR) family members, and cadherin-related family member 3 (CDHR3), preferably intercellular adhesion molecule 1 (ICAM-1), and is configured to reduce the binding of one or more human rhinoviruses to the intercellular adhesion molecule 1 (ICAM-1).

The invention discloses application of METTL14 in inhibition of pituitary tumor cell proliferation and prognosis evaluation, and relates to the technical field of medicines. Experiments prove that when METTL14 is knocked out, E-cadherin can be lowered, and N-cadherin and waveform protein can be increased, so that the migration ability and proliferation and invasion ability of GH3 cells are promoted, and the tumor forming ability and in-vivo hormone level of pituitary growth hormone tumors are improved. Therefore, the METTL14 can be used for preparing a product for diagnosing or treating pituitary growth hormone adenoma, which is beneficial to theoretically researching pituitary adenoma and developing a novel targeted drug, and provides a new direction for finding a tumor marker or a new treatment strategy related to novel pituitary growth hormone adenoma diagnosis and controlling pituitary growth hormone adenoma.

Disclosed are inhibitors for the β-catenin / T-cell factor interaction. The inhibitors are selective for β-catenin / T-cell factor over β-catenin / phosphocadherin, and β-catenin / phosphoAPC interactions. Methods of using the disclosed compounds to treat cancer are also disclosed.

This invention relates to the field of pharmaceutical technology, specifically to the preparation of sine kinase nanoliposomes and their application in inhalation therapy for acute lung injury. The sine kinase nanoliposomes provided by this invention possess good water solubility, biocompatibility, and biocompatibility. After entering the body, they can target the lungs, reducing the expression levels of inflammatory factors such as IL-6, IL-1β, and TNF-α, thus alleviating inflammation; simultaneously, they can increase the expression levels of proteins such as ZO-1, VE-Cadherin, and Claudin5, alleviating damage to the lung barrier. Therefore, the sine kinase nanoliposomes provided by this invention can be used to prepare drugs for treating acute lung injury, and their therapeutic effect is significantly superior to that of free sine kinase monomers.

The invention discloses application of 2-fluorofucose in preparation of a medicine for relieving acute kidney injury, and belongs to the technical field of biology. In-vitro cell experiments and animal experiments prove that 2-fluorofucose can inhibit core fucosylation, competitively inhibit the activity of fucosyltransferase, down-regulate the expression of FUT8 and reduce the core fucosylation level in kidney tissues and renal tubular epithelial cells; by inhibiting core fucosylation, effectively reversing EMT phenotypic transformation induced by hypoxia reoxygenation or ischemia reperfusion, up-regulating E-cadherin expression, down-regulating alpha-SMA and Snail expression and reducing cell migration ability, phosphorylation activation of an ERK pathway is remarkably inhibited, and downstream inflammatory factor release and cell injury signal transduction are blocked, so that the ERK pathway can be used for inhibiting ERK pathway phosphorylation activation. The invention provides application of 2-fluorofucose to preparation of a medicine for relieving acute kidney injury. The invention provides a new choice for treating acute kidney injury, has the outstanding advantages of remarkable curative effect, high safety and the like, and has a wide application prospect.

To provide epithelial cadherin-specific antibodies, and their use in the diagnosis and treatment of diseases such as cancer. [Solution] The above problem is solved by an antibody or antigen-binding fragment that specifically binds one or more O-mannosylated threonine residues of E-cadherin, wherein the one or more O-mannosylated threonine residues are located within amino acid positions 467 to 472 of the E-cadherin sequence.

The invention discloses pharmaceutical application of RNA helicase DHX8, including application of the RNA helicase DHX8 in aortic dissection diagnosis, treatment and drug development. It is found for the first time that DHX8 is significantly down-regulated in aortic dissection patients, animal models and vascular endothelial cells, and overexpression of DHX8 can effectively up-regulate endothelial cell tight connection related genes and repair the endothelial barrier function. The Si DHX8 is used for transfecting human umbilical vein endothelial cells (HUVECs), and the DHX8 is knocked down, so that the tight connection gene OCLN is obviously reduced; when the OE DHX8 plasmid is used for transfecting the HUVECs and overexpressing the DHX8, the tight connection genes OCLN, JAM-A, ZO-1 and VE-cadherin are found to be obviously up-regulated. The DHX8 is used as a new target for aortic dissection diagnosis and treatment, and a detection reagent, a gene therapy vector and an agonist drug of the DHX8 have important clinical transformation values.

The invention discloses application of a small molecule compound in preparation of a medicine for protecting pulmonary vascular endothelial cells, and relates to the technical field of medicine, the application of the small molecule compound in preparation of the medicine for protecting the pulmonary vascular endothelial cells comprises the small molecule compound, and the small molecule compound serves as an active component of the medicine; the small molecule compound is used for inhibiting damage of OSM to an endothelial cell barrier. The medicine takes a small molecule compound as an active ingredient of the medicine and is used for inhibiting damage of OSM to an endothelial cell barrier, and the use dosage of the medicine is 1-10 [mu] M; the small molecule compound in the medicine is used for inhibiting the reduction of vascular epithelial cell VE-cadherin expression caused by OSM; the permeability of the endothelial cells is reduced, the damage to the endothelial barrier is prevented, and the obvious application prospect in the protection of the lung vascular endothelial cells is realized.

The invention relates to the technical field of biological medicine, in particular to application of a TMEM43 inhibitor in preparation of an anti-gastric cancer drug. According to the application disclosed by the invention, the expression profiles of the gastric cancer primary lesion and the peritoneal metastasis lesion are compared and analyzed through a single cell sequencing technology, and the TMEM43 is found to be abnormally high in expression in the peritoneal metastasis lesion. A further research proves that after the expression of the TMEM43 gene in the human gastric cancer cells is knocked down, the migration ability and the clone formation ability of the cells are obviously reduced; meanwhile, the expression levels of various markers related to the intracellular epithelial-mesenchymal transition (EMT) process also present different degrees of down-regulation (N-Cadherin, Snail, Twist1 and TMEM43 up-regulation) or up-regulation (E-cadherin up-regulation), and finally, the therapeutic effect of inhibiting the gastric cancer progress can be exerted. The key effect of TMEM43 in occurrence and development of gastric cancer is defined, and brand new theoretical guidance and technical direction are provided for research and development of gastric cancer treatment drugs.

Provided is an antitumor drug having antitumor effect and safety. Provided is an anti-cadherin 17 antibody comprising a heavy chain variable region and a light chain variable region, a drug conjugate thereof, and a composition containing the anti-cadherin 17 antibody or the drug conjugate thereof, and an application thereof as a drug.

This invention provides an antitumor drug with excellent therapeutic effects, exhibiting superior antitumor efficacy and safety. It also provides an anti-cadherin 17 antibody comprising a heavy chain variable region and a light chain variable region, a drug conjugate thereof, and a composition containing an anti-cadherin 17 antibody or a drug conjugate thereof, and their use as a drug.

This invention provides a method for promoting the differentiation of induced pluripotent stem cells (iPSCs) into three germ layers and its application in differentiation potential detection, relating to the field of biotechnology. The method includes seeding iPSCs into a culture medium containing 5 μM~20 μM E-cadherin activator 1, shaking culture to form embryoids, adding differentiation medium for differentiation culture, obtaining embryoids with activated three germ layer differentiation potential; seeding the embryoids with activated three germ layer differentiation potential into a container coated with a cell adhesion matrix, adding differentiation medium for further differentiation culture, inducing differentiation into three germ layer cells. This invention solves the technical problems in existing technologies where induction of iPSC differentiation into three germ layers via the embryoid pathway results in poor embryoid formation, poor embryoid state, poor long-term maintenance, and poor adhesion after embryoid transfer, leading to poor endoderm differentiation and migration abilities.

The invention provides an application of USP7 (ubiquitin-specific protease 7) as a target spot in preparation of drugs for treating vascular abnormal leakage diseases, and relates to the technical field of biomedicine, USP7 (ubiquitin-specific protease 7) as a deubiquitination enzyme not only regulates tumor, nerve and immune related diseases, but also is closely related to vascular endothelial cell functions. In the vascular homeostasis, the USP7 can maintain the integrity of a vascular barrier and inhibit pathological leakage by stabilizing endothelial connexin such as VE-cadherin and beta-catenin; under the inflammation or hypoxia condition, through deubiquitination of HIF-1alpha or NF-kappa B pathway components (such as I kappa B alpha), vascular endothelial cell activation can be promoted, VEGF signal-driven abnormal angiogenesis or release of inflammatory factors can be aggravated, and diabetic retinopathy, tumor vascular hyperplasia and sepsis-related vascular leakage can be participated. According to the application, verification experiments prove that USP7 has a certain protection effect on vascular permeability, and a treatment strategy is provided for vascular abnormal leakage diseases clinically.

The application of the biomarker combination in the preparation of a drug for fulminant myocarditis belongs to the field of drugs. The application is characterized in that the biomarker combination comprises Siglec-5; the biomarker combination is further selected from the group consisting of sST2, PAI-1, Siglec-5, CD163, CD40, P-Cadherin, CD14, CTLA4. The application finds that the expression of the biomarker in the plasma of a patient with fulminant myocarditis is increased, and confirms the role of the biomarker as a drug target in relieving and / or improving fulminant myocarditis. The level of the biomarker can be controlled by a drug, the diagnosis and subsequent treatment of the disease can be more intensified, and the biomarker has great application value in clinical practice.

The application discloses application of a petroleum ether extract of a root of a roadside green plant in preparation of a drug for treating colorectal cancer by regulating a PI3K / AKT / MDM2 / p53 pathway. In the application, the petroleum ether extract of the root of the roadside green plant for treating colorectal cancer is obtained by petroleum ether reflux extraction of the root of the roadside green plant. Pharmacological experiments show that the petroleum ether extract of the root of the roadside green plant treats colorectal cancer by regulating the PI3K / AKT / MDM2 / p53 signal pathway through down-regulating p-PI3K / PI3K and p-AKT / AKT ratio, up-regulating p-MDM2 and down-regulating p53 level; the extract has an anti-malignant proliferation effect, induces G1 phase arrest by targeting CDK2, up-regulating p21, down-regulating Cyclin E1-CDK2 and Cyclin D1-CDK4; the extract induces HCT-116 cell apoptosis through a mitochondrial pathway by up-regulating Bax / Bcl-2, reducing ΔΨm, releasing Cyt C, activating Caspase-9 / 3 and cleaving PARP; the extract inhibits migration and invasion of HCT-116 cells by targeting MMP9, down-regulating MMP-2, MMP-9 and N-cadherin expression and up-regulating E-cadherin expression. In addition, the extract inhibits growth of a transplanted tumor in a nude mouse transplanted tumor model by inducing apoptosis of transplanted tumor cells.

The invention belongs to the technical field of traditional Chinese medicine, and particularly relates to a sperm-nourishing seed jade decoction and application thereof to improvement of endometrial receptivity, the sperm-nourishing seed jade decoction is composed of 30 g of radix rehmanniae preparata, 15 g of cornus officinalis, 15 g of radix paeoniae alba and 15 g of angelica sinensis, by inhibiting the epithelial-mesenchymal transition (EMT) process, the expression of E-cadherin and beta-catenin is up-regulated, the expression of Vimentin is down-regulated, and the endometrial receptivity is improved. Therefore, the stability and integrity of endometrial epithelium are maintained, intimal thickening, gland hyperplasia and angiogenesis are promoted, and an effective treatment strategy can be provided for infertility caused by thin endometrium.