12 results about "GATA4" patented technology

The invention discloses application of a composition containing lycium barbarum polysaccharide. The lycium barbarum polysaccharide is used for achieving the effects of resisting aging and removing lipofuscin, particularly, the specific lycium barbarum polysaccharide LBP1C can more remarkably reduce the level of transcription factors GATA4, activate key transcription regulatory factors of autophagy, reduce aging-related secretion phenotypes and inhibit accumulation of lipofuscin, and the lycium barbarum polysaccharide LBP1C has the effects of delaying aging, whitening skin and promoting healthy aging.

The invention discloses a GATA4 gene-based MAFLD animal model construction method and application in prevention and treatment drugs, and belongs to the field of mouse model construction, and the GATA4 gene-based MAFLD MASH animal model construction method comprises the following steps: S1, hybridizing a GATA flox transgenic hybrid mouse and a Vil1-Cre transgenic mouse to obtain an F1 generation, and hybridizing the GATA flox transgenic hybrid mouse and a Vil1-Cre transgenic mouse with the genotype of GATA4 flox / +, Vil1-Cre transgenic mouse in the F1 generation to obtain a GATA4 flox / +, Vil1-Cre transgenic mouse to obtain a GATA4 flox / +, Vil1-Cre transgenic mouse; the method comprises the following steps: S1, carrying out selfing on transgenic mice with GATA4 flox / flox and Vil1-Cre to obtain F2-generation mice, and S2, sequentially giving GATA4 intestinal specific knockout mice with genotypes of GATA4 flox / flox and Vil1-Cre in the F2-generation mice with high-fat and high-cholesterol feed (HFD), and inducing to obtain an intestinal GATA4 specific knockout metabolism-related steatohepatitis (MASH) and hepatic fibrosis mouse model. The invention provides a model construction method of MASH and hepatic fibrosis animals in which the intestinal GATA4 gene is specifically knocked out, and application of the intestinal GATA4 serving as a target to preparation of drugs for preventing and treating related diseases such as liver injury and liver diseases caused by the MASH, and the intestinal GATA4 has an important clinical prospect.

The present invention discloses the use of apolipoprotein D in the preparation of drugs for treating intervertebral disc degeneration, and relates to the field of biotechnology. APOD undergoes S-palmitoylation, which competitively inhibits its ubiquitination and degradation process mediated by GNB2. S-palmitoylated APOD changes extracellular matrix metabolism and regulates cellular oxidative stress by inhibiting the GATA4-P65 signaling pathway, thereby inhibiting the aging of nucleus pulposus cells and delaying the progression of intervertebral disc degeneration. In the results of the examples of the present application, the role of S-palmitoylation in the pathogenesis of intervertebral disc degeneration is elucidated for the first time, and the in vivo supplementation is verified. Etc. The degenerative phenotype of the intervertebral disc can be significantly reversed. This application provides a new intervention target for the treatment and prognosis of intervertebral disc degeneration, and is expected to provide a potential new strategy for clinical patients with intervertebral disc degeneration to restore joint homeostasis.

The invention relates to cellular microcompartments, each microcompartment successively comprising the following layers, which are organised around at least one lumen: —at least one inner layer of human cells undergoing cardiac differentiation, expressing at least one gene chosen from PDGFRα, MESP-1, NKX2-5, GATA4, MEF2C, TBX20, ISL1 and TBX5, —at least one intermediate layer of isotonic aqueous solution, and—at least one outer hydrogel layer. The invention also relates to the cardiac tissues obtained from said microcompartments and the use thereof, particularly in the treatment of heart disease.

The invention relates to a new isolated ribonucleic acid molecule, which is a long non-coding RNA (lncRNA) molecule, and that regulates the activity of the GATA4 transcription factor. The invention discloses the use in therapy of this molecule, as well as of any interference nucleic acid molecule able to quenched it. Particular methods to induce cell differentiation and the obtention of organoids are also disclosed.

A method of detecting a predisposition to, or the incidence of, cancer in a sample comprises detecting an epigenetic change in at least one gene selected from an NDRG4 / NDRG2 subfamily gene, GATA4, OSMR, GATA5, SFRP1, ADAM23, JPH3, SFRP2, APC, MGMT, TFPI2, BNIP3, FOXE1, SYNE1, SOX17, PHACTR3 and JAM3, wherein detection of the epigenetic change is indicative of a predisposition to, or the incidence of, cancer. Also described are pharmacogenetic methods for determining suitable treatment regimens for cancer and methods for treating cancer patients, based around selection of the patients according to the methods of the invention. The present invention is also concerned with improved methods of collecting, processing and analyzing samples, in particular body fluid samples. These methods may be useful in diagnosing, staging or otherwise characterizing various diseases. The invention also relates to methods for identifying, diagnosing, staging or otherwise characterizing cancers, in particular gastrointestinal cancers such as colorectal cancers, gastric cancers and oesophageal cancers. The methods of the invention relate, inter alia, to isolating and analyzing the human DNA component from faecal samples and blood-based samples.

A senescence reprogramming composition and methods of use thereof, kits containing the composition, and their use in tissue repair, tissue regeneration, organ regeneration, reversal of senescence, or any combination thereof. In particular, SOX1, SOX2, SOX3, RCOR2, GMNN, GATA1, GATA2, GATA3, GATA4, GATA6, FOXA2, SOX7, SOX17, NKX3.1, NR5A2, C / EBP alpha, OCT4, PAX1, Klf4, Klf2, GLIS1 and c-MYC are used as inducible factors for reprogramming cells, tissues or organs to a young state. Compositions in the form of engineered nucleic acids, engineered cells, engineered proteins, chemical agents, or any combination thereof are provided for treating disease, preventing disease, modulating tissue repair, modulating tissue regeneration, or any combination thereof.

An aging reprogramming composition, a use method therefor, a kit containing the composition, and the use of the composition in tissue repair, tissue regeneration, organ regeneration, aging reversion, or any combination thereof. The present invention relates to SOX1, SOX2, SOX3, RCOR2, GMNN, GATA1, GATA2, GATA3, GATA4, GATA6, FOXA2, SOX7, SOX17, NKX3.1, NR5A2, C / EBPα, OCT4, PAX1, Klf4, Klf2, GLIS1 and c-MYC, which are used as inducing factors to reprogram cells, tissues or organs to restore a youthful state. Provided is a composition of an activation inducing factor in the form of an engineered nucleic acid, an engineered cell, an engineered protein, a chemical agent, or any combination thereof, wherein the composition is used for treating diseases, preventing diseases, modulating tissue repair, modulating tissue regeneration, or any combination thereof.

The invention discloses an application of an MCP-1 inhibitor in preparation of a medicine for preventing and treating aging-related pathological myocardial hypertrophy, the experiment reveals that MCP-1 is an aging-related pathological myocardial hypertrophy core regulatory factor for the first time, and the MCP-1 is used for up-regulating the protein expression of GATA4, IL-17A, NF-kB-p65 signals, alpha-SMA and Collagen I by activating an IL-17A / MCP-1 / CCR2 / IL-17A signal loop, so that the effect of preventing and treating the aging-related pathological myocardial hypertrophy is achieved. Further, myocardial cell senescence and senescence-related secretory phenotypes, hypertrophy and fibrosis are induced. Experiments prove that the MCP-1 inhibitor can be used for preventing and treating the SA-PCH, can improve the SA-PCH induced by Ang II and / or IL-17A, is free of liver and kidney toxicity and can obviously improve liver and kidney function decline induced by Ang II, and a new way is provided for clinical treatment of the SA-PCH.

The invention discloses a histone H3 hypoacetylation mediated heart gene expression regulation method, and relates to the technical field of biological medicines. Comprising the following steps: inducing a low acetylation state of a specific site of histone H3 in heart tissue by applying a histone acetylation inhibitor so as to inhibit gene expression of embryo transcription factors GATA4 and MEF2C; the low acetylation status is directed against lysine sites of histone H3, including at least one of H3K4, H3K9, and H3K27. The accurate epigenetic regulation and control mechanism is different from the traditional gene knockout or overexpression technology, and the transcriptional activity of the key gene for embryonic heart development is accurately regulated and controlled by regulating histone acetyl under the condition that a DNA sequence is not changed.

A diastolic function improving agent according to the present embodiment comprises a polynucleotide encoding a reprogramming factor polypeptide Gata4.

The application discloses application of palmitoyltransferase ZDHHC11 in preparation of a drug for treating osteoarthritis. ZDHHC11 catalyzes S-palmitoylation of a substrate APOD by specific binding, and then inhibits a GATA4-P65 signal pathway related to aging, and plays a protective role on aged cartilage cells. Increasing the expression level of Zdhhc11 in vivo helps to regulate extracellular matrix metabolism, inhibit cartilage cell aging, and delay the progression of osteoarthritis. The application first identifies ZDHHC11 as a key palmitoyltransferase, the expression level of which influences cartilage cell aging and osteoarthritis phenotype, and clarifies a downstream molecular mechanism of S-palmitoylation mediated by ZDHHC11 in delaying the progression of osteoarthritis, and verifies that increasing the expression level of Zdhhc11 in vivo can significantly reverse the osteoarthritis phenotype.