53results about "Cell cycle regulated proteins" patented technology

The invention belongs to the field of biology, and discloses a cdc42 gene knockout HCT-8 cell line and application thereof, the taxonomic name of the cdc42 gene knockout HCT-8 cell line is Homo sapiens, the cdc42 gene knockout HCT-8 cell line is preserved in Guangdong Microbial Culture Collection Center, and the preservation number is GDMCC NO: 66616; the preservation date is July 01, 2025; the preservation address is the fifth floor of building 59, No.100 courtyard, Xianlie Middle Road, Guangzhou City, Guangdong Province. According to the invention, a cdc42 gene in an HCT-8 cell is knocked out by adopting a CRISPR-Cas9 technology so as to construct a cdc42 gene knocked-out HCT-8 cell line, and the cdc42 gene knocked-out HCT-8 cell line is used as a cryptosporidium parvum cell infection model.

The present invention addresses the problem of providing: a human astrocyte population obtained by differentiation induction from astrocyte precursor cells derived from human iPS cells; a method for producing the human astrocyte population; and a method for evaluating a test substance using the human astrocyte population. According to the present invention, provided is a human astrocyte population obtained by differentiation induction from astrocyte precursor cells derived from human iPS cells, the human astrocyte population comprising at least 90% of human astrocytes, the human astrocytes comprising at least 90% of the human astrocytes, and the human astrocytes comprising at least 90% of the human astrocytes, the human astrocytes comprising at least 90% of the human astrocytes, and the human astrocytes comprising at least 90% of the human astrocytes. A) CDKN2A is positive, b) at least one gene marker selected from the group consisting of IGFBP5, NNMT, HLA-DRB1, and HLA-DRB5 is positive, and c) the C3 expression level standardized with GAPDH of a reference gene is 0.05 copy number / copy number or less.

Provided herein are complexes, methods, and therapeutic uses for inducing and / or enhancing the ubiquitination of proteins such as NRF2 by beta-transducin repeat containing E3 ubiquitin protein ligase (BTRC).

The invention discloses an oncolytic virus and application of the oncolytic virus in preparation of tumor inhibition drugs. The oncolytic virus is a lentiviral vector, and the lentiviral vector comprises polynucleotide encoding p16 protein or a bioactive part of the p16 protein containing CDKN2A gene, and can effectively inhibit growth of cancer related to CDKN2A gene mutation, so that the problem that the existing oncolytic virus has biological safety risk in delivery of cancer suppressor genes is effectively solved.

This disclosure provides for engineered T cell Receptors (TCRs), cells comprising the TCRs, and methods of making and using the TCRs. The current disclosure relates to TCRs that specifically recognize epitope(s) from tumor antigen NDC80 CT. Accordingly, aspects of the disclosure relate to an engineered T-cell Receptors (TCRs), nucleic acids encoding the TCRs, and cells comprising the nucleic acids and TCRs. Also provided are compositions comprising the cells, nucleic acids, or engineered TCRs of the disclosure, methods of making the cells and methods of using the embodiments of the disclosure for therapeutic treatments.

Described herein is a chimeric antigen receptor (CAR) platform with the ability to (a) serve as an ON / OFF switch (with the ability for tenability / titrability), (b) sense multiple antigens and perform logic computations, and / or (c) independently regulate multiple signaling pathways. The compositions provided herein permit the degree of control and discrimination necessary to optimize CAR T cell therapy. Also described herein are cells comprising such compositions and the use of these compositions and / or cells in the treatment of cancer.

This document provides methods and materials for assessing and / or treating mammals (e.g., humans) having prostate cancer. For example, methods and materials that can be used to determine whether or not a prostate cancer (e.g., a castration-resistant prostate cancer (CRPC)) is likely to respond to a particular cancer treatment (e.g., treatment with one or more one or more lutetium-177 (177Lu)-PSMA therapies) are provided. Methods and materials for using one or more cancer treatments to treat a mammal (e.g., a human) identified as likely to respond to a particular cancer treatment are also provided.

Described are affinity purification system that includes a carrier / surface that is non-cellular, and sliding clamp (SC) protein, and methods for purifying proteins that bind to the SC. The SC is associated with the carrier / surface via covalent / non-covalent interactions. To attain control of coupling site, the SC can be mutated via site-directed mutagenesis to introduce an exogenous residue and, the exogenous internal residue is conjugated to the non-cellular surface through the linker. The SC can also be coupled to the carrier via non-covalent interactions such as the affinity interactions involved in ligand / binding partner complex formation.The SC-based affinity purification system are used in a purification column as bait proteins, to isolate SC binding partners or non SC-binding proteins engineered to contain a SC binding site prior to its purification.

The present disclosure provides a pharmaceutical association for use in the treatment, prevention and / or diagnostic of a neoplastic disease, said association comprising at least one growth factor receptor-binding compound, which activates at least one growth factor receptor of a neoplastic cell, and at least one bioactive carrier forming at least one covalent or non-covalent interaction with said at least one growth factor receptor-binding compound, and wherein said association reduces or suppresses, in the neoplastic cell, the gene expression of at least one cyclin D and / or reduces or suppresses the formation of at least one complex formed between said at least one cyclin D and at least one of cyclin dependent-kinase 4 or 6.

The present disclosure provides a pharmaceutical association for use in the treatment, prevention and / or diagnostic of a neoplastic disease, said association comprising at least one growth factor receptor-binding compound, which activates at least one growth factor receptor of a neoplastic cell, and at least one bioactive carrier forming at least one covalent or non-covalent interaction with said at least one growth factor receptor-binding compound, and wherein said association reduces or suppresses, in the neoplastic cell, the gene expression of at least one cyclin D and / or reduces or suppresses the formation of at least one complex formed between said at least one cyclin D and at least one of cyclin dependent-kinase 4 or 6.

A genetic construct is described having a nucleotide sequence A (Cre+ERT2) with a nucleotide sequence SEQ ID NO. 1 coding for an enzyme recombinase Cre and a sequence SEQ ID NO. 2 coding for a mutated receptor for estrogen ERT2; or a nucleotide sequence A′ with a nucleotide sequence SEQ ID NO. 3 coding for the fragment A of the diphtheria toxin (DTA); and a nucleotide sequence B with a nucleotide sequence SEQ ID NO. 4 coding for the inhibitor of a mutant cyclin dependent kinase (CDK) p27K−.

The disclosure relates to adeno-associated (AAV) particles comprising viral genomes encoding cyclin-dependent kinase-like 5 (CDKL5) proteins and peptides, compositions comprising said AAV particles, and methods for making and delivering said AAV particles to a cell or subject. The AAV particles, compositions, and methods of the present disclosure are useful for the treatment of subjects who have, have been diagnosed with having, or are at risk of having a CDKL5 deficiency disorder (CDD), developmental and epileptic encephalopathy 2, atypical Rett syndrome, and / or other CDKL5-related disorders or at least one symptom thereof.

This disclosure provides for engineered T cell Receptors (TCRs), cells comprising the TCRs, and methods of making and using the TCRs. The current disclosure relates to TCRs that specifically recognize epitope(s) from tumor antigen NDC80 CT. Accordingly, aspects of the disclosure relate to an engineered T-cell Receptors (TCRs), nucleic acids encoding the TCRs, and cells comprising the nucleic acids and TCRs. Also provided are compositions comprising the cells, nucleic acids, or engineered TCRs of the disclosure, methods of making the cells and methods of using the embodiments of the disclosure for therapeutic treatments.

Provided herein are modified cyclin F polypeptides and nucleic acid molecules encoding the same. In particular, provided herein are modified cyclin F polypeptides that have increased cytoplasmic targeting compared to wild-type cyclin F polypeptides, and functional, truncated modified cyclin F polypeptides, and nucleic acid molecules encoding the same. Also provided herein is the use of the modified cyclin F polypeptides and encoding nucleic acid molecules for enhancing motor neuron survival, inhibiting motor neuron degeneration and treating neurodegenerative conditions, in particular those associated with neuronal TDP-43 proteinopathy.

The present invention relates to the technical field of biology, in particular to a porcine bone marrow macrophage, a construction method therefor, and the use thereof. The method comprises a method of performing electroporation on a primary porcine bone marrow macrophage to introduce pTERT, pCDK4(R24C) and pCCND1 genes into same so as to immortalize the porcine bone marrow macrophage; a method of continuously constructing, on the basis of the cell, a porcine bone marrow macrophage cell line stably expressing the Cre gene; and a method of removing a screening marker gene on a gene-deleted recombinant virus strain by means of using the cell line. The methods comprise: by means of electroporation, separately introducing into the primary porcine bone marrow macrophage transposon vectors and transposase vectors which respectively contain pTERT, pCDK4(R24C) and pCCND1, and screening out an immortalized porcine bone marrow macrophage; and continuing to perform electroporation on the immortalized porcine bone marrow macrophage to introduce the Cre gene so as to enable same to stably express a Cre protein. The present invention can be used for removing screening marker genes during the process of constructing gene-deleted recombinant virus strains.

The present invention concerns genetically modified immune cell, which (a) overexpresses p21 compared to a corresponding non-genetically modified immune cell, (b) expresses at its surface a recombinant antigen binding domain, and (c) is a monocyte, a macrophage, or a dendritic cell, as well as methods for producing them, pharmaceutical compositions comprising them, and their use as a medicament, in particular in the treatment of a subject suffering from a cell proliferative disorder, in particular cancer.

The present invention provides CDCA1-derived epitope peptides having the ability to induce cytotoxic T cells. The present invention also provides polynucleotides encoding the peptides, antigen-presenting cells presenting the peptides, and cytotoxic T cells targeting the peptides, as well as methods of inducing antigen-presenting cells or CTLs. The present invention also provides compositions and pharmaceutical compositions containing them as active ingredients. Furthermore, the present invention provides methods of using the peptides, polynucleotides, antigen-presenting cells, cytotoxic T cells, or pharmaceutical compositions of the present invention to treat and / or prevent cancer, and / or prevent postoperative recurrence thereof. Methods of inducing an immune response against cancer are also provided.

An object of the present invention is to provide a human astrocyte cell population that is differentiated from astrocyte progenitor cells derived from human iPS cells, a manufacturing method for the human astrocyte cell population; and an evaluation method for a test substance using the human astrocyte cell population. According to the present invention, there is provided a human astrocyte cell population that is differentiated from astrocyte progenitor cells derived from human iPS cells, the human astrocyte cell population including at least 90% of human astrocytes, in which in the human astrocytes, a) CDKN2A is positive, b) at least one gene marker selected from the group consisting of IGFBP5, NNMT, HLA-DRB1, and HLA-DRB5 is positive, and c) an expression level of C3, which is standardized with GAPDH of a reference gene, is 0.05 copies / copies or less.

The present invention provides CDCA1-derived epitope peptides having the ability to induce cytotoxic T cells. The present invention also provides polynucleotides encoding the peptides, antigen-presenting cells presenting the peptides, and cytotoxic T cells targeting the peptides, as well as methods of inducing antigen-presenting cells or CTLs. The present invention also provides compositions and pharmaceutical compositions containing them as active ingredients. Furthermore, the present invention provides methods of using the peptides, polynucleotides, antigen-presenting cells, cytotoxic T cells, or pharmaceutical compositions of the present invention to treat and / or prevent cancer, and / or prevent postoperative recurrence thereof. Methods of inducing an immune response against cancer are also provided.

The present disclosure relates to methods of coupling antic-cancer agents and anti-cancer treatments to improve the efficacy of the overall treatment. The anti-cancer agent reduces stroma in the tumor microenvironment, in part by killing stroma producing cells such as TAFs and TAMs. Reduction of tumor stroma not only improves immune cell function, including immune cells administered in a second treatment, but also allows allowing other anti-cancer treatments to better access to tumor cells.

The present application provides methods and compositions that involve BRCA1 agents (e.g., BRCA1 mRNA, proteins, genome editing agents) for treating, preventing or delaying diseases such as cancer. In some cases, the BRCA1 agents correspond to only a fragment of BRCA1 wildtype protein.

Provided herein are methods comprising administering to a cancer patient an agent that modifies expression of a gene or function of a product encoded by the gene, wherein the gene is a human ortholog of a gene that maps to a mouse Chromosome 15 quantitative trait locus (QTL), for example, the human NCF4 gene.

The invention belongs to the technical field of tumor treatment, and particularly relates to a CRISPR library screening method of genes related to ovarian cancer cell growth, tumor formation and immune escape. The sgRNA library comprises sgRNA which is selected from 80 genes in a MusCK library in a targeting manner. According to the invention, a targeted MusCK library of 922 genes related to the starting, progression and immunoregulation of tumors is used, and a P53- / -Carm1OE Ccne1OE KrasOE mouse ovarian cancer cell line, a C57BL / 6 mouse and a BALB / c-nu mouse are respectively adopted for high-throughput screening, so that the immunoregulation of tumors is realized. A series of confirmed and unverified key genes for high-grade serous ovarian cancer cell growth, tumor formation and immune escape function exertion are successfully screened, and an important theoretical and experimental foundation is laid for finding a novel treatment target of the high-grade serous ovarian cancer; and breakthrough in targeted therapy of high-grade serous ovarian cancer is facilitated.

To provide inhibitors of cyclin-dependent kinase 2 (CDK2), as well as pharmaceutical compositions thereof, and methods of treating cancer using the same.SOLUTION: A compound of Formula (I) or a pharmaceutically acceptable salt thereof is provided. The compound inhibits cyclin-dependent kinase 2 (CDK2), and is useful in treating cancer.SELECTED DRAWING: None

The invention relates to expression of the transcription factor Myc and / or pTEF-b and their use as medicaments for inducing proliferation in cells with limited proliferative potential, such as cardiomyocytes. Also described are methods for the prevention and treatment of diseases, such as heart disease, associated with the loss of cells or cell death.

The application provides a PCNA binding protein, a preparation method and application, and relates to the technical field of biology. The PCNA binding protein contains a complementarity determining region of a heavy chain variable region and a complementarity determining region of a light chain variable region, the complementarity determining region of the heavy chain variable region comprises an amino acid sequence identical to VH-CDR1, VH-CDR2 and VH-CDR3 of the heavy chain variable region shown in SEQ ID NO. 1, and the complementarity determining region of the light chain variable region comprises an amino acid sequence identical to VL-CDR1, VL-CDR2 and VL-CDR3 of the light chain variable region shown in SEQ ID NO. 2. The binding protein has good specific binding capacity with PCNA, and can be used for identification of PCNA antibodies or PCNA antigens, and auxiliary diagnosis and detection of PCNA antibody positive diseases.

The disclosure relates to a composition comprising BRINP3 variants and methods of using the same for treatment of obesity, weight gain, diabetes, MASH, or MASLD in subjects in need thereof.

The present application provides imidazolyl pyrimidinylamine inhibitors of cyclin-dependent kinase 2 (CDK2), as well as pharmaceutical compositions thereof, and methods of treating cancer using the same.

A quality improving agent for iPS cells that comprises a polynucleotide, said polynucleotide containing H1foo gene and a regulatory sequence. When the H1foo gene is introduced into cells, the regulatory sequence can regulate the amount and / or timing of the presence of H1foo protein expressed by the H1foo gene in the cells.