7 results about "Activating transcription factor" patented technology

The present disclosure provides genetically modified iPSC-derived γδT cells and their precursors. A double genomic disruption in the suppressor of cytokine signaling 1 (SOCS1) gene and the cytokine-inducible sh2-containing protein (CISH) gene are provided, as is a triple genomic disruption in genes for SOCS1, CISH, and Bcl-2 interacting mediator of cell death (BIM), as is a quadruple genomic disruption in genes for SOCS1, CISH, BIM, and cell surface death receptor (FAS), as is a quintuple genomic disruption in genes for SOCS1, CISH, BIM, β-2-Microglobulin (B2M), and class II transactivator (CITTA), as is a sextuple genomic disruption in genes for SOCS1, CISH, BIM, B2M, CITTA, and FAS. Also provided is genetically modified iPSC-derived γδT cells and their precursors with improved proliferation and tumor killing activity. Also provided are genetically modified iPSC-derived γδT cells and their precursors further comprising CD19 CAR. The present disclosure further provides methods making and using such cells, as well as gene editing systems.

The present disclosure provides genetically modified iPSC-derived γδT cells and their precursors. A double genomic disruption in the suppressor of cytokine signaling 1 (SOCS1) gene and the cytokine-inducible sh2-containing protein (CISH) gene are provided, as is a triple genomic disruption in genes for SOCS1, CISH, and Bcl-2 interacting mediator of cell death (BIM), as is a quadruple genomic disruption in genes for SOCS1, CISH, BIM, and cell surface death receptor (FAS), as is a quintuple genomic disruption in genes for SOCS1, CISH, BIM, β-2-Microglobulin (B2M), and class II transactivator (CIITA), as is a sextuple genomic disruption in genes for SOCS1, CISH, BIM, B2M, CIITA, and FAS. Also provided is genetically modified iPSC-derived γδT cells and their precursors with improved proliferation and tumor killing activity. Also provided are genetically modified iPSC-derived γδT cells and their precursors further comprising CD19 CAR. The present disclosure further provides methods making and using such cells, as well as gene editing systems.

The present invention relates to novel compounds (I') which inhibit the Signal Transducer and Activator of Transcription protein 6 (STAT6). This invention also relates to pharmaceutical compositions containing them, processes for their preparation and their use in the treatment of several disorders.

The application discloses application of an anti-IFN-gamma antibody loaded hydrogel in preparation of a drug for treating bisphosphonate-related osteonecrosis of the jaw. The research result of the application shows that ZOL treatment can promote secretion of IFN-gamma by gamma delta T cells, enhance glycolysis of osteoclasts, induce histone H3K18 lactic acidification of lactic acid generated by glycolysis, activate transcription factor IKZF1 and downstream effector molecule ZBP1, finally drive necrotic apoptosis of osteoclasts and damage bone remodeling function. By locally applying GelMA@ab at a BRONJ lesion, controllable release of the anti-IFN-gamma antibody can be realized, IFN-gamma activity can be effectively blocked, necrotic apoptosis of osteoclasts and local inflammatory reaction can be significantly reduced, and a rat BRONJ-like lesion can be improved. Therefore, the application provides an effective strategy for treatment of BRONJ and provides experimental feasibility support for clinical conversion application of the composite hydrogel.

Compounds (1-2) as modulators of Activating Transcription Factor 6 (ATF6) are provided. The compounds may find use as therapeutic agents for the treatment of diseases or disorders mediated by ATF6 and may find particular use in the treatment of viral infections, neurodegenerative diseases, vascular diseases, or cancer. (Formula (1-2))

The disclosure relates to methods of inhibiting cellular senescence involving expressing Activating Transcription Factor 3 (ATF3) in a cell at a level sufficient to inhibit senescence of the cell. In some embodiments, ATF3 is delivered to a cell via administration of a messenger ribonucleic acid comprising an open reading frame encoding ATF3.

The present invention provides compositions and methods for the sensitization of tumor cells to immune killing and to improve anti-tumor immunotherapy. The methods of treating cancer include administering to the subject a therapeutically effective amount of an activator of Activating Transcription Factor 6 (ATF6). Methods and compositions for enhancing immune checkpoint blockade therapy in are also provided and include administering an effective amount of an activator of Activating Transcription Factor 6 (ATF6) before, during or after administration of an immune checkpoint blockade therapy.