The present disclosure provides methods of treating a subject having asthma or at risk of developing asthma, and methods of identifying subjects having an increased risk of developing asthma.

The present disclosure relates to methods for increasing telomere length in one or more human cells and/or increasing genome stability of one or more human cells, for example by contacting one or more human cells with an agent that increases expression of Zscan4 in the one or more human cells. Methods of treating a subject in need of telomere lengthening, treating a disease or condition associated with a genomic and/or chromosome abnormality, of rejuvenating one or more human cells, of rejuvenating tissues or organs, and of rejuvenating a subject in need thereof, for example by contacting one or more human cells in the subject with an agent that increases expression of Zscan4, or by administering to a subject in need thereof, an agent that increases expression of Zscan4 are also provided.

The present disclosure relates to methods for increasing telomere length in one or more human cells and/or increasing genome stability of one or more human cells, for example by contacting one or more human cells with an agent that increases expression of Zscan4 in the one or more human cells. Methods of treating a subject in need of telomere lengthening, treating a disease or condition associated with a genomic and/or chromosome abnormality, of rejuvenating one or more human cells, of rejuvenating tissues or organs, and of rejuvenating a subject in need thereof, for example by contacting one or more human cells in the subject with an agent that increases expression of Zscan4, or by administering to a subject in need thereof, an agent that increases expression of Zscan4 are also provided.

The present disclosure provides methods comprising administering to the individual an effective amount of an agent that decreases or inhibits TIGIT expression and/or activity and an anti-cancer agent and/or an anti-cancer therapy. Further provided are kits comprising an anti-cancer agent, an agent that decreases or inhibits TIGIT expression and/or activity, or both, as well as instructions for use thereof.

The present disclosure provides methods comprising administering to the individual an effective amount of an agent that decreases or inhibits TIGIT expression and/or activity and an anti-cancer agent and/or an anti-cancer therapy. Further provided are kits comprising an anti-cancer agent, an agent that decreases or inhibits TIGIT expression and/or activity, or both, as well as instructions for use thereof.

The present disclosure provides methods comprising administering to the individual an effective amount of an agent that decreases or inhibits TIGIT expression and/or activity and an anti-cancer agent and/or an anti-cancer therapy. Further provided are kits comprising an anti-cancer agent, an agent that decreases or inhibits TIGIT expression and/or activity, or both, as well as instructions for use thereof.

Methods of increasing T cell effector function in a T cell population are provided that involve inhibiting one or more genetic subunits of the SAGA (Spt-Ada-Gcn5-acetyltransferase) gene regulation complex in the T cell population. Also provided are methods of using such T cell populations in the treatment of cancer patients.

A modified oligonucleotide having an activity of inhibiting Ataxin 3 expression and having any one of the following nucleobase sequences or a nucleobase sequence of 17 contiguous bases contained in the nucleobase sequences:

TABLE-US-00001 (SEQ ID NO: 239) (1) TCGGGTAAGTAGATTTTC, (SEQ ID NO: 240) (2) GAAGTATCTGTAGGCCTA, (SEQ ID NO: 241) (3) GGACTGTATAGGAGATTA, (SEQ ID NO: 242) (4) GGTTATAGGATGCAGGTA, (SEQ ID NO: 243) (5) AGGTTATAGGATGCAGGT, (SEQ ID NO: 244) (6) GAAGCTAAGTAGGTGACT, (SEQ ID NO: 245) (7) TGAAGCTAAGTAGGTGAC, (SEQ ID NO: 246) (8) CCTAGTCACTTTGATAGA, (SEQ ID NO: 247) (9) GGAACATCTTGAGTAGGT, (SEQ ID NO: 248) (10) GGTGTTCAGGGTAGATGT, (SEQ ID NO: 249) (11) GGATACTCTGCCCTGTTC, (SEQ ID NO: 250) (12) GGTGTCAAACGTGTGGTT, (SEQ ID NO: 251) (13) CCGTGTGCTAGTATTTGT, (SEQ ID NO: 252) (14) TAGTAGAGTTTTGCTTGG, (SEQ ID NO: 253) (15) GATGTAGTAGAGTTTTGC, (SEQ ID NO: 254) (16) TGATGTAGTAGAGTTTTG, (SEQ ID NO: 255) (17) CTGATGTAGTAGAGTTTT, (SEQ ID NO: 256) (19) GCAAGTTGGTTTGTGGTA, (SEQ ID NO: 257) (20) TCTAGGCAATTGTGGTGG, (SEQ ID NO: 258) (21) GTAACTCTGCACTTCCCA, (SEQ ID NO: 259) (22) GTCATCCCTATGTCTTAT, (SEQ ID NO: 260) (23) GTCATATGGTCAGGGTAT, (SEQ ID NO: 261) (24) TGTCATATGGTCAGGGTA, (SEQ ID NO: 262) (25) ATGTCATATGGTCAGGGT, and (SEQ ID NO: 263) (26) TATGTCATATGGTCAGGG.

The present invention relates to a composition for preventing or treating Alzheimer’s disease, containing an inhibitor of ATL2, and a method of diagnosing the disease based on the measurement of the ATL2. In the present invention, it was found that PS1 mutants may result in mitochondrial dysfunction, such as increased binding between endoplasmic reticulum and mitochondria, increased mitochondrial ROS production, decreased mitochondrial membrane potential, decreased ATP production, decreased complex I activity, and decreased peroxidase activity, in brain glioma cells and that the PS1 mutants may abnormally increase the binding between endoplasmic reticulum and mitochondria by elevating the expression of the ATL2 in the brain. In addition, when the ATL2 was knocked down, it was observed that the binding between endoplasmic reticulum and mitochondria was lowered and that the expression of the ATL2 was elevated in the brains of Alzheimer’s disease animal models and patients. Accordingly, it is expected that it may possible to effectively prevent or treat Alzheimer’s disease by inhibiting the expression or activity of the ATL2 and that it may possible to diagnose the disease, predict the risk of developing the disease, and screen therapeutic agents for the disease, by measuring the level of the expression or activity of the ATL2.

The present invention relates to a composition for preventing or treating Alzheimer’s disease, containing an inhibitor of ATL2, and a method of diagnosing the disease based on the measurement of the ATL2. In the present invention, it was found that PS1 mutants may result in mitochondrial dysfunction, such as increased binding between endoplasmic reticulum and mitochondria, increased mitochondrial ROS production, decreased mitochondrial membrane potential, decreased ATP production, decreased complex I activity, and decreased peroxidase activity, in brain glioma cells and that the PS1 mutants may abnormally increase the binding between endoplasmic reticulum and mitochondria by elevating the expression of the ATL2 in the brain. In addition, when the ATL2 was knocked down, it was observed that the binding between endoplasmic reticulum and mitochondria was lowered and that the expression of the ATL2 was elevated in the brains of Alzheimer’s disease animal models and patients. Accordingly, it is expected that it may possible to effectively prevent or treat Alzheimer’s disease by inhibiting the expression or activity of the ATL2 and that it may possible to diagnose the disease, predict the risk of developing the disease, and screen therapeutic agents for the disease, by measuring the level of the expression or activity of the ATL2.