Abstract: Inhibitory nucleic acids, e.g., antisense oligonucleotides (ASO) against PAR-TERRA RNA or other chromosome-specific TERRA transcripts (i.e., inclusive of chromosome-specific subtelomeric sequences), and methods of use thereof to downregulate expression of escapee genes on the inactive X chromosome, expression from the active X chromosome, subtelomeric autosomal loci (e.g., FSHD locus), or expression of autosomal genes involved in growth control and apoptosis, e.g., in cells and subjects with supernumerary X chromosomes and/or cancer and other human diseases.

Abstract: Inhibitory nucleic acids, e.g., antisense oligonucleotides (ASO) against PAR-TERRA RNA or other chromosome-specific TERRA transcripts (i.e., inclusive of chromosome-specific subtelomeric sequences), and methods of use thereof to downregulate expression of escapee genes on the inactive X chromosome, expression from the active X chromosome, subtelomeric autosomal loci (e.g., FSHD locus), or expression of autosomal genes involved in growth control and apoptosis, e.g., in cells and subjects with supernumerary X chromosomes and/or cancer and other human diseases.

Abstract: Inhibitory nucleic acids, e.g., antisense oligonucleotides (ASO) against PAR-TERRA RNA or other chromosome-specific TERRA transcripts (i.e., inclusive of chromosome-specific subtelomeric sequences), and methods of use thereof to downregulate expression of escapee genes on the inactive X chromosome, expression from the active X chromosome, subtelomeric autosomal loci (e.g., FSHD locus), or expression of autosomal genes involved in growth control and apoptosis, e.g., in cells and subjects with supernumerary X chromosomes and/or cancer and other human diseases.

Abstract: Inhibitory nucleic acids, e.g., antisense oligonucleotides (ASO) against PAR-TERRA RNA or other chromosome-specific TERRA transcripts (i.e., inclusive of chromosome-specific subtelomeric sequences), and methods of use thereof to downregulate expression of escapee genes on the inactive X chromosome, expression from the active X chromosome, subtelomeric autosomal loci (e.g., FSHD locus), or expression of autosomal genes involved in growth control and apoptosis, e.g., in cells and subjects with supernumerary X chromosomes and/or cancer and other human diseases.

Abstract: Methods are provided to increase resistance to cell damage in a subject. The increase in resistance to cell damage in a subject in the subject is accomplished by decreasing activity of eEF2 kinase in the subject. The eEF2 kinase activity can be decreased by decreasing the amount of functional eEF2 kinase produced by the subject, including contacting the eEF2 kinase with a compound that inhibits phosphorylation of eEF2 kinase substrate or decreasing the amount of functional eEF2 kinase is decreased by reducing expression of a gene encoding the eEF2 kinase.

Abstract: Methods are provided to increase resistance to cell damage in a subject. The increase in resistance to cell damage in a subject in the subject is accomplished by decreasing activity of eEF2 kinase in the subject. The eEF2 kinase activity can be decreased by decreasing the amount of functional eEF2 kinase produced by the subject, including contacting the eEF2 kinase with a compound that inhibits phosphorylation of eEF2 kinase substrate or decreasing the amount of functional eEF2 kinase is decreased by reducing expression of a gene encoding the eEF2 kinase.

Abstract: Methods are provided to increase resistance to cell damage in a subject. The increase in resistance to cell damage in a subject in the subject is accomplished by decreasing activity of eEF2 kinase in the subject. The eEF2 kinase activity can be decreased by decreasing the amount of functional eEF2 kinase produced by the subject, including contacting the eEF2 kinase with a compound that inhibits phosphorylation of eEF2 kinase substrate or decreasing the amount of functional eEF2 kinase is decreased by reducing expression of a gene encoding the eEF2 kinase.