The present invention relates to an inhibitor of the TGS1 enzyme and/or compositions comprising such inhibitor and one or more excipients for the therapeutic treatment of clinical conditions characterized and/or caused by telomeropathies.

Methods and kits are disclosed for measuring activity of a methyltransferase or a radical SAM enzyme or for screening for an inhibitor of a methyltransferase or a radical SAM enzyme, where the methods and kits comprise, respectively, deaminase TM0936 for a MTase coupled assay and deaminase PA3170 for a radical SAM coupled assay.

The present invention relates to a marker that can be used as aging biomarker. More specifically, the present invention relates to the analysis of nucleolar size as a biomarker for aging and metabolic health and its relation to the virtual age, or the life expectancy of animals, including humans. The aging biomarker of the invention can be used to study the effect of medication, food compounds and/or special diets on the wellness and virtual age, or the life expectancy of animals, including humans.

The present invention relates to methods and pharmaceutical composition for the treatment of T-helper type 2 (Th2)-mediated diseases. More particularly, the present invention relates to an inhibitor of the Suv39h1-HP1a silencing pathway for use in the treatment of a T-helper type 2 (Th2)-mediated disease, in particular allergic asthma.

The present invention relates to a melanogenesis detection method using FAM86A, and the like. The level of FAM86A of the present invention decreases according to an increase in the amount of melanin secretion or formation, and thus the present invention can whiten the skin by using protein FAM86A or an agonist thereof, and can prevent, treat or alleviate melanin-deficiency diseases such as vitiligo since the formation and secretion of melanin is promoted when FAM86A is inhibited. Therefore, the present invention is expected to be used in various ways, such as a composition for skin whitening using protein FAM86A or an agonist thereof, and as a composition for preventing and treating melanin deficiency diseases including vitiligo and canities by using a FAM86A inhibitor.

Methods for diagnosing non-alcoholic steatohepatitis (NASH) and NASH with or without advanced liver fibrosis in a subject are provided, such methods including the detection of levels of a variety of biomarkers diagnostic of NASH versus simple steatosis and NASH with advanced liver fibrosis versus NASH without advanced liver fibrosis. The invention also provides methods treating NASH (e.g., NASH with or without advanced liver fibrosis) by administering a biomarker or an agent that modulates a biomarker of NASH or fibrosis. Compositions in the form of kits and panels of reagents for detecting the biomarkers of the invention are also provided.

Compositions and methods for carboxymethylation of cytosine containing DNA and applications thereof for direct sequencing of 5mC are disclosed.

The present disclosure relates to chemical compounds that inhibit HP1-mediated heterochromatin formation, pharmaceutical compositions containing such compounds, methods of identifying such compounds, and their use in the treatment of disorders related to heterochromatin formation such as, for example, a disorder of cellular proliferation (e.g., cancer). This abstract is intended as a scanning tool for purposes of searching in the particular art and is not intended to be limiting of the present invention.

The present invention relates to a use for, by using the protein arginine methyltransferase 1 (PRMT1) protein or a gene encoding the same, preventing or treating a neuromuscular disease induced by motor neurons, particularly, damage to motor neurons caused by oxidative stress in the neuromuscular junction; and a method for screening a candidate material for activating the expression of PRMT1. PRMT1 deficiency in the motor nerve or neuromuscular junction induces aggravated degenerative motor nerve damage caused by aging, and DNA damage caused by oxidative stress and inflammation, thereby enabling the induction of neuromuscular disease, and thus the disease may be treated through the overexpression and activity of the PRMT1 protein and a gene encoding the same.

The invention relates to inhibition of wild-type and certain mutant forms of human histone methyltransferase EZH2, the catalytic subunit of the PRC2 complex which catalyzes the mono- through tri-methylation of lysine 27 on histone H3 (H3-K27). In one embodiment the inhibition is selective for the mutant form of the EZH2, such that trimethylation of H3-K27, which is associated with certain cancers, is inhibited. The methods can be used to treat cancers including follicular lymphoma and diffuse large B-cell lymphoma (DLBCL). Also provided are methods for identifying small molecule selective inhibitors of the mutant forms of EZH2 and also methods for determining responsiveness to an EZH2 inhibitor in a subject.