The invention provides novel personalized therapies, kits, transmittable forms of information and methods for use in treating patients having cancer, wherein the cancer is MTAP-deficient and/or MTA-accumulating and thus amenable to therapeutic treatment with a PRMT5 inhibitor. Kits, methods of screening for candidate PRMT5 inhibitors, and associated methods of treatment are also provided.

Provided herein are method of treating cancer using agents that inhibit the interaction between Methyltransferase like 3 (METTL3) and Eukaryotic Translation Initiation Factor 3 Subunit H (EIF3h), and optionally agents that inhibit Bromodomain-containing protein 4 (BRD4). The present disclosure demonstrates the topology of individual polyribosomes with single METTL3 foci found in close proximity to 5′ cap-binding proteins, revealing a previously unknown direct physical and functional interaction between METTL3 and the eukaryotic translation initiation factor 3 subunit h (eIF3h).

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.

Transgenic plants with blue flower color, or their inbred or outbred progeny, or their propagules, partial plant bodies, tissues or cells, are provided. A buckwheat-derived C-glucosyltransferase (CGT) gene or its homolog is transferred into a host plant to cause delphinidin-type anthocyanins and flavone mono-C-glycosides to be copresent in the plant cells.

Compositions and methods are provided for the silencing of the NSD3 gene. Specifically, siRNA compositions are provided that contain siRNA molecules that target the wild-type NSD3 gene or the NSD3.sub.T1232A mutant. Methods for using these compositions for treating cancer also are provided.

Provided herein are methods and compositions for producing alpha-N-methylated peptides in vitro and in vivo. This disclosure also provides in vivo and in vitro methods for producing highly diverse alpha-N-methylated peptide libraries by methylating natural or non-natural alpha-N-methyltransferase target peptides.

Methods for increasing specificity of RNA-guided genome editing, e.g., editing using CRISPR/Cas9 systems, using truncated guide RNAs (tru-gRNAs).

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.

The present invention provides methods of systems and methods of site specific methylation.

The present disclosure provides a method of treating a subject having a cancer. The method comprises reducing expression of a Carm 1 gene and/or a Carm 1 effector gene in a cell of the subject, and/or reducing activity of a Carm 1 protein and/or a Carm 1 effector protein in a cell of the subject. The cancer is resistant to immunotherapy and/or checkpoint blockade treatment.