The present invention relates to an immobilized capping enzyme, preferably an immobilized Vaccinia virus capping enzyme. Furthermore, the present invention relates to an immobilized cap-specific nucleoside 2′-O-methyltransferase, preferably an immobilized Vaccinia virus cap-specific nucleoside 2′-O-methyltransferase. Moreover, the present invention relates to a method for immobilizing said enzymes and to a method of using said enzymes for the addition of a 5′-cap structure to RNAs. Moreover, the present invention relates to an enzyme reactor for performing the capping reaction using said immobilized enzymes and the subsequent separation of the 5′-capped RNA product. In addition, the present invention relates to a kit comprising the capping enzyme and/or the cap-specific nucleoside 2′-O-methyltransferase.

The disclosure provides an ex vivo method to prepare regulatory T cells, a population of regulatory T cells with enhanced properties and methods of using the population or complexes useful to induce Tregs in a mammal. The ex vivo methods allows for the generation and expansion of super regulatory T cells for the prevention, inhibition or treatment of autoimmune disorders.

Methods for reactivating genes on the inactive X chromosome that include administering one or both of a DNA methyltransferase (DNMT) Inhibitor and/or a topoisomerase inhibitor, e.g., etoposide and/or 5′-azacytidine (aza), optionally in combination with an inhibitor of XIST RNA and/or an Xist-interacting protein, e.g., a chromatin-modifying protein, e.g., a small molecule or an inhibitory nucleic acid (such as a small inhibitory RNA (siRNAs) or antisense oligonucleotide (ASO)) that targets XIST RNA and/or a gene encoding an Xist-interacting protein, e.g., a chromatin-modifying protein.

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.

Provided is a variant strain of the genus Yarrowia. More specifically, provided are a variant strain of the genus Yarrowia, in which activity of phosphatidylethanolamine N-methyltransferase (PEMT) or phospholipid methyltransferase is inactivated, and a method of increasing a fat in the strain, including culturing the strain, or a method of preparing a fat.

The present disclosure provides SETD7 modulators (e.g., polypeptides, polynucleotides, vectors, compositions, micelles, or pharmaceutical composition) which reduce or abolish SETD7 translocation to the nucleus, e.g., in response to stimuli such as increases in glucose levels. In some aspects, the SETD7 modulators mimic phosphorylated STED7, competing with STED7 and reducing or abolishing SETD7 nuclear translocation. In turn, the reduced SETD7 nuclear translocation results in a decrease in histone monomethylation. In some aspects, the SETD7 modulator is a catalytically inactive SETD7 protein. In some aspects, the SETD7 modulator is a polypeptide (e.g., a phosphomimetic polypeptide). In other aspects, the SETD7 modulator is a polynucleotide encoding a SETD7 polypeptide modulator, e.g., a phosphomimetic polypeptide or a mutant SETD7 protein. The SETD7 modulators of the present disclosure can be used to treat type diabetes or cancer.

The present disclosure relates to a novel use of CMTR1 having the activity of enhancing the production and function of siRNA, and more particularly, to a composition for enhancing the production of siRNA including a cap1 2′-O-ribose methyltransferase (CMTR1) protein as an active ingredient, and a composition for enhancing the gene silencing activity by siRNA, and also to a method for producing siRNA for gene silencing in vitro. According to the present disclosure, the CMTR1 may enhance the production of siRNA for gene silencing and at the same time, ultimately enhance the production and function of siRNA without artificial chemical modification of siRNA by enhancing the formation of holo-RNA-induced silencing complex (RISC) that acts on silencing of a target gene in an RNAi mechanism. Therefore, the CMTR1 of the present disclosure can be usefully used in the development of pharmaceuticals using siRNA as a therapeutic agent.

The present disclosure is directed to methods of inducing rejuvenation in a population of adult glial progenitor cells, and methods of treating a subject having a myelin deficiency. The method of inducing rejuvenation in a population of adult glial progenitor cells, may comprise: administering, to the population of adult glial progenitor cells, one or more nucleic acid molecules encoding microRNAs, wherein administering suppresses the signal transducer and activator of transcription 3 (STAT3) signaling pathway; and/or administering microRNAs, wherein administering suppresses the E2F transcription factor 6 (E2F6) signaling pathway; and/or administering microRNAs, wherein administering suppresses the Myc-associated factor X (MAX) signaling pathway, wherein said one or more nucleic acid molecules are administered in an amount sufficient to induce rejuvenation in the population of adult glial progenitor cells.

Disclosed herein is a method of treating a cancer in a subject having or suspected of having the cancer that has a mutated PREX2 expressed thereon. According to the embodiment of the present disclosure, the mutation is G258V, S1113R, E1346D or K400fs. The method includes the step of administering an effective amount of a composition to the subject, wherein the composition includes a therapeutic molecule for producing a polypeptide that exhibits a binding affinity to the mutated PREX2 protein expressed in the cancer in the subject.

Provided herein is a non-naturally occurring microbial organism (NNOMO) having a methanol metabolic pathway (MMP) that can enhance the availability of reducing equivalents in the presence of methanol. Such reducing equivalents can be used to increase the product yield of organic compounds produced by the microbial organism, such as succinate. Also provided herein are methods for using such an organism to produce succinate.