The present disclosure provides T7 RNA polymerase variants with enhanced transcriptional activity, and methods of using such variants to produce modified oligonucleotides, such as 2′-modified oligonucleotides. These polymerase variants and methods thereof improve the transcription yield of modified oligonucleotides.

The disclosure provides method and kits for characterizing spliced m RNA isoforms. The disclosure also provides methods of screening for mutations and oligonucleotides that modulate splicing.

Novel processes and compositions are described which use viral capsid proteins resistant to hydrolases to prepare virus-like particles to enclose and subsequently isolate and purify target cargo molecules of interest including nucleic acids such as siRNAs and shRNAs, miRNAs, messenger RNAs, small peptides and bioactive molecules.

The present invention refers to a modified D-amino acid oxidase (DAAO). In particular, the modified DAAO of the present invention has the activity of catalyzing the oxidation of D-glufosinate into PPO. Further, the modified DAAO of the present invention has increased activity of catalyzing the oxidation of D-glufosinate into PPO and/or increased stability as compared to SEQ ID NO: 4. The present invention also refers to the polynucleotide encoding the modified DAAO of the present invention, the vector and host cell expressing the modified DAAO of the present invention, and the method of producing L-glufosinate with the modified DAAO and host cell of the present invention.

Anti-cytokine therapy has revolutionized immunological disease treatment, but is not always effective and subject to treatment resistance as the cytokine cascade is highly redundant and multiple cytokines are involved in inflammation. Targeting a critical common regulator of inflammatory effectors is desirable. Lipopolysaccharide (LPS)-responsive beige-like anchor (LRBA) is a master regulator of multiple genes important for inflammation. Subcellular localization shows that LRBA translocated to the nucleus upon LPS stimulation and colocalized with multiple proteins associated with the endosome membrane system, indicating a critical role in membrane/vesicle trafficking essential for deposition, secretion and signal transduction of immune effectors. Deregulation, deficiency, down-regulation and overexpression of LRBA causes defective trafficking and signaling of immune effector molecules, resulting in immunodeficiency and autoimmunity diseases associated with a broader spectrum of severe symptoms when compared to other CVID genes. Modulating LRBA through antibodies, dominant negative mutants, or small interference RNA can be used to treat inflammatory diseases.

Disclosed are components and systems for cell-free glycoprotein synthesis (CFGpS). In particular, the components and systems include and utilize prokaryotic cell lysates from engineered prokaryotic cell strains that have been engineered to enable cell-free synthesis of glycoproteins.

This disclosure provides SERPIN B1 polypeptides that possess neutrophil or pancreatic elastase inhibitory activity, and the elastase inhibition activity is resistant to oxidation by free radicals. The free radicals may a reactive oxygen species, or a reactive nitrogen species, or both. In some embodiments, the SERPIN B1 polypeptide comprises an amino acid substitution at residue 344 as compared to SEQ ID NO: 1. The SERPIN B1 polypeptides disclosed herein can be used to treat a patient having a disease or a genetic condition that is associated with the increased production of free radicals as compared to a normal individual or increased exposure to free radicals in environmental sources.

A method is provided for generating RNA nanoparticles having modified nucleotides and/or having increased nuclease resistance where the RNA nanoparticles are formed cotranscriptionally by T7 RNA polymerase in the presence of manganese ions.

The present invention relates to agents for use in the treatment of glioma, in particular astrocytoma WHO IΓ and 111°, as well as IV0 (glioblastoma), in a subject.

Provided herein are novel .sup.10Fn3 domains which specifically bind to PD-L1, as well as imaging agents based on the same for diagnostics.