The present invention includes a method of increasing, stimulating, inducing, promoting, enhancing or maintaining the genomic stability of a cell of a subject, the method comprising decreasing, reducing, inhibiting, suppressing, limiting or controlling loss of methylation of heterochromatin in the cell and/or modulating heterochromatin dysfunction in a cell of a subject, the method comprising activating, eliciting, stimulate ng, inducing, promoting, increasing or enhancing expression or activity in the cell of one or more DNA methyltransferase (DNMT).

Disclosed is a dTAG system comprising small molecule degraders of mutant BET family protein-tagged proteins via recruitment of an E3 ubiquitin ligase and uses thereof.

Provided herein are compositions and methods for assessing arrestin-dependent signaling. The provided compositions include fusion proteins comprising arrestin polypeptides that bind strongly to G protein-coupled receptors (GPCRs). In some instances, the fusion proteins may also bind to non-GPCR proteins, such as single transmembrane receptors and non-receptor proteins. Also provided are nucleic acids, vectors, constructs, and host cells that encode or express such fusion proteins. Also provided are methods of using such fusion proteins to assess arrestin trafficking, localization, and other functions including, for example, arrestin-mediated GPCR signaling as well as non-GPCR protein activity or signaling.

The present invention relates to compositions comprising factor VIII coagulation factors linked to extended recombinant polypeptide (XTEN), isolated nucleic acids encoding the compositions and vectors and host cells containing the same, and methods of making and using such compositions in treatment of factor VIII-related diseases, disorders, and conditions.

Described herein are compositions and methods for modulating protein abundance in a target-specific manner via degron tags.

An auxin-inducible degron system kit that controls degradation of a target protein in a non-plant-derived eukaryotic cell, the kit containing a first nucleic acid that encodes a mutant TIR1 family protein having a mutation at an auxin-binding site, an auxin analog that has an affinity to the mutant TIR1 family protein and a second nucleic acid that encodes a degradation tag containing at least a part of an Aux/IAA family protein and having an affinity to a complex of the mutant TIR1 family protein and the auxin analog.

The type V-U1 system from the bacterium Mycobacterium mucogenicum CCH10-A2 (Mmu) has a nuclease which binds dsDNA but it does not cleave it. Additionally, after dsDNA binding by the nuclease an RuvC-dependent interference of nascent transcript (mRNA) takes place and this mechanism has not been described before for any CRISPR system. CRISPR based gene manipulation can therefore use CRISPR endonucleases from the Type V-U1 system from Mycobacterium mucogenicum, including variant and modified endonucleases, so as to provide for methods of expression control and gene editing in cells of any living organism or of any nucleic acid in vitro.

The present disclosure provides compositions and methods related to transcription factor systems. Such systems provide for modular and tunable protein expression driven by regulated transcriptional activity.

Compounds and compositions that have an asialoglycoprotein receptor (ASGPR) binding ligand bound to an extracellular protein binding ligand for the selective degradation of the target extracellular protein in vivo to treat disorders mediated by the extracellular protein are described.

The present disclosure relates to engineered polypeptides comprising degradation domains, compounds, compositions, and methods for their preparation and use as for degrading engineered proteins in cells.