The present disclosure features compositions and methods for producing one or more isoprenoid compounds, such as E-copalol, in a host cell, such as a yeast cell, that is genetically modified to express the enzymes of an isoprenoid biosynthetic pathway, such as a pathway for making E-copalol. Using the compositions and methods of the present invention, the host cell may be genetically modified to express one or more enzymes of an isoprenoid biosynthetic pathway, such as a copalyl-diphosphate (CPP) pyrophosphatase. The host cell may then be cultured in a medium, for example, in the presence of an agent that regulates expression of the one or more enzymes. The host cell may further be incubated for a time sufficient to allow for production of an isoprenoid compound, such as E-copalol, by the host cell. The isoprenoid compound may then be separated from the host cell or from the medium.

The present invention provides breast cancer markers based on RECQL mutations, and related methods, uses, agents, and kits. The invention includes methods for determining the susceptibility of a subject to developing breast cancer, and methods for detecting, diagnosing, treating, and predicting responses to treatment for breast cancer.

The present invention provides breast cancer markers based on RECQL mutations, and related methods, uses, agents, and kits. The invention includes methods for determining the susceptibility of a subject to developing breast cancer, and methods for detecting, diagnosing, treating, and predicting responses to treatment for breast cancer.

Compositions and methods are provided for treating lymphoma in an individual by targeting engineered phagocytes to lymphoma cells. In particular, the phagocytes provided for administration to an individual, who has lymphoma, are engineered to express a chimeric antigen receptor (CAR) that specifically binds to an antigen present on lymphoma cells. The CAR localizes the engineered phagocytes to sites where lymphoma cells are present. In some embodiments, phagocytic activity of the phagocytes is enhanced by further engineering the phagocytes to express a hyperactive Rac GTPase.

The present invention relates to methods of modifying pathogen resistance in plants and plants having modified pathogen resistance. In particular, the present invention relates to modification of expression or activity of a negative regulator of plant immunity.

The present inventions provide a concise panel of chromatography-based stability-indicating methods for evaluating in vitro transcribed (IVT) mRNA under various conditions, including varying types and degrees of stress conditions, as part of a forced degradation study. The inventions also provide that addition of EDTA to the mRNAs prior to heat exposure reduces the extent of mRNA degradation, that the transcripts are fragmenting via a divalent metal-ion mediated pathway. The inventions also provide the application of the methods to evaluate the critical quality attributes (CQAs) of mRNAs as well as to detect intrinsic process and product related impurities.

The present disclosure provides a C6-substituted locked nucleic acid-modified cap analog and a use thereof, wherein the cap analog improves the stability of mRNA and/or the translation efficiency of mRNA.

The present disclosure relates, in part, to a composition comprising a nucleic acid, wherein the nucleic acid encodes a protein which has a reduced abundance in a GTPase IMAP family 5 (GIMAP5) deficient subject or at least partially inhibits expression of a protein which has an increased abundance in a GIMAP5 deficient subject, as compared to a healthy subject. In certain embodiments, the composition is a nucleic acid-lipid particle. In certain embodiments, the composition is a polymer-based vehicle. In another aspect, the present disclosure relates to a recombinant viral vector comprising a nucleic acid encoding a protein which has a reduced abundance in a GIMAP5 deficient subject as compared to a healthy subject. In yet another aspect, the present disclosure provides a method of treating, ameliorating, and/or preventing liver disease and/or portal hypertension in a subject with administration of one or more compositions and/or vectors of the present disclosure.

The present disclosure provides a C6-substituted locked nucleic acid-modified cap analog and a use thereof, wherein the cap analog improves the stability of mRNA and/or the translation efficiency of mRNA.