Modified E1a regulatory sequences are provided, wherein at least one Pea3 binding site, or a functional portion thereof, is deleted. Also provided are modified E1a sequences that selectively express particular isoforms. Also provided is an E1b-19K clone insertion site. These modified sequences can be used individually, or in combination with one another, to provide tumor-selective expression of proteins.

The present invention discloses a recombinant bacteriophage comprising a phage genome polynucleotide including a gene encoding a heterologous antigen protein(s) and a killing gene encoding a protein that is capable of killing a host bacterium. Such a recombinant bacteriophage is designed to prime a subject's immune response and to kill the bacterium that it infects such that the prime and kill bacteriophage provides two lines of protection against infectious disease.

The present invention relates to insect cells for producing parvoviral vectors with mosaic, chimeric and/or modified capsids. The insect cells of the invention comprise separate expression cassettes for the VP1 capsid protein and for the VP2 and VP3 proteins, which allow for the production of parvoviral vectors in which the VP1 capsid protein is of a different parvovirus or of a different serotype than the VP2 and VP3 protein and/or for the production of parvoviral vectors in which the VP1 capsid protein is modified, e.g. by the insertion of an exogenous amino acid sequence. Such exogenous amino acid sequence can e.g. encode a single domain antibody that targets the parvoviral vector to a specific tissue or type of cell. The invention further relates to method wherein the insect cells of the invention are used for the production of parvoviral vectors with mosaic, chimeric and/or modified capsids.

The present disclosure provides compositions and methods for the treatment of ocular diseases associated with angiogenesis, particularly wet age-related macular degeneration.

The present invention provides a nucleic acid sequence comprising at least one miRNA binding site sequence containing at least one miRNA binding site. Those miRNA binding site sequences are located within and/or immediately 3 or 5 of the 5 UTR of a gene to reduce the off-target side effects and allow a cell type specific expression from the nucleic acid sequence within the target organ or organs. The invention further provides pharmaceutical compositions, as well as a method of promoting cell-type specific expression, comprising the nucleic acid sequence according to the invention for use in therapy.

Embodiments herein describe systems and methods to enhance RNA stability and uses thereof. Many embodiments alter the sequence of an RNA therapeutic molecule (e.g., vaccines) to encode for a variant peptide while maintaining and/or increasing stability of the RNA therapeutic.

The invention relates to the use of a virus, preferably an adenovirus, for producing a medicament. Said virus is replication-deficient in cells which do not contain YB-1 in the core and codes for an oncogene or ongogene product, especially an oncogene protein, which transactivates at least one viral gene, preferably an adenoviral gene, said gene being selected among the group comprising E1B55kDa, E4orf6, E4orf3, and E3ADP.

Disclosed are a recombinant expression vector and a host cell that contains the vector.

The present invention relates generally to a gene expression system utilizing an alphavirus replicon and T7 promoter. The system is capable of expressing proteins in the cell cytoplasm without integrating the gene of interest into the genome of a host cell. The invention has a wide range of applications such as producing induced pluripotent cells and vaccines against pathogens and cancers.

The present invention relates in some aspects to super-enhancers and related compositions, methods, and agents that are useful for modulating expression of cell type-specific genes that are required for maintenance of cell identity (e.g., embryonic stem cell identity) or maintenance of a disease state (e.g., cancer).