Abstract: Certain genes controlled by endogenous miRNA are actually upregulated upon the transfection of exogenous mi/siRNA. Based on this, methods of determining whether administration of mi/siRNA will have a deleterious effect by upregulating certain genes are provided. Comparison of sequences of exogenous mi/siRNA allows selection of exogenous miRNA to be administered to cell to enhance or limit this affect, and therefore to control unwanted disregulation, or to upregulate an endogenous miRNA-regulated gene of interest.

Abstract: An object of the present invention is to provide a novel marker for rheumatoid arthritis (RA), and more specifically, to provide a marker whose expression may be specifically increased or decreased in RA. Another object of the present invention is to confirm whether or not miRNA serving as the marker is involved as the etiology of RA, and to provide an inspection method for RA and a therapeutic agent for RA each using the miRNA involved. The marker includes miRNA (for example, miR124a) whose expression is specifically increased or decreased in RA synovial cells based on a small RNA expression profile in the RA synovial cells. In addition, the therapeutic agent for RA includes miRNA (for example, miR124a) as an active ingredient.

Abstract: A double-strand oligonucleotide including two complementary oligonucleotide sequences forming a hybrid, each including at one of their 3? or 5? ends, one to five unpaired nucleotides forming single-strand ends extending beyond the hybrid, one of the oligonucleotide sequences being substantially complementary to a target sequence belonging to a DNA or RNA molecule to be specifically repressed, the target sequence belonging to a DNA or RNA molecule of a gene coding an angiogenic factor.

Abstract: The present invention includes compositions and methods for contacting one or more cells with a random RNA-containing library, treating the contacted cells and with a denaturing agent or digestion with one or more nucleases, and extracting from the cells one or more internalized nucleic acids resistant to the nucleases or denaturants.

Abstract: A method of treating cancer in a subject in need thereof is disclosed. The method comprises administering to the subject a siRNA molecule capable of inducing degradation of an mRNA encoding a polypeptide of SEQ ID NO: 1 in cells of the cancer thereby treating the cancer in the subject.

Abstract: The invention relates to a method for influencing the miR-92 expression in a cell, comprising the following steps: (a) providing a cell; and (b1) reducing the miR-92 expression in the cell in order to promote the vascularization or vessel repair by introducing an antisense molecule against miR-92 into the cell, or (b2) increasing the miR-92 expression in the cell for an inhibition of the tumor angiogenesis by introducing a construct into the cell, wherein the construct includes an expressible miR-92 sequence. Furthermore, the invention relates to a pharmaceutical composition, comprising an agent for reducing the miR-92 activity or expression in a cell in the form of an antisense molecule against miR-92, or an agent for increasing the miR-92 expression in a cell in the form of a construct for expressing miR-92.

Abstract: The invention relates to a method for inhibiting the expression of a target gene in a eukaryotic cell. The method includes the following steps: a) providing at least one eukaryotic cell, the cell being capable of RNA interference, b) transfecting the eukaryotic cell with a composition that includes a genetic construct that includes an siRNA tag, and a target gene that forms a transcription unit together with the siRNA tag, and c) introducing at least one siRNA that is complementary to the siRNA tag of the transfected genetic construct to inhibit the expression of the target gene.

Abstract: The present invention provides a method of preventing or reducing restenosis, neointima formation, graft failure, atherosclerosis, angiogenesis and/or solid tumor growth in a subject The method comprises administering to the subject a prophylactically effective dose of a nucleic acid which decreases the level of c-Jun mRNA, c-Jun mRNA translation or nuclear accumulation or activity of c-Jun. It is preferred that the nucleic acid is a DNAzyme that targets c-Jun mRNA.

Abstract: Antisense oligonucleotides against cPLA2 are provided, which are capable of inhibiting cPLA2 expression as well as superoxide production, especially in phagocytes. These antisense oligonucleotides are powerful agents for the treatment of inflammatory conditions, in particular arthritis, as well as in neurodegenerative diseases. The antisense oligonucleotides or compositions comprising the same may be used in methods of treatment of such diseases.

Abstract: Described herein are polynucleotides associated with prostate and lung cancer. The polynucleotides are miRNAs and miRNA precursors. Related methods and compositions that can be used for diagnosis, prognosis, and treatment of those medical conditions are disclosed. Also described herein are methods that can be used to identify modulators of prostate and lung cancer.

Abstract: The present invention relates to a group of noel viral RNA regulatory genes, here identified as “viral genomic address messenger genes”or “VGAM genes”, and as “Viral genomic record”or “VGR genes”. VGAM genes selectively inhibit translation of known host target genes, and are believed to represent a pervasive viral attack mechanism. VGR genes encode an “operon”-like cluster of VGAM genes. VGAM and viral VGR genes may therefore be useful in diagnosing, preventing and treating viral disease. Several nucleic acid molecules are provided respectively encoding several VGAM genes, as are vectors and probes, both comprising the nucleic acid molecules, and methods and systems for detecting VGAM genes, and for counteracting their activity.

Abstract: The invention relates to the therapeutic use of stabilized oligoribonucleotides as immune modulatory agents for immune therapy applications. Specifically, the invention provides RNA-based oligoribonucleotides with improved nuclease and RNase stability and that selectively induce immune modulatory activity through TLR7.

Abstract: Methods and means are provided for reducing the phenotypic expression of a nucleic acid of interest in eukaryotic cells by providing aberrant, preferably unpolyadenylated, target-specific RNA to the nucleus of the host cell. Preferably, the unpolyadenylated, target-specific RNA is provided by transcription of a chimeric gene comprising a promoter and a DNA region encoding the target-specific RNA.

Abstract: The present invention is directed to methods for suppressing the growth of oral squamous-cell carcinoma cells. The methods include introducing at least one gene selected from miR-137 or miR-193a into oral squamous-cell carcinoma cells.

Abstract: An inducible system and methods for controlling expression of siRNA are provided. An inducible system for producing siRNA only in the presence of HIV TAT, and methods for inhibiting HIV-1 gene expression in cells comprising such inducible system also are provided.

Abstract: There is provided a method of identifying DNA responsible for conferring a particular phenotype in a cell which method comprises a) constructing a cDNA or genomic library of the DNA of the cell in a suitable vector in an orientation relative to a promoter(s) capable of initiating transcription of the cDNA or DNA to double stranded (ds) RNA upon binding of an appropriate transcription factor to the promoter(s), b) introducing the library into one or more of the cells comprising the transcription factor, and c) identifying and isolating a particular phenotype of the cell comprising the library and identifying the DNA or cDNA fragment from the library responsible for conferring the phenotype.

Abstract: The invention relates to the therapeutic use of stabilized oligoribonucleotides as immune modulatory agents for immune therapy applications. Specifically, the invention provides RNA based oligoribonucleotides with improved nuclease and RNase stability and that have immune modulatory activity through TLR7 and/or TLR8.

Abstract: The present invention uses an RPN2 gene expression inhibitor as a cancer cell growth inhibitor, which further includes a drug showing an anti-cancer action if desired, and is administered in combination with atelocollagen if desired. In addition, the present invention is an anti-cancer agent including such cancer cell growth inhibitor.

Abstract: Compounds, compositions and methods are provided for modulating the expression of exportin 5. The compositions comprise oligonucleotides, targeted to nucleic acid encoding exportin 5. Methods of using these compounds for modulation of exportin 5 expression and for diagnosis and treatment of diseases and conditions associated with expression of exportin 5 are provided.

Abstract: Compounds, compositions and methods are provided for modulating the expression of transthyretin. The compositions comprise oligonucleotides, targeted to nucleic acid encoding transthyretin. Methods of using these compounds for modulation of transthyretin expression and for diagnosis and treatment of diseases and conditions associated with expression of transthyretin are provided.