The present disclosure relates to the treatment of Hutchinson-Gilford Progeria Syndrome (HGPS) and diseases related to vascular ageing and in the treatment of smooth muscle cells diseases, in particular an inhibitor of a metalloprotease the treatment of smooth muscle cells diseases. The disclosure subject matter describes a more effective therapies for the treatment of Hutchinson-Gilford Progeria Syndrome and diseases related to vascular ageing, or namely by the use of an inhibitor of a metalloprotease.

The present disclosure provides compositions and methods for reactivating latent immunodeficiency virus and/or reducing transcription of HIV integrated into the genome of an HIV-infected cell. The present disclosure provides compositions and methods for treating an immunodeficiency virus infection.

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.

The present invention relates to methods for upregulating immune responses using combinations of anti-RGMb and anti-PD-1 agents.

Provided is a composition and method for reducing a cellular senescence level by inhibiting the activity or expression of one or more of DCUN1D3 protein or gene encoding same and a polynucleotide having a nucleotide sequence of SEQ ID NO: 5, as well as a method of treating a disease or a disease symptom associated with an increased cellular senescence level in a mammal.

Provided is a composition and method for reducing a cellular senescence level by inhibiting the activity or expression of one or more of DCUN1D3 protein or gene encoding same and a polynucleotide having a nucleotide sequence of SEQ ID NO: 5, as well as a method of treating a disease or a disease symptom associated with an increased cellular senescence level in a mammal.

Disclosed herein are methods of controlling insect pests, in particular Leptinotarsa spp. which infest crop plants, and methods of providing plants resistant to such pests. Also disclosed are polynucleotides and recombinant DNA molecules and constructs useful in such methods, insecticidal compositions such as topical sprays containing insecticidal double-stranded RNAs, and solanaceous plants with improved resistance to infestation by Leptinotarsa spp. Further disclosed are methods of selecting target genes for RNAi-mediated silencing and control of Leptinotarsa spp.

The present invention provides a screening method for a pain suppressor, which method comprises using FLRT3 to select a substance capable of inhibiting FLRT3 expression or a substance capable of inhibiting FLRT3 transport to the spinal cord. In addition, the present invention provides a pharmaceutical composition for prevention or treatment of pain, which pharmaceutical composition comprises, as an active ingredient, a substance capable of inhibiting FLRT3 expression or a substance capable of inhibiting FLRT3 transport to the spinal cord.

Compositions and methods for down-regulating genes through oral administration of RNAi molecule encapsulated in plant cells are provided.

The present invention provides a c-Rel-specific siRNA and its use for preventing and treating autoimmune psoriasis. In particular, the c-Rel-specific siRNAs have sequences as shown in SEQ ID Nos. 1-2 or SEQ ID Nos. 3-4. In the present invention, small interfering RNA (siRel) specific to c-Rel are employed to inhibit c-Rel biosynthesis, and prevent and treat autoimmune psoriasis by inhibiting inflammatory factors relating to IL-23/IL-17A inflammatory axis.