Abstract: Compounds, compositions and methods are provided for selectively activating chaperone-mediated autophagy (CMA), protecting cells from oxidative stress, proteotoxicity and lipotoxicity, and/or antagonizing activity of retinoic acid receptor alpha (RAR?) in subjects in need thereof.

Abstract: Methods and compositions are disclosed for rapid functional analysis of gene variants based on analysis of protein-protein and protein-nucleic acid interactions.

Abstract: The disclosure provides polypeptides that specifically bind to HLA-DQ8 for treating Type 1 Diabetes (TID) and methods using same for reducing autoimmune destruction of pancreatic islet beta cells. In particular, the present disclosure relates to peptides containing at least one D-amino acid that are capable of blocking the presentation of antigenic islet peptides (e.g., lnsB:9-23) by HLA-DQ8, and to their uses, especially as it relates to the prevention and/or treatment of TID.

Abstract: Methods, pharmaceutical compositions and vaccines comprising an attenuated bacteria that expresses a recall antigen are disclosed for treatment of cancer.

Abstract: The application discloses methods and compositions for inhibiting functions associated with vascular endothelial growth factor-A (VEGF-A). The methods and compositions may involve the use of pan-variant specific aptamers for binding to VEGF-A, and preventing or reducing association of VEGF-A with Flt-1, KDR, or Nrp-1. The methods and compositions may include one or more aptamers that bind to receptor binding face of VEGF-A. The methods and compositions may include one or more aptamers that bind to a receptor binding domain of VEGF-A. The application further provides anti-VEGF-A aptamers for the treatment of ocular diseases or disorders. In some cases, the anti-VEGF-A aptamers may have a stem-loop secondary structure.

Abstract: Methods, pharmaceutical compositions and vaccines comprising an attenuated bacteria that expresses a recall antigen are disclosed for treatment of cancer.

Abstract: Synthetic fragment antigen-binding (Fab) antibodies are disclosed that bind to an N-terminal activation site of BCL-2-associated X-protein (BAX) and inhibit BAX activation. Also disclosed are methods of using the Fabs for measuring inactive monomeric BAX levels, screening for small molecules that bind to an N-terminal activation site of BAX, inhibiting apoptotic cell death, and predicting the ability of a cancer therapy to promote apoptotic cell death.

Abstract: Microvesicles produced by stem cells grown on a silk scaffold for enhancing stem cell self-renewal/proliferation and promoting tenogenesis in damaged tendons, and their use in tendon wound repair and tendinopathy treatment. Also provided are compositions containing the microvesicles and devices for obtaining them.

Abstract: Described herein are phenylsulfonamido-benzofuran derivatives, and pharmaceutically acceptable salts thereof. Also provided are pharmaceutical compositions, methods, uses, and kits involving compounds of Formulae (I), (II), (III), (IV), (V), or (VI) for treating and/or preventing proliferative diseases (e.g. cancers, inflammatory diseases, and autoimmune diseases) in a subject. The compounds and pharmaceutical compositions as described herein inhibit at least one protein of the BCL-2 family in a biological sample or subject to treat and/or prevent a proliferative disease. In certain embodiments, compounds described herein are selective inhibitors of MCL-1, a BCL-2 family member protein.

Abstract: Compositions and methods to increase the in vivo capacity of CD8+ T cells to kill HIV-infected and reactivated latent HIV-infected T cells (LHITC) to functionally cure HIV infection or improve the clinical course. Compositions and methods to increase the in vivo capacity of CD8+ T cells to kill CMV or CMV-infected cells are also provided.

Abstract: Systems and methods for treating cancer and for preventing metastasis using low intensity focused ultrasound in combination with an anti-cancer therapy are disclosed.

Abstract: This invention relates generally to the use of 5?-methylthioadenosine phosphorylase (MTAP) inhibitors for the treatment of lung diseases associated with inflammation, such as cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD). Small molecule inhibitors of MTAP can sustain accumulation of endogenous MTA to therapeutically beneficial levels resulting in decreased inflammation in CF and COPD.

Abstract: Methods are disclosed for treating acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) using compounds that inhibit p21 protein (Cdc42/Rac)-activated kinase (PAK1).

Abstract: Provided herein are methods of determining a subject's level of exposure to radiation and methods of determining a subject's risk of subsequent development of radiation disease or risk of poor prognosis from radiation exposure that include determining a level of one or more miRNAs selected from the group consisting of mouse and human homologues of mouse miR-130a-3p, miR-150-5p, miR-17-3p, miR-187-3p, miR-194-5p, miR-27a-3p, miR-30a-3p, miR-30c-5p, miR-142-5p, miR-342-3p, miR-34b-3p, miR-126-3p, miR-320-3p, miR-136-5p, miR-33-5p, miR-142a-3p, miR-706, miR-375-3p, miR-29a-5p, miR-193a-3p, miR-99b-5p, miR-151-3p, miR-let-7d-3p, miR-486-5p, miR-423-5p, miR-30b-5p, miR-191-5p, miR-497a-5p, miR-32-5p, miR-214-5p, miR-326-3p, miR-1195, miR-122-5p, miR-1839-3p, miR-500-3p, miR-30e-3p, miR-322-3p, miR-709, miR-486-3p, miR-133a-3p, miR-676-3p, miR-744-5p, miR-29a-3p, miR-1839-5p, miR-30a-5p, miR-199b-5p, miR-125a-5p, miR-133b-3p, miR-24-3p, miR-21a-5p, miR-503-5p, miR-328-3p, miR-let-7g-5p, miR-362-3p, miR-199a-5p, miR

Abstract: Heritable mutations in the BRCA1 and BRCA2 and other genes in the DNA double-strand break (DSB) repair pathway increase risk of breast, ovarian and other cancers. In response to DNA breaks, the proteins encoded by these genes bind to each other and are transported into the nucleus to form nuclear foci and initiate homologous recombination. Flow cytometry-based functional variant analyses (FVAs) were developed to determine whether variants in BRCA1 or other DSB repair genes disrupted the binding of BRCA1 to its protein partners, the phosphorylation of p53 or the transport of the BRCA1 complex to the nucleus in response to DNA damage. Each of these assays distinguished high-risk BRCA1 mutations from low-risk BRCA1 controls. Mutations in other DSB repair pathway genes produced molecular phenocopies with these assays. FVA assays may represent an adjunct to sequencing for categorizing VUS or may represent a stand-alone measure for assessing breast cancer risk.

Abstract: Recombinant herpes simplex virus 2 (HSV-2) vaccine vectors, virions thereof, compositions and vaccines comprising such, and methods of use thereof are each provided.

Abstract: Heritable mutations in the BRCA1 and BRCA2 and other genes in the DNA double-strand break (DSB) repair pathway increase risk of breast, ovarian and other cancers. In response to DNA breaks, the proteins encoded by these genes bind to each other and are transported into the nucleus to form nuclear foci and initiate homologous recombination. Flow cytometry-based functional variant analyses (FVAs) were developed to determine whether variants in BRCA1 or other DSB repair genes disrupted the binding of BRCA1 to its protein partners, the phosphorylation of p53 or the transport of the BRCA1complex to the nucleus in response to DNA damage. Each of these assays distinguished high-risk BRCA1 mutations from low-risk BRCA1 controls. Mutations in other DSB repair pathway genes produced molecular phenocopies with these assays. FVA assays may represent an adjunct to sequencing for categorizing VUS or may represent a stand-alone measure for assessing breast cancer risk.

Abstract: A system and a method for identifying a cognate ligand molecules for known proteins.

Abstract: The present invention is related to the development of therapeutics and prophylactics for the treatment and/or prevention of filovirus infection in humans and other mammals. A new class of small molecules is disclosed that inhibits the interaction of naturally processed (i.e., proteolytically cleaved) filovirus glycoprotein (GPCL) with its host receptor Niemann-Pick C1 (NPC1) protein and thus block infection of host cells by filoviruses. Also disclosed are methods of using the small molecule inhibitors in the treatment/prevention of filovirus infection.

Abstract: Methods of treating a wound in a subject are provided comprising administering to the subject an amount of an inhibitor of Fidgetin-like 2. Compositions and pharmaceutical compositions comprising an amount of an inhibitor of Fidgetin-like 2 are also provided. Methods are also provided for identifying an inhibitor of Fidgetin-like 2.