The disclosure provides inducible caspase polypeptides, compositions comprising inducible caspase polypeptides and sequences encoding the same, cells modified to express the polypeptides and compositions of the disclosure, as well as methods of making and methods of using same for adoptive cell therapy.

Compositions comprising peptide sequences with high cytotoxicity to cancer cell lines are provided. Pharmaceutical compositions comprising peptide sequences with high cytotoxicity to cancer cell lines are provided. A method for treating cancer is provided.

Bag3 is a multifunctional protein expressed predominantly in the heart, the skeletal muscle, the central nervous system and in many cancers. Although BAG3 was cloned only a decade ago, studies have shown that genetic variants, particularly those that result in haplo-insufficiency, can lead to severe left ventricular dysfunction; however, the full mechanisms responsible have remained obscure. To obviate the influence of heart failure itself on the biology of Bag3, ransgenic mice harboring a single allele knock-out were studied between 8 and 10 weeks of age before any obvious signs of heart failure were evident. The results were surprising and informative. First, it was found that despite a normal phenotype, young Bag3.sup.+/− had marked changes in the proteome that were characterized by changes in proteins associated with metabolism and apoptosis. Consistent with this finding, a decrease in the levels of critical proteins charged with maintaining the mitochondrial membrane potential was observed. It was also found that young mice shifted from a balance between the extrinsic and intrinsic pathways of apoptosis. However, in the presence of stress and the absence of Bag3 there was a shift from a balanced to an extrinsic dominant system (cleaved caspase 8). The diverse array of critical pathways regulated by Bag3 suggests a more important role especially during stress and that this role might include serving as an intracellular glue that holds proteins where they can be most effective rather than having them meet accidentally.

The present disclosure provides danoprevir/NS3a complex reader (DNCR) and grazoprevir/NS3a complex readers (GNCR) polypeptides, fusion proteins, and combinations and their use.

Provided herein are peptides that bind Mcl-1. Also provided are compositions containing these polypeptides and methods of using such peptides in the treatment of cancer that include administering to a subject one of the polypeptides.

The present invention provides an antagonist of a Bcl-2 prosurvival protein containing a BH3-like domain. The antagonist of the invention comprises ARTS and any fragment or peptide that comprises a BH3-like domain. The invention further provides compositions, combined compositions and kits as well as methods for treating Bcl-2 over-expressing disorders.

Provided herein are recombinant peptides useful for inhibiting the function of autophagy-related 8 (Atg8) proteins. The recombinant peptides can be used in the preparation of imaging agents for monitoring autophagy in a cell or subject and treating autophagy related diseases, such as cancer.

The disclosure provides BI-1 modulating peptides and methods for treating cancer in a subject by administering an effective amount of a BI-1 modulating peptide.

In one aspect, a method of altering programmed cell death includes administering to an individual in need thereof a therapeutically effective amount of isomyosmine or a pharmaceutically acceptable salt thereof. In other aspects, isomyosmine is administered to treat a wound, hemochromatosis, traumatic brain injury, or disorders associated with chronic oxidative stress. In other aspects, isomyosmine is administered to increase blood oxygen saturation levels.

The present invention relates to a method of using family and/or regulatory members of the PD-1/PD-L1 pathway as predictive markers for risk of skin cancer development and as targets for therapeutic prevention of pre-malignant (or pre-cancerous) skin lesions and non-melanoma skin cancer (NMSC). This invention will allow for quantitative measurements of UV-induced expression of PD-1/PD-Li signaling pathway family members (e.g., PD-1, PD-L1, PD-L2) and/or PD-1/PD-L1 regulatory factors including AP-1 and NFκB family members in skin tissue of individuals to determine an individual's 1) risk for skin cancer development and 2) appropriate prophylactic treatment strategy to prevent skin cancer development. This information will facilitate identification of those patients at risk for pre-malignant (or pre-cancerous) skin lesions or subsequent NMSC lesions who would benefit from a PD-1/PD-L1 pathway suppressing therapy to prevent skin cancer development.