Abstract: Provided herein are methods, kits, and assays for identifying and quantifying a mitochondrial protein in a sample using mass spectrometry. Also provided herein are methods, kits, and assays for determining a mitochondrial protein biomarker signature for a subject using mass spectrometry.

Abstract: Methods of treating or inhibiting ischemia and reperfusion injury are provided.

Abstract: In alternative embodiments, the invention provides cell-permeable recombinant or synthetic proteins to modulate autophagy, including a Tat-Atg5K130R (inhibitor of autophagy) and a Tat-Beclin 1 (stimulant or activator of autophagy), and nucleic acids expressing them and methods for making and using them, e.g., to treat conditions and disorders responsive to autophagy modulation (e.g., where autophagy is dysregulated), including neurodegeneration, cystic fibrosis, cancer, heart failure, diabetes, obesity, sarcopenia, aging, ischemia/reperfusion, inflammatory disorders including Crohns, ulcerative colitis, biliary cirrhosis, lysosomal storage diseases, infectious diseases associated with intracellular pathogens including viruses, bacteria, and parasites such as Trypanosomes and malaria.

Abstract: The invention provides methods and compositions for detecting and measuring the amount of autophagosomes in cells or tissues, including biopsy samples, in vitro, in situ and/or in vivo. By detecting and measuring the amount of autophagosomes in cells or tissues, the methods and compositions of the invention also measure the amount of autophagic activity in a cell or a tissue. In one aspect, the invention can be adapted to a plate-reader format for high-throughput screening of drugs that modulate autophagy, i.e., high-throughput detection of autophagic (autophagosome) activity in cells or tissues. In alternative embodiments, the compositions of the invention can localize into autophagosomes (AV), and these compositions can comprise any detectable moiety or group, e.g., a cadaverine, a radioactive, fluorescent-, bioluminescent and/or paramagnetic-conjugated reagent.

Abstract: The invention provides methods and compositions for treating, ameliorating or preventing diseases or conditions caused by or aggravated by lost and/or impaired mitochondrial Complex I function, including treating, ameliorating or preventing an ischemia and/or reperfusion injury, Parkinson's disease, myopathic diseases, cardiolipin deficiency, neurodegenerative diseases, aging, diabetes, obesity, sepsis and other conditions in which mitochondrial Complex I function is lost and/or impaired.

Abstract: Methods of treating or inhibiting ischemia and reperfusion injury are provided.

Abstract: Methods of treating or inhibiting ischemia and reperfusion injury are provided.

Abstract: Methods of treating or inhibiting ischemia and reperfusion injury are provided.

Abstract: The present invention relates to therapeutic methods for treating diseases characterized by an accumulation of high molecular weight DNA in mucous, thereby contributing to the viscosity of the mucous. Such diseases include cystic fibrosis and chronic bronchitis. Treatment includes administration of weak organic acids to promote acidification of cells and consequently apoptosis-induced DNA fragmentation. The invention also relates to therapeutic apparatus for administering the acid compositions.