Abstract: The present invention relates to cardiac performance, in particular to regulating cardiac performance via recombinant troponin I (TnI) protein and nucleic acids encoding recombinant TnI. The present invention provides nucleic acids encoding gain of function TnI proteins (e.g., cTnlA164H), vectors containing such nucleic acids, host cells containing such vectors, transgenic animals carrying a gain of function TnI protein (e.g., a cTnlA164H transgene), and therapeutic agents (e.g., comprising recombinant TnI, TnI analogues, synthetic TnI, or the like) or agents for gene therapy of heart failure or disease for research and therapeutic uses.

Abstract: Peptide analogs of oxyntomodulin (OXM, glucagon-37), which have been modified to be resistant to cleavage and inactivation by dipeptidyl peptidase IV (DPP-IV) and to increase in vivo half-life of the peptide analog while enabling the peptide analog to act as a dual GLP-1/glucagon receptor (GCGR) agonistm are described. The peptide analogs are useful for treatment of metabolic disorders such as diabetes and obesity.

Abstract: The present invention relates to cardiac performance, in particular to regulating cardiac performance via recombinant troponin I (TnI) protein and nucleic acids encoding recombinant TnI. The present invention provides nucleic acids encoding gain of function TnI proteins (e.g., cTnlA164H), vectors containing such nucleic acids, host cells containing such vectors, transgenic animals carrying a gain of function TnI protein (e.g., a cTnlA164H transgene), and therapeutic agents (e.g., comprising recombinant TnI, TnI analogues, synthetic TnI, or the like) or agents for gene therapy of heart failure or disease for research and therapeutic uses.

Abstract: Cells and non-human transgenic animals have been engineered to be deficient in the gene encoding agouti-related protein (AgRP). AgRP deficient transgenic animals have a reduced day time respiratory quotient (RQ), indicating that AgRP is involved in the regulation of energy metabolism, resulting in the reduced usage of fat as an energy source. These AgRP deficient transgenic animals can be used to select for and test potential modulators of AgRP. This data allows for methods of screening for AgRP modulators which regulate energy metabolism and caloric utilization. The disclosure also relates to a NPY/AgRP double knockout mouse which can be used to select for and test potential modulators (e.g., agonists or antagonists) of AgRP and/or NPY.