Abstract: The invention features compositions comprising in vitro generated beta cells capable of glucose-stimulated insulin secretion, methods of inducing beta cell maturation from embryonic or induced pluripotent stem cell-derived beta-like cells, and methods of using in vitro generated beta cells for the treatment of type 1 diabetes, type 2 diabetes, or a related disorder.

Abstract: Methods of assembling modified adenoviruses, libraries of adenoviral gene modules and compositions thereof are provided herein.

Abstract: The method provides methods and compositions for treating metabolic disorders such as impaired glucose tolerance, elevated blood glucose, insulin resistance, dyslipidemia, obesity, and fatty liver.

Abstract: Provided herein are methods and compositions for improving muscle performance and increasing endurance. Agonists of AMP-activated protein kinase (AMPK) and agonists of peroxisome proliferator-activated receptor delta (PPAR?) can be used in such treatments.

Abstract: Anti-cancer adenoviruses, methods of use and methods of making the same are provided herein.

Abstract: Provided are methods of promoting browning of white adipose tissue (WAT) in a subject. Such methods can include administering to a subject (e.g., via the gastrointestinal tract) a therapeutically effective amount of fexaramine in combination with a therapeutically effective amount of a compound that mimics or increases sympathetic nervous system activity (e.g., one or more beta-adrenergic agonists and/or compounds that increase epinephrine secretion).

Abstract: The method provides methods and compositions for treating metabolic disorders such as impaired glucose tolerance, elevated blood glucose, insulin resistance, dyslipidaemia, obesity, and fatty liver.

Abstract: The present disclosure provides methods for modulating the interaction between a TAM ligand and a lipid membrane containing phosphatidyl serine (PtdSer). In one example, such methods use a TAM receptor agonist having a PtdSer-containing lipid bilayer membrane with Gas6 and/or Protein S bound to the membrane to activate signaling from one or more TAM receptors and treat an autoimmune disease. In another example, methods are provided for treating a subject with a pathological condition characterized by overactivation of TAM signaling and/or reduction in Type I IFN response, such as infection by an enveloped virus, by use of agents that decrease the interaction between a TAM ligand and PtdSer. Also provided are methods for classifying a virus as susceptible to anti-TAM therapy. Methods of identifying an agent that blocks virus infectivity are also provided.

Abstract: The present invention relates to mutants of the plant aminotransferase VAS1 and to transgenic plants expressing said mutant protein that exhibit a modulated response to shade. In certain embodiments, the mutations of VAS1 uncouple VAS1 metabolic coordination of auxin and ethylene homeostasis, so that reduction of auxin is no longer linked (via VAS1) to reduction of ethylene. Such uncoupling allows for the generation of plants carrying a VAS1 mutant transgene that demonstrate a modulated response to shade, for example, less hypocotyl growth.

Abstract: Provided herein are methods and compositions relating to the synthesis of isoprenoid diphosphates using a mutated isopentenyl phosphate kinase.

Abstract: Cyclic CRF antagonist peptides having improved properties of “drugability”. The peptides are 33 residues in length with a lactam bond between the residues in position 22 and 25; however, they may be N-terminally shortened by up to 3 residues.

Abstract: This application provides methods of increasing vascularization, muscle performance, muscle rehabilitation, and/or mitochondrial activity in subjects in need thereof, by administering a therapeutically effective amount of one or more agents that increases ERR? activity to the subject. Such agents can include one or more ERR? agonists. In some examples the method does not require that the subject exercise, and as such, the subject may be sedentary (such as bedridden or in a wheelchair).

Abstract: ETP1 and ETP2 bind to EIN2 and modulate plant ethylene sensitivity.

Abstract: The present invention relates to a chimeric protein that includes an N-terminus coupled to a C-terminus, where the N-terminus includes a portion of a paracrine fibroblast growth factor (“FGF”) and the C-terminus includes a C-terminal portion of an FGF19 molecule. The portion of the paracrine FGF is modified to decrease binding affinity for heparin and/or heparan sulfate compared to the portion without the modification. The present invention also relates to pharmaceutical compositions including chimeric proteins according to the present invention, methods for treating a subject suffering from diabetes, obesity, or metabolic syndrome, and methods of screening for compounds with enhanced binding affinity for the ?Klotho-FGF receptor complex involving the use of chimeric proteins of the present invention.

Abstract: The method provides methods and compositions for treating metabolic disorders such as impaired glucose tolerance, elevated blood glucose, insulin resistance, dyslipidaemia, obesity, and fatty liver.

Abstract: This application provides methods of increasing vascularization, muscle performance, muscle rehabilitation, and/or mitochondrial activity in subjects in need thereof, by administering a therapeutically effective amount of one or more agents that increases ERR? activity to the subject. Such agents can include one or more ERR? agonists. In some examples the method does not require that the subject exercise, and as such, the subject may be sedentary (such as bedridden or in a wheelchair).

Abstract: The present disclosure relates to chimeric polypeptide having TGF-beta activity, nucleic acids encoding the polypeptides, and host cells for producing the polypeptides.

Abstract: The relationship between F-box proteins and proteins involved in the ethylene response in plants is described. In particular, F-box proteins may bind to proteins involved in the ethylene response and target them for degradation by the ubiquitin/proteasome pathway. The transcription factor EIN3 is a key transcription factor mediating ethylene-regulated gene expression and morphological responses. EIN3 is degraded through a ubiquitin/proteasome pathway mediated by F-box proteins EBF1 and EBF2. The link between F-box proteins and the ethylene response is a key step in modulating or regulating the response of a plant to ethylene. Described herein are transgenic plants having an altered sensitivity to ethylene, and methods for making transgenic plant having an altered sensitivity to ethylene by modulating the level of activity of F-box proteins. Methods of altering the ethylene response in a plant by modulating the activity or expression of an F-box protein are described.

Abstract: The method provides methods and compositions for treating metabolic disorders such as impaired glucose tolerance, elevated blood glucose, insulin resistance, dyslipidaemia, obesity, and fatty liver.

Abstract: The present invention relates to methods of treating or preventing a metabolic disorder in a subject, methods of treating or preventing coronary artery disease in a subject with a metabolic disorder, as well as methods of reducing hepatic glucose production in a subject. Such methods include, but are not limited to, the administration to the subject of inhibitors or activators of CaMKII, IP3Rs, calcineurin, p38, MK2/3, HDAC4, Dach1, Dach2, or any combination thereof. The invention also provides methods of identifying a compound that inhibits the activity of CaMKII, IP3Rs, calcineurin, p38, MK2/3, HDAC4, Dach1 or Dach2, or reduces the activity and/or activation of CaMKII, IP3Rs, calcineurin, p38, MK2/3, HDAC4, Dach1 or Dach, or activates CaMKII, IP3Rs, calcineurin, p38, MK2/3, HDAC4, Dach1 or Dach2.