University of Massachusetts

Silvia Corvera

Michael P Czech

Emmanouela Tsagkaraki

Sarah M Nicoloro

Provided herein are methods and compositions for disrupting expression of nuclear receptor interacting protein 1 (Nrip1) in adipose cells, and methods of use of such adipose cells for treating, or reducing risk of, a condition associated with an elevated body mass index (BMI).

Targeting Nrip1 to alleviate metabolic disease

Methods for preparation of prospectively identified human adipose stem cells enriched populations thereof, e.g., for therapy.

Human adipose tissue white and 'brown-on-white' progenitors for reconstructive and metabolic therapies

The invention features methods of enhancing whole body insulin sensitivity by modulating the endoplasmic reticulum (ER) stress response pathway in adipose cells. In one aspect, the methods involve targeting chaperone proteins important in the ER stress response pathway, for example, BiP and ERO-1. Another aspect features targeting the upstream transcription factors (e.g., CHOP-1 and XBP-1) of the genes encoding the chaperone proteins (and/or other ER proteins). Screening assays for identification of modulators of these ER proteins and/or transcription factors are also featured.

Methods and compositions for controlling appetite and modulating insulin sensitivity

The invention discloses a chimeric GLUT transporter including a GLUT receptor polypeptide fused to a domain of a detectable heterologous polypeptide and cells expressing such reporter constructs. Cells expressing a detectably-tagged chimeric GLUT transporter are used in methods of screening candidate compounds for their ability to agonize or antagonize an interaction between a ligand and a receptor, e.g., insulin. In addition, a 30 amino acid intracellular retention sequence is disclosed.

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Westborough, MA, United States of America

Silvia Corvera