The Magnuson lab is focused on understanding the regulatory processes that resolve pancreatic islet and acinar cell fate, initiate islet cell differentiation, and distinguish the pancreatic b-cell differentiation program from the other islet cell differentiation programs. They have been making use of site-specific DNA recombinases to accelerate the modification of specific gene loci in both mouse ES cells and mice. The Magnuson Laboratory is currently applying these methods to the study of several genes. These genes include: 1) Ptf1a, a transcription factor that plays a key role in both the development and function of the vertebrate pancreas, 2) Insm1, a snail/slug-related transcriptional repressor involved in the process known as Epithelial-Mesenchymal Transition (EMT) that may place an important role in the delamination of pancreatic epithelial cells as they are induced to differentiate towards a pancreatic endocrine fate, and 3) Pianissimo (also called RICTOR or mAVO3), an mTOR binding protein which is part of the rapamycin-insensitive mTOR complex 2.

NEWEST PUBLICATIONS

mTOR complex 2 is required for the development of prostate cancer induced by Pten loss in mice.  2009 Cancer Cell 15: 148-159

Differential structure of atrial and ventricular KATP: atrial KATP channels require SUR1.  2008 Circulation Research 103: 1458-1465

A Rictor-My1c complex participates in dynamic cortical actin events in 3T3-L1 adipocytes.  2008 Molecular Cell Biology 28: 4215-4226

Pdx-1 and Ptf1a concurrently determine fate specification of pancreatic multipotent progenitor cells.  2008 Developmental Biology 316: 74-86

A nonclassical bHLH Rbpj transcription factor complex is required for specification of GABAergic neurons independent of Notch signaling.  2008 Genes & Development 22: 166-178