Maureen Gannon, Ph.D.
Department of Medicine, Division of Diabetes, Endocrinology and Metabolism
Department of Molecular Physiology and Biophysics
Department of Cell and Developmental Biology
Vanderbilt University Medical Center
2213 Garland Avenue
MRB IV 7435
Nashville, TN 37232
office: (615) 936-2676
lab: (615) 936-2683
fax: (615) 936-1667
Hometown: Goshen, Indiana
Education: B.A. in Biology from Hanover College
Prostaglandins are important modulators of an array of physiologic functions including insulin secretion and systemic inflammation. EP3 and EP4 play opposing roles in many cell types due to signaling through different G proteins, resulting in Gi inhibition (EP3) or Gs stimulation (EP4) of adenylyl cyclase. We hypothesize that EP3 and EP4 play opposing roles in regulating β-cell mass expansion. Signaling via EP3 is predicted to inhibit β-cell proliferation whereas activation of EP4 is predicted to enhance β-cell proliferation and survival. I am using genetic and pharmacological tools to examine the effects of EP3 and EP4 signaling in β-cell proliferation and survival in vivo and in ex vivo studies using rodent and human islets.
Hometown: Franklin, TN
Education: BA in Molecular Biology from Colgate University
I am interested in understanding the role of the transcription factor Oc1 (Onecut1) in pancreas development and disease. Oc1 is essential for development of the endocrine pancreas, so I am investigating its interaction its cofactor Pdx1 in that role. I have thus far determined that proper dosage of both Oc1 and Pdx1 is necessary for endocrine cell differentiation and that defects established during development persist into adulthood. I am also interested in the role of Oc1 in development of the exocrine pancreas, especially the digestive-enzyme secreting acinar cells. To that end, I am working to identify the targets of Oc1 during pancreas development through both ChIP-Seq and RNA-Seq. I am further determining the role of Oc1 in acinar cell development by inactivating Oc1 specifically in differentiated acinar cells. These studies will shed light on how developmental defects due to Oc1 misexpression could lead to adult diseases such as diabetes, pancreatitis, and pancreatic cancer.