Postdoctoral Fellows

D. Jacobs Damon Jacobs Ph.D., Postdoctoral Fellow
Mentor: Pamela Tran

Research interest: Obesity is a growing epidemic in industrialized nations of the world and is the primary cause of several life-threatening metabolic disorders, such as hypertension, liver disease, and diabetes. Primary cilia are antennae-like extensions present on most cells of the body, they contain receptors (such as Hedgehog, Wnt, PDGFa, ...etc.) that are important for communicating signals from the extracellular environment into the cell. ‘Ciliopathies' arise due to defects in proteins that localize to primary cilia and can cause developmental and postnatal defects such as polydactyly, cystic kidney disease and obesity. Thm1 is a critical ciliary protein that is important in maintaining proper cell signaling programs, and I am working with a THM1-/- mouse model to characterize the postnatal obesity phenotype and examine the physiological and neurological causes of obesity onset. We are working toward identifying potential therapeutic targets for controlling the onset of obesity.
S Jasti Susmita Jasti Ph.D., Postdoctoral Fellow
Mentor: Margaret Petroff

My research work involves understanding the association between parity and cancer risk. During pregnancy, the foreign antigens present on fetal tissues elicit an immune response leading to the presence of anti-fetal T cells in the mother. One such antigen include shared placenta/tumor antigens. These are protein molecules that are expressed by placenta and many tumors, and are either absent or minimally expressed in normal tissues. I am using a mouse model of a surrogate shared placenta/tumor antigen, Ovalbumin to test the hypothesis that maternal T cells against these antigens are elicited during pregnancy, and subsequently provide immune protection against cancer bearing the same antigen in the parous mothers.
T Tanaka Tomohiro Tanaka Ph.D., Postdoctoral Fellow
Mentor: Hiroshi Nishimune

Pathology of Amyotrophic lateral sclerosis (ALS), a fatal motor neuron disease. Our previous research suggested that the denervation rate of motor axons in ALS model mice is significantly increased, even before the degeneration of their cell bodies(dying-back neuropathy). However, the mechanism causing dying-back neuropathy has not been elucidated. My research is focused on the phenomena typically found in motor neurons of ALS model mice, emerging both neuromuscular junction and cell bodies, and see if there is a time lag between these two compartments. This project will uncover what is responsible for dying-back neuropathy in ALS.
N Wilson Natalie Wilson, Ph.D., Postdoctoral Fellow
Mentor: Doug Wright

My research interests focus on the glyoxalase enzyme system and its ability to protect against the development of diabetic neuropathy.  This enzyme system breaks down highly reactive dicarbonyls, and is composed of 2 enzymes of which glyoxalase 1 (GLO1) is rate limiting enzyme. The activity of GLO1 differs among mouse strains; we are currently utilizing GLO1 overexpressing mouse lines to further demonstrate the beneficial role of this enzyme system against the development of diabetic neuropathy.  We are also investigating if GLO1 expression differences also occur in human patients and whether this system can be targeted to improve diabetic neuropathy in patients.

Last modified: Aug 25, 2014