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Postbac Seminar Series: September 12, 2019

Series: Science Skills; Speaking

Sep 12, 2019

This event is recommended for: Postbacs.

Science isn't complete until the results have been shared with others, and talking about your results is one of the important ways of making them public. The Postbac Seminar Series provides a unique opportunity for two Postbacs each month to present their research to a diverse audience of their peers.  The atmosphere is relatively informal and non-threatening.  The series allows Postbacs who attend to learn about the different types of biomedical research being conducted at the NIH while meeting other postbacs.  Read more about the seminar series.

This month's presenters are:

Name: Upneet Kaur


Research Title: Unroofing Alpha-Synuclein Membrane Interactions

Research Summary: α-Synuclein, despite being a widely studied neuronal protein involved in the pathology of Parkinson’s disease, remains an enigma because its physiological functions are not well understood.  Membrane association of α-syn suggests that the properties of the cellular membrane are likely important for its biological behavior. To mimic the cytoplasmic surface of cellular membranes, we are unroofing cells. Preliminary data shows that α-syn co-localizes with the unroofed cells in a punctate pattern, which may be due to local membrane curvature that has been known to enhance α-syn binding. Also, performing a concentration-dependent series of α-syn with unroofed cells shows that increasing concentrations of α-syn may remodel unroofed cells. This study elucidates α-syn membrane interactions by using a membrane mimetic that encapsulates the spatial and topological complexity of cellular membranes.

Bio: Upneet graduated from the University of Massachusetts Amherst with honors in Biochemistry and Molecular Biology. She completed her thesis in the lab of Dr. Anne Gershenson, investigating protein folding of serine protease inhibitors.  Currently, Upneet works with Dr. Jennifer Lee, exploring alpha-synuclein membrane interactions and its implications in Parkinson’s disease. She is applying to MD/PhD programs in biophysics.


Name: Louise Stolz


Research Title: PET imaging of phosphodiesterase-4 identifies affected dysplastic bone in McCune-Albright syndrome, a genetic mosaic disorder

Research Summary: In McCune-Albright syndrome (MAS), a mutation in the GNAS gene results in constitutive activation of Gsα leading to increased cAMP signaling and therefore an upregulation of phosphodiesterase-4 (PDE4). It is unknown whether fibrous dysplasia and other symptoms of MAS is related to increased PDE4 activity. We sought to evaluate changes in the cAMP cascade both in the brain and peripheral organs of individuals with MAS to determine whether these increases in activity correlate with known areas of fibrous dysplasia. PET imaging of [11C](R)-rolipram, which binds to PDE4, reflects cAMP cascade activity. We have shown that subjects with MAS show greater rolipram binding than controls in areas known to be affected by the disorder.

Bio: Louise graduated from Brown University with a B.Sc. in Neuroscience. At Brown, she completed her thesis work under Dr. David Badre comparing demand avoidance in cognitive versus physical effort. She also worked with Dr. Wael Asaad on a project analyzing credit assignment in severe OCD patients before and after they received laser lesion surgery. At the NIH with Dr. Robert Innis, she has used PET imaging to research the cAMP cycle in McCune-Albright syndrome patients as well as to study inflammation in patients with variations of dementia.


Name: Samuel Chauvin


Research Title: XMEN Disease: A novel congenital disorder of glycosylation

Research Summary: X-linked immunodeficiency with magnesium defect, Epstein-Barr virus (EBV) infection, and neoplasia (XMEN) disease is a primary immunodeficiency caused by the genetic loss of the magnesium transporter protein 1 (MAGT1) gene. XMEN disease is marked by chronic EBV infection, EBV induced lymphomas and decreased expression of the Natural Killer Group 2, member D (NKG2D) receptor. Recently, we discovered broader pathogenesis of XMEN disease which included lymphadenopathy (LAD), liver disease, cavum septum pellucidum, and an inverted CD4: CD8 ratio. MAGT1 is homologous to the yeast ost3/6 proteins which are involved in glycosylation, so we performed glycoproteomic analysis of XMEN samples. We discovered a small subset of glycoproteins is affected, with a preferential defect in sites that are close to transmembrane regions. Our results show that XMEN is a mild congenital disorder of glycosylation with multi-system abnormalities, which has important ramifications for the diagnosis and treatment of patients.

Bio: Samuel graduated from Cornell University in 2018. Since then, he has worked in Dr. Mike Lenardo’s section of the Laboratory of Immune System Biology at NIAID. While studying the molecular mechanism of extremely rare genetic diseases, Sam has fallen in love with clinical immunology and wishes to continue studying it throughout medical school and beyond.