People in the Bassell Lab

bassell-gary-150x210.jpgGary J. Bassell, PhD
Professor and Chair
gbassel@emory.edu

Gary J. Bassell, Ph.D. joined the faculty at Emory University School of Medicine in 2005, where he is currently Professor and Chair of the Department of Cell Biology http://cellbio.emory.edu. Prior to moving Emory, Dr. Bassell was a member of the faculty at the Albert Einstein College of Medicine, in the Department of Anatomy and Structural Biology (1995-1998) and subsequently in the Department of Neuroscience and Rose Kennedy Center for Mental Retardation (1998-2005). Read More

Dr. ShiLiang Shi, PhD
Associate Scientist
liang.shi@emory.edu

My overall research focuses on understanding mechanisms of axonal mRNA transport and local protein synthesis in neurons. In particular, I am studying the role of the Fragile X Mental Retardation Protein (FMRP) in cultured neurons using fluorescence microscopy and live cell imaging methods. This will expand our understanding of Fragile X Syndrome and promote development of therapeutic strategies.

   

Dr. ShiBethleham "Betty" Bekele
Graduate Student (PhD program, Neuroscience)
bethlehem.bekele@emory.edu

My current research is focused on understanding the molecular and neurobiological mechanisms that contribute to brain pathology in Myotonic Dystrophy Type 1 (DM1). I use the Muscleblind-like protein 2 (MBNL2)- deficient DM1 mouse model as well as patient-derived induced pluripotent stem cells (iPSCs) to study CNS deficits DM1. The findings from my research will help design novel therapies that mitigate the behavioral/cognitive impact of the disease.

   

Mingee "Tony" Chungraj-nisha-150x210.jpg
Research Specialist
tony.chung@emory.edu

My interests revolve around the overlapping genetics and pathogenesis that lead to C9 ALS/FTD. As a research specialist, I am working jointly with Zachary McEachin to understand the role of chimeric dipeptide repeats in C9orf72-ALS/FTD pathogenesis. More broadly we are interested in understanding splicing defects associated with TDP-43 proteinopathies. By utilizing model systems such as patient-specific induced pluripotent stem cells (iPSCs), organoid models, and patient tissues, we are attempting to uncover and model the disease pathway underlying C9orf72-ALS/FTD.

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Kamyra Edokpolor, PhD
Lead Research Specialist
kamyra.edokpolor@emory.edu

My research centers around using mouse models to elucidate neural mechanisms underlying impairments in inhibitory brain circuits in Myotonic Dystrophy Type 1 (DM1). DM1 is a neuromuscular, neurodegenerative, and multisystemic disease with many of its central nervous system symptoms, such as emergence and recovery from anesthesia and hypersomnia under-researched. My research examines how sequestration of Muscle blind like protein 2 (MBNL2) RNA-binding protein alters the expression of specific inhibitory receptors, which may play a role in delayed emergence and recovery from anesthesia and increased sleep phenotypes observed in DM1.

 

A Janusz-Kaminska

Aleksandra Janusz-Kaminska, PhD
Associate Scientist

I’m interested in the mechanisms of structural neuronal plasticity and its contribution to learning, neurodevelopment and pathology. My current research project is focused on mechanisms of mRNA transport, localization and translation in neurons in the context of DM1 (Myotonic Dystrophy type I). For this, I utilize a variety of methods to visualize proteins and mRNA granules in living and fixed cells.

 

 

 

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Luke Knudson
Graduate Student (PhD program, Biomedical Engineering)
luke.knudson@emory.edu

I am currently investigating the interaction between Muscleblind-like (MBNL) RNA-binding protein and kinesin motor proteins and the role that this interaction plays in proper localization of mRNA in neurons. mRNA mislocalization due to MBNL nuclear sequestration is one of the major pathogenic contributors to myotonic dystrophy.

 

 

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Adam Kosti, PhD
Postdoctoral Fellow
akosti@emory.edu

I am broadly interested in how neurons leverage post-transcriptional regulation to control plasticity. My current research is centered around the altered RNA interference pathway in Fragile X Syndrome. Utilizing both animal and human models, I am identifying dysregulated microRNAs in Fragile X neurons. I will subsequently evaluate whether restoring these altered microRNAs will stop Fragile X Syndrome phenotypes, such as excess protein synthesis and neuronal hyperexcitability.

Zachary Mceachin

Zachary Mceachin, PhD
Assistant Professor of Human Genetics and Cell Biology
zmceach@emory.edu

My research is focused on understanding shared mechanisms between C9 ALS/FTD and Spinocerebeallar Ataxia type 36 (SCA36).  These diseases are caused by a similar hexanucleotide repeat expansion in the first intron of C9orf72 (C9ALS) and NOP56 (SCA36).  To investigate the molecular etiology and pathogenesis of these disorders we are using a variety of model systems such as patient specific induced pluripotent stem cells (iPSCs).

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GiaLinh (Linda) Nguyen, MPH
Senior Research Administrative Coordinator
Linda.gia@emory.edu

As the Research Administrative Coordinator for the Bassell Lab, I ensure that the lab is in compliance with Emory’s research policies. My primary duties include overseeing daily lab activities, tracking laboratory expenditures, monitoring grant budgets, ordering laboratory consumables and chemical reagents, and maintaining laboratory records, biosafety manuals, chemical stock, and communal lab space in accordance with laboratory and biosafety regulations. I also assist the graduate students and research staff with various administrative tasks as needed.

Ryan Purcell

Ryan Purcell, PhD
Instructor
ryan.purcell@emory.edu

3q29 deletion is a recurrent copy number variant and is the highest known genetic risk factor for schizophrenia. However, the molecular basis for this risk has not been identified and is a major unanswered question. The goal of my research is to characterize the neuronal consequences of 3q29 deletion using both a mouse model and human cells. My primary focus is the generation of neurons from patient-derived induced pluripotent stem cells for morphological and signaling pathway analysis. These studies will help us to better understand the cellular and molecular consequences of this genetic variant and may also provide important insights into the molecular basis of schizophrenia.

Nisha Raj, PhDraj-nisha-150x210.jpg
Postdoctoral Fellow
nraj2@emory.edu

I am interested in studying the molecular mechanisms underlying specific cognitive, cellular and synaptic impairments seen in FXS, 15q13DS, DiGeorge syndrome and other autism related neurodevelopmental disorders. I am using induced pluripotent stem cell (iPSC)-derived neurons from patients with known genetic mutations to investigate abnormalities in neuronal morphology, signaling and protein synthesis, as well as to screen potential therapeutic interventions. 

Maxine RobinetteRobinette-Maxine-150x210.jpg
Graduate Student (PhD program, Neuroscience)
maxine.robinette@emory.edu

My research focuses on the underlying cellular and molecular mechanisms of 3q29 microdeletion syndrome (3q29Del), a major genetic risk factor for schizophrenia. I am using human iPSC derived neural stem cell models of individuals with the genetic mutation and a diagnosis of schizophrenia to investigate aberrant cellular function and potential downstream outcomes on neuronal development.

Camille TrautmanTrautman
Graduate Student (PhD program, Neuroscience)
camille.trautman@emory.edu 

I’m interested in understanding how interactions between disease-associated RNA binding proteins regulate synaptic function. Currently, I am studying the functional consequences of fragile X messenger ribonucleoprotein (FMRP) and fused in sarcoma (FUS) interactions in both healthy and ALS/FTD contexts.