Wolverine Foundation Research Team
The Wolverine Foundation is currently engaging in a variety of innovative and cutting edge initiatives to expand research into MAPK8IP3 genetic disease studies to address this issue, but we are constantly seeking out new, innovative and cutting edge research initiatives. The Wolverine Foundation (“WF”) is sponsoring the following research studies which are investigating possible treatments for the MAPK8IP3 genetic mutation.
Research teams
The Ferguson Lab at YSM
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Dr. Ferguson
About Dr Ferguson →
In 2010, he established his independent laboratory in the Department of Cell Biology at Yale School of Medicine which focuses on the intersection between fundamental cell biology questions and neurological disease mechanisms He currently holds the rank of Associate Professor (tenured) and has a secondary appointment in Neuroscience.
The Chung Lab at BCH
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Dr. Chung
About Dr Chung →
Dr. Chung directs NIH funded research programs in human genetics of birth defects including congenital diaphragmatic hernia, congenital heart disease, and esophageal atresia, autism, neurodevelopmental disorders, pulmonary hypertension, cardiomyopathy, obesity, diabetes, and breast cancer. She leads Pediatrics at Boston Children’s Hospital and is a member of the National Academy of Medicine. She has authored over 450 peer reviewed papers and 75 reviews and chapters in medical texts.
BCH Team
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Alexa Geltzeiler
About
The Gowrishankar Lab at UIC
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Dr. Gowrishankar
We are sponsoring Dr. Swetha Gowrishankar Assistant Professor in the Department of Anatomy and Cell Biology at The College of Medicine at The University of Illinois Chicago. Her initiative is focused on evaluating efficacy of candidate compounds for rescuing lysosome defects in MAPK8ip3 KO iNeurons.
Summary of Gowrishankar Lab Recent Results:
Our lab investigates the cellular changes in neurons resulting from loss of JIP3/MAPK8IP3 as well as de novo MAPK8IP3 mutations. Using human iPSC derived neurons as well as mouse models that were a kind gift from the Wolverine Foundation, we examine how organelle distribution (lysosomes, mitochondria and Golgi), axon specification and development are altered under these conditions.
Our results thus far have led us to focus on how MAPK8IP3 mutations alter neuronal polarity including axon initial segment integrity. Using an unboased approach of compartment-specific proteomics that we recently validated on our KO model, we also intend to identify unanticipated changes in axons of the mutant cultured neurons. We also use the mouse models to determine physiological consequences of the mutations starting with health and survival. We will extend our results from cultured neurons to the mouse model to determine if there is cell type specificity as well as age-specific effects to the cellular changes arising from the MAPK8IP3 mutations. Lastly, we examine the physiological consequences arising from cellular changes we have observed.
About Dr Gowrishankar →
The Precision Medicine Institute at UAB
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Dr. Might
About Dr Might →
From 2016 to 2018, Dr. Might was a Strategist in the Executive Office of the President in The White House. At The White House, he worked primarily on President Obama’s Precision Medicine Initiative with both the NIH and the Department of Veterans Affairs. In 2015, Dr. Might joined the faculty of the Department of Biomedical Informatics at Harvard Medical School as a visiting professor. At DBMI, his research focused on rare disease discovery and diagnosis, and on the development of personalized therapeutics for rare disease.
UAB Team
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Dr. Crowder
About
Cammie joined UAB’s Hugh Kaul Precision Medicine Institute as the Assistant Director of Education, Research, and Science Communication in 2020. As a senior laboratory scientist at PMI, she uses CRISPR-Cas9 mutagenesis to develop patient-guided zebrafish models of rare-genetic disorders associated with neurodevelopmental and neuropsychiatric disease. Through her research, she aims to describe molecular mechanisms contributing to patient symptoms and complete drug screens in zebrafish models to identify potential therapeutic options that could be repurposed to treat patients. She uses research in her teaching and has developed a series of laboratory-based curriculum for UAB undergraduate programs in the areas of genetics, molecular biology, and precision medicine. Cammie is an Assistant Professor of Neurobiology at UAB Birmingham.
Prior to her current position, she was awarded an NIH Institutional Research and Academic Career Development Award (IRACDA) and completed her postdoctoral fellow at UAB examining endocrinological disease and rare-human genetic disorders in the labs of Dr. Daniel Gorelick and Dr. Matt Might. She received her PhD in 2016 from Oregon State University in Corvallis, OR. She is originally from Birmingham, AL.
Crowder Lab Research
The Crowder Lab has recapitulated Loss Of Function microscopic phenotypes in MAPK8IP3 zebrafish at UAB facilities (axon swelling and truncation), and established a high-throughput phenotyping assay that can be used for drug screening (morphological, behavioral, locomotive).
The Yu Lab at BCH
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Dr. Yu
About Dr Yu →
BCH Team
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Dr. Demirbas
About
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Megan Seferian
About
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Dr. Davis
Previous Research Work with Dr Roger Davis
Dr. Roger J. Davis is an Investigator of the Howard Hughes Medical Institute and is the H. Arthur Smith Professor and Chair, Program in Molecular Medicine at the University of Massachusetts Medical School. He received his initial training as a student at Cambridge University. He also trained as a Damon Runyon Cancer Research Foundation fellow with Michael P. Czech at the University of Massachusetts Medical School. He subsequently joined the faculty of the University of Massachusetts Medical School and was a founding member of the Program in Molecular Medicine.
Dr. Davis’ studies of signal transduction mechanisms led to the molecular cloning of the first human stress-activated MAP kinase, the cJun NH2-terminal kinase (JNK). Subsequent studies defined the molecular structure of the JNK pathway, including the identification of upstream and down-stream pathway components and scaffold proteins. This signaling pathway is activated in response to many pathological / physiological stimuli and is implicated in inflammatory diseases (e.g. arthritis), cancer, stroke, heart disease, and diabetes. The overall goal of Dr. Davis’ research is to understand the molecular basis for these diseases and to design novel therapeutic strategies.
About Dr. Davis →
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