D. J. Sidjanin, PhD

DJ_SidjaninAssociate Professor

Medical College of Wisconsin
Department of Cell Biology, Neurobiology & Anatomy
8701 Watertown Plank Road
Milwaukee, WI 53226-0509

(414) 955-7810 | (414) 955-6517 (fax) | dsidjani@mcw.edu

BS Biochemistry, The University of Rochester, Rochester, NY, 1989
PhD Biological Sciences, Northern Illinois University/Argonne National Laboratory, IL, 1995

Graduate Programs
Program in Cell and Developmental Biology
Program in Neuroscience

Research Area

Warburg Micro Syndrome

We recently discovered that mutations in the TBC1D20 gene cause Warburg Micro syndrome, a genetically heterogeneous disorder characterized by developmental eye, brain, and genital abnormalities. However, very little is known about TBC1D20 cellular function and how disrupted TBC1D20 function cases aberrant development. In order to address these questions, we are utilizing classical forward and reverse genetic approaches. Our studies to date have shown that TBC1D20 functions as a GTPase-activating protein (GAP) and facilitates the GTP hydrolysis of an “active” GTP-bound RAB1 to the “inactive” GDP-bound form. RAB1 belongs to the superfamily of RAB proteins that act as key regulators of membrane trafficking including vesicle formation, transport along cytoskeletal networks, docking, and vesicle fusion. Our current research focuses on characterization of the TBC1D20-mediated vesicular pathways and their roles during eye and brain development in mouse models. Eye phenotypes in control and TBC1D20-deficient miceOur future goals are to test if TBC1D20-mediated pathways established in mice facilitate similar mechanisms in humans by utilizing induced pluripotent stem cells (iPSCs) to model human tissue development. Currently, we are enrolling individuals and family members affected with Warburg Micro syndrome, polymicrogyria or other cortical malformations to participate in our genetic study. If you are interested in participating in our study or would like to get more information please email us at dsidjani@mcw.edu.

ADAM10 and ADAM17

Model of ADAM17 functionADAM10 and ADAM17 are two closely related members of the ADAM (a disintegrin and metalloprotease) family of proteins that proteolytically cleave or “shed” ectodomains of cell surface proteins. In the cell culture, ADAM10 and ADAM17 shed numerous overlapping ligands, which led to the hypothesis that in vivo ADAM10 and ADAM17 have overlapping and compensatory functions. Results from our laboratory revealed that in mice ADAM17 mediates the development of ocular anterior segment by shedding EGFR ligands, transactivating the EGFR receptor and facilitating cell migration. While ADAM10 is also indispensable for ocular development, our findings indicate that ADAM10 has a distinct function from ADAM17. Our current efforts focus on establishing the independent and overlapping roles of ADAM10 and ADAM17 during ocular development.


Sidjanin Lab

D. J. Sidjanin, PhD Lab

Sidjanin lab graduate and medical student alumni:

Eryn Hassemer PhD, Assistant Professor, Milwaukee School of Engineering, Milwaukee, WI
Kate Merath, PhD, Patent Scientist, Law Firm of Michael Best and Friedrich, LLP, Chicago IL
Joe Toonen PhD, Postdoctoral Fellow, Washington University School of Medicine, St. Louis MO
Ryan Liegel, PhD, Postdoctoral Fellow, Cincinnati Children’s Hospital, Cincinnati, OH
Todd Jackson, MD, Ophthalmology, Prestige Laser & Cataract Institute, Las Vegas, NV
Matthew Koeberl, MD, Radiology, Lakeshore Radiology, Manitowoc, WI
Anna Park, Medical Student (M3), Medical College of Wisconsin, Milwaukee, WI

Recent Publications