Two Postdoctoral Associate Positions In Disease Modeling, Nuclear Architecture and Molecular Clearance
- Rutgers University
- Location: Newark, NJ
- Job Number: 7060289
- Posting Date: Sep 12, 2019
- Application Deadline: Open Until Filled
Job DescriptionTwo Postdoctoral Associate Positions In Disease Modeling, Nuclear Architecture and Molecular Clearance
We are searching for motivated recent Ph.D. graduates with strong interest in molecular mechanisms of human neurodegenerative diseases and experience in protein biochemistry (western blots, immunodetection), confocal microscopy, cloning, and iPSC cell culture. Candidates experienced in stem cell biology, CRISPR/Cas9 techniques, and advanced confocal microscopy are particularly encouraged to apply.
One future postdoctoral associate will be involved in determining mechanisms by which Alzheimer disease (AD)-associated mutations in presenilin, tau and other genes affect nuclear calcium signaling that regulates molecular clearance pathways (autophagy, endocytosis, lysosomal degradation, etc).
One future postdoctoral associate will be involved in testing the hypothesis that cellular aging and AD-related changes in nuclear morphology affect RNA and regulatory protein shuttling in and out of the nucleus driving brain aging and promoting disease onset.
Both projects will be realized using available CRISPR/Cas9-edited human iPSC-derived cells (neurons, astrocytes and other) and novel optogenetic tools that disrupt nuclear architecture and signaling. Live-cell imaging and a variety of novel as well as conventional cell biological methods will be used to realize these projects.
The principal focus of research is on the molecular mechanisms leading to neuronal death in Alzheimer and Parkinson disease. We have recently identified novel intracellular signaling cascades that regulate the autophagy-lysosomal pathway and molecular clearance. The long-term goal of our laboratory is to define changes in major cellular signaling pathways (mTOR and others) regulating RNA and protein stability and their degradation. We investigate these alterations in vivo in mouse and Drosophila models, and in vitro in several isogenic human iPSC derived cell types.
Interested candidates should contact Dr. Radek Dobrowolski via email ( firstname.lastname@example.org ) and forward their CV, including contact information to three (3) reference letter writers.