Post Doc in neurodegenerative disease

Location
Johns Hopkins Hospital, Baltimore
Salary
$55,000 with benefits
Posted
Aug 19, 2021
Closes
Oct 18, 2021
Ref
HopkinsPostDoc
Position Type
Full Time
Level
Entry Level

We are looking for highly motivated postdoctoral candidates to participate in studies of the pathophysiology of nuclear transport and the nuclear pore complex in neurodegenerative disorders including in ALS and dementias in the laboratory of Jeffrey Rothstein MD, PhD at Johns Hopkins University.

Work in the laboratory is focussed on understanding the underlying defect(s) of the nuclear pore complex (NPC) and its regulation as a disease initiating event in amyotrophic lateral sclerosis, Alzheimer’s disease and other dementias along with the development of therapies to mitigate NPC damage.  For the last decade we have employed human and rodent models to explore the role of the NPC in neurodegeneration pathophysiology.  The model systems include a very large population of highly characterized induced pluripotent cel lines for ALS , FTD and AD along with transgenic rodent models of these diseases.   Most recently we identified a specific set of nucleoporins that initiate a cascade of NPC failure and have now identified an underlying initiating event, including ESCRT3 pathway and gene therapies to mitigate damage/disease.  Projects include:

  1. Nuclear Biology in Neurodegeneration: to address fundamental questions on implicating nuclear pore complex and nuclear transport in dementia and ALS (Donnelley et al, Neuron, 2013; Zhang et al Nature 2015; Grima et al, Neuron 2017; Eftekharzadeh, Neuron 2018; Zhang et al, Cell, 2018, Coyne et al, Neuron 2020) and other related neurodegenerative diseases.
  2. Development of therapies targeting the regulation of nuclear pore and nuclear transport in neurodegeneration. These studies may involve collaboration with biotechnology companies interested in this new therapeutic target and its potential widespread disease engagement.
  3. Development of new iPS and rodent transgenic models of nuclear pore and nuclear pore regulation defects present in familial and sporadic ALS/dementia.

Experimental approaches, including biochemistry, genetics, molecular imaging and cell biology, from human and in vivo/in vitro rodent to mammalian systems are employed. New techniques applied in the lab include iPSC, genome editing, single cell analysis, whole genome analytics and metabolic studies. Access to the largest library of human iPS cell lines (~750) for ALS and dementia along with full omics data thru our ANSWER ALS Program (https://dataportal.answerals.org/home). Candidates with a strong background in molecular biology, advanced imaging (confocal, structured illumination microscopy/Cryo EM), cellular biology, and/or biochemistry are encouraged to apply.

Position Information: Candidates should have a doctoral degree and strong research background. Please send a statement of research experience and career goals, a copy of Curriculum Vitae, and contact information of at least one or two references to Dr. Jeffrey D. Rothstein at jrothstein@jhmi.edu. The post doc position is for at least 2 years or more and is fully funded.  Candidates can start at any time.  

The Johns Hopkins Medical Institutions provide a stimulating and collaborative environment for biomedical research. Our lab is located in the Brain Science Institute and affiliated with the Depts of Neurology and Neuroscience at the School of Medicine. The Baltimore/Washington D.C. area also offers rich professional and living (county hiking and water activities) opportunities

Selected Recent Relevant Publications:

  • Coyne et al. Nuclear accumulation of CHMP7 initiates nuclear pore complex injury and subsequent TDP-43 dysfunction in sporadic and familial ALS. Science Trans Med, 2021, in press.
  • Coyne AN, et al. G4C2 Repeat RNA Initiates a POM121-Mediated Reduction in Specific Nucleoporins in C9orf72 ALS/FTD. Neuron. 2020;107(6):1124-40 
  • Eftekharzadeh B, et al. Tau Protein Disrupts Nucleocytoplasmic Transport in Alzheimer's Disease. Neuron. 2019;101(2):349.: 
  • Zhang K.  Stress granule formation disrupts nucleocytoplasmic transport. Cell. 2018;173(4):958-71
  • Zhang K et al. The C9orf72 repeat expansion disrupts nucleocytoplasmic transport. Nature. 2015;525(7567):56-61. 

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