ד"ר אברהם[אבי] אשכנזי

  • סגל אקדמי בכיר בביולוגיה תאית והתפתחותית
ביולוגיה תאית והתפתחותית סגל אקדמי בכיר
ד"ר אברהם[אבי] אשכנזי
טלפון פנימי: 4521
טלפון חיצוני: 073-3804521
משרד: רפואה-סאקלר, 705

Biography

 

Dr. Ashkenazi received his B.Sc. (cum laude)  from the Technion in 2006 and M.Sc. (cum laude) from Ben Gurion University in 2008 both in Biotechnology Engineering. He then continued to his Ph.D. studies at the Weizmann Institute of Science under the supervision of Prof. Yechiel Shai. In 2013 he received The Elchanan E. Bondi Memorial Prize of the Weizmann Institute for Excellence in PhD StudiesIn 2013, Dr. Ashkenazi joined the laboratory of Prof. David Rubinsztein at the University of Cambridge, UK as a Postdoctoral Fellow supported by the FEBS Long Term Fellowship. He joined the Faculty of Medicine at Tel Aviv University in 2018.

Research Interests

 

Our research utilizes state-of-the-art technologies to elucidate cellular mechanisms of neurological disorders. Some of these disorders progress late in life, such as Huntington's disease and Parkinson's disease. A common characteristic in these disorders is the accumulation of proteins that are not folded properly and can form aggregates in cells. ​

Research in the lab is currently focused on the proteasome-ubiquitin and autophagy pathways, the main routes by which aggregate-prone proteins are degraded. Also, these pathways are important for cells to cope with various stress conditions.   ​

We aim to elucidate novel regulatory pathways of protein homeostasis in cells to better understand the basis of these devastating diseases and to identify future therapeutic targets.    

publications

 

1. Puri, C., Vicinanza, M., Ashkenazi, A., Gratian, M. J., Zhang, Q., Bento, C. F., Renna, M., Menzies, F. M. and Rubinsztein, D. C. (2018) The RAB11A-Positive Compartment Is a Primary Platform for Autophagosome Assembly Mediated by WIPI2 Recognition of PI3P-RAB11A. Developmental Cell 45, 114-131 

2. Ejlerskov, P., Ashkenazi, A. and Rubinsztein, D. C. (2018) Genetic enhancement of macroautophagy in vertebrate models of neurodegenerative diseases. Neurobiology of Disease 18, 30110-30114 

3. Ashkenazi, A., Bento, C. F., Ricketts, T., Vicinanza, M., Siddiqi, F., Pavel, M., Squitieri, F., Hardenberg, M. C., Imarisio, S., Menzies, F. M., and Rubinsztein, D. C. (2017) Polyglutamine tracts regulate beclin 1-dependent autophagy. Nature 545, 108–111 

  • News and Views: Martin, D. D. O., and Hayden, M. R. (2017) Neurodegeneration: Role of repeats in protein clearance. Nature 545, 33–34 
  • Highlight: Strzyz, P. (2017) Excessive polyQ tracts curb autophagy. Nature Reviews Molecular Cell Biology 18, 344 

4. Menzies, F. M., Fleming, A., Caricasole, A., Bento, C. F., Andrews, S. P., Ashkenazi, A., Fullgrabe, J., Jackson, A., Jimenez Sanchez, M., Karabiyik, C., Licitra, F., Lopez Ramirez, A., Pavel, M., Puri, C., Renna, M., Ricketts, T.,
Schlotawa, L., Vicinanza, M., Won, H., Zhu, Y., Skidmore, J., and Rubinsztein, D. C. (2017) Autophagy and Neurodegeneration: Pathogenic Mechanisms and Therapeutic Opportunities. Neuron 93, 1015-1034 

5. Bento, C. F., Ashkenazi, A., Jimenez-Sanchez, M., and Rubinsztein, D. C. (2016) The Parkinson's disease-associated genes ATP13A2 and SYT11 regulate autophagy via a common pathway. Nature Communications 7, 11803 

6. Bento, C. F., Renna, M., Ghislat, G., Puri, C., Ashkenazi, A., Vicinanza, M., Menzies, F. M., and Rubinsztein, D. C. (2016) Mammalian Autophagy: How Does It Work? Annual Review of Biochemistry 85, 685-713 

7. Vicinanza, M., Korolchuk, V. I., Ashkenazi, A., Puri, C., Menzies, F. M., Clarke, J. H., and Rubinsztein, D. C. (2015) PI(5)P regulates autophagosome biogenesis. Molecular Cell 57, 219-234 

For full list of publications see:

https://www.ncbi.nlm.nih.gov/pubmed/?term=avraham+ashkenazi

אוניברסיטת תל-אביב, ת.ד. 39040, תל-אביב 6997801
UI/UX Basch_Interactive