David Rubinsztein
Born
David Chaim Rubinsztein

1963 (age 60–61)
Alma materUniversity of Cape Town (MBChB, PhD)
Known forautophagy and polyglutamine expansions
Awards
Scientific career
FieldsAutophagy
Neurodegenerative diseases[4]
InstitutionsUniversity of Cambridge
Cambridge Institute for Medical Research
Cambridge Drug Discovery Institute
ThesisMonogenic hypercholesterolemia in South Africans: familial hypercholesterolemia in Indians and familial defective apolipoprotein B-100 (1993)
Doctoral advisorProf. D.R. van der Westhuyzen
Website

David Chaim Rubinsztein (born 1963) FRS[3] FMedSci[5] is the Deputy Director of the Cambridge Institute of Medical Research (CIMR),[6] Professor of Molecular Neurogenetics at the University of Cambridge[7] and a UK Dementia Research Institute Professor.

Education

Rubinsztein completed his Bachelor of Medicine, Bachelor of Surgery (MB ChB) in 1986 and PhD in 1993 in the Medical Research Council/University of Cape Town Unit for the Cell Biology of Atherosclerosis. In 1993 he went to Cambridge as a senior registrar in Genetic Pathology.[8]

Career

In 1997, Rubinsztein acquired his Certificate of Completion of Specialist Training at the University of Cambridge. He was appointed to a Personal Readership at the University of Cambridge in 2003. In 2005, he was promoted to Professor of Molecular Neurogenetics at the University of Cambridge (personal chair). He has been an author on more than 400 scientific papers,[4][9] and was ranked as the 4th most cited European author from 2007 to 2013 in cell biology.[10] Rubinsztein has been invited to give talks at major international conferences, including Gordon Research Conferences and Keystone Symposia.[11][12][13]

Research

Rubinsztein has made major contributions to the field of neurodegeneration[4] with his laboratory's discovery that autophagy regulates the levels of intracytoplasmic aggregate-prone proteins that cause many neurodegenerative diseases, including Huntington's, Parkinson's and Alzheimer's disease.[14][15][16][17][18] His lab has found that autophagy may be inhibited in various neurodegenerative diseases[19] and has elucidated the pathological consequences of autophagy compromise.[20] In addition his research has advanced the basic understanding of autophagy, identifying the plasma membrane as a source of autophagosome membrane[21] and characterising early events in autophagosome biogenesis,.[22][23][24] Furthermore, he studied how lysosomal positioning regulates autophagy.[25] His goal is to understand the links between these diseases and autophagy. He is currently focused on understanding how to induce autophagy in vivo to remove toxic proteins and avoid the development of neurodegenerative disease[6][26]

Honours and awards

Rubinsztein has won numerous awards including:

References

  1. ^ "14 Academy Fellows elected to the Royal Society in 2017 | the Academy of Medical Sciences".
  2. ^ a b "EMBO people: David C. Rubinsztein". people.embo.org.
  3. ^ a b c Anon (2017). "Professor David Rubinsztein FRS". London: royalsociety.org.
  4. ^ a b c David C. Rubinsztein publications indexed by Google Scholar Edit this at Wikidata
  5. ^ a b Anon (2004). "Professor David Rubinsztein FMedSci". acmedsci.ac.uk. London: Academy of Medical Sciences. Archived from the original on 4 March 2016. Retrieved 26 November 2015.
  6. ^ a b "Professor David C. Rubinsztein". University of Cambridge.[permanent dead link]
  7. ^ "Professor David Rubinsztein :: Cambridge Neuroscience". www.neuroscience.cam.ac.uk. Retrieved 8 January 2018.
  8. ^ F1000 Prime Faculty Member
  9. ^ Research Gate
  10. ^ "Publication analysis 2007–2013, Cell Biology" (PDF). Archived from the original (PDF) on 4 March 2016. Retrieved 26 November 2015.
  11. ^ "Centre for Science and Policy". University of Cambridge.
  12. ^ Renna, M.; Jimenez-Sanchez, M.; Sarkar, S.; Rubinsztein, D. C. (2010). "Chemical Inducers of Autophagy That Enhance the Clearance of Mutant Proteins in Neurodegenerative Diseases". Journal of Biological Chemistry. 285 (15): 11061–11067. doi:10.1074/jbc.R109.072181. ISSN 0021-9258. PMC 2856980. PMID 20147746. Open access icon
  13. ^ Renna, M.; Jimenez-Sanchez, M.; Sarkar, S.; Rubinsztein, D. C. (2010). "Chemical Inducers of Autophagy That Enhance the Clearance of Mutant Proteins in Neurodegenerative Diseases". The Journal of Biological Chemistry. 285 (15): 11061–11067. doi:10.1074/jbc.R109.072181. PMC 2856980. PMID 20147746.
  14. ^ Rubinsztein, D. C. (2012). "Autophagy modulation as a potential therapeutic target for diverse diseases". Nature Reviews Drug Discovery. 11 (9): 709–730. doi:10.1038/nrd3802. PMC 3518431. PMID 22935804.
  15. ^ Ravikumar, B.; Rubinsztein, D. C. (2004). "Inhibition of mTOR induces autophagy and reduces toxicity of polyglutamine expansions in fly and mouse models of Huntington disease". Nature Genetics. 36 (6): 585–595. doi:10.1038/ng1362. PMID 15146184.
  16. ^ Analytics, Clarivate. "David Rubinsztein Interview - Special Topic of Autophagy - ScienceWatch.com". archive.sciencewatch.com. Retrieved 8 January 2018.
  17. ^ Davies, J. E.; Rubinsztein, D. C. (2005). "Doxycycline attenuates and delays toxicity of the oculopharyngeal muscular dystrophy mutation in transgenic mice". Nature Medicine. 11 (6): 672–677. doi:10.1038/nm1242. PMID 15864313. S2CID 13190118.
  18. ^ Sarkar, S.; Rubinsztein, D. C. (2007). "Small molecules enhance autophagy and reduce toxicity in Huntington's disease models". Nature Chemical Biology. 3 (6): 331–338. doi:10.1038/nchembio883. PMC 2635561. PMID 17486044.
  19. ^ Winslow, A. R.; Rubinsztein, D. C. (2010). "α-Synuclein impairs macroautophagy: implications for Parkinson's disease". The Journal of Cell Biology. 190 (6): 1023–1037. doi:10.1083/jcb.201003122. PMC 3101586. PMID 20855506.
  20. ^ Ravikumar, B.; Rubinsztein, D. C. (2005). "Dynein mutations impair autophagic clearance of aggregate-prone proteins". Nature Genetics. 37 (7): 771–776. doi:10.1038/ng1591. PMID 15980862. S2CID 7628772.
  21. ^ Ravikumar, B.; Rubinsztein, D. C. (2010). "Plasma membrane contributes to the formation of pre-autophagosomal structures". Nature Cell Biology. 12 (8): 747–757. doi:10.1038/ncb2078. PMC 2923063. PMID 20639872.
  22. ^ Moreau, K.; Rubinsztein, D. C. (2011). "Autophagosome precursor maturation requires homotypic fusion". Cell. 146 (2): 303–317. doi:10.1016/j.cell.2011.06.023. PMC 3171170. PMID 21784250.
  23. ^ Puri, C.; Rubinsztein, D. C. (2013). "Diverse autophagosome membrane sources coalesce in recycling endosomes". Cell. 154 (6): 1285–1299. doi:10.1016/j.cell.2013.08.044. PMC 3791395. PMID 24034251.
  24. ^ Vicinanza, M.; Rubinsztein, D. C. (2015). "PI(5)P regulates autophagosome biogenesis". Molecular Cell. 57 (2): 219–234. doi:10.1016/j.molcel.2014.12.007. PMC 4306530. PMID 25578879.
  25. ^ Korolchuk, V. I.; Rubinsztein, D. C. (2011). "Lysosomal positioning coordinates cellular nutrient responses". Nature Cell Biology. 13 (4): 453–460. doi:10.1038/ncb2204. PMC 3071334. PMID 21394080.
  26. ^ "Autophagy, a guardian against neurodegeneration - Part 2 - David Rubinsztein". SENS Research Foundation. 27 November 2013. Archived from the original on 8 December 2015. Retrieved 8 January 2018.
  27. ^ "Wellcome Trust". Archived from the original on 2 October 2015. Retrieved 26 November 2015.
  28. ^ "Editor biographies". Nature.
  29. ^ "Funded People and Projects - Grant Funding | Wellcome".
  30. ^ a b Thomson Reuters
  31. ^ "Labtimes: Publication Statistics: Cell Biology". Archived from the original on 29 July 2017. Retrieved 12 April 2016.
  32. ^ "2017 Award Winners". biochemistry.org. Archived from the original on 4 June 2016. Retrieved 12 April 2016.
  33. ^ "Highly Cited Researchers - the Most Influential Scientific Minds".
  34. ^ "Highly Cited Researchers".
  35. ^ "Main Programme 212th Scientific Meeting of the Pathological Society of Great Britain & Ireland".[permanent dead link]
  36. ^ "Highly Cited Researchers".
  37. ^ "Highly Cited Researchers". Archived from the original on 24 November 2021. Retrieved 24 November 2021.
  38. ^ "Member > Rubinsztein David".
  39. ^ "Highly Cited Researchers".
  40. ^ "Highly Cited Researchers".
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