Wikipedia

Dimitri Krainc

Dimitri Krainc is a Slovenian-born American physician-scientist who is the Aaron Montgomery Ward Professor and Chairman of the Ken & Ruth Davee Department of Neurology and Director of the Feinberg Neuroscience Institute and the Simpson Querrey Center for Neurogenetics at Northwestern University Feinberg School of Medicine.[1] After completing his medical training at the University of Zagreb, Krainc spent more than two decades at the Massachusetts General Hospital and Harvard Medical School, where he completed his research and clinical training and served on faculty until relocating to Northwestern University in 2013.[2] He has dedicated his scientific career to studying molecular pathways in the pathogenesis of neurodegeneration. Informed by genetic causes of disease, his work has uncovered key mechanisms across different neurodegenerative disorders that have led to pioneering design and development of targeted therapies. He has received numerous awards and recognitions for his work, including the Javits Neuroscience Investigator Award[3] and the Outstanding Investigator award from NIH,[4] and was elected to the Association of American Physicians, the National Academy of Medicine, the National Academy of Inventors[5] and the Croatian Academy of Sciences and Arts[6] He is the principal founding scientist of two biotech companies[7] and serves as Venture Partner at OrbiMed.[8] Krainc is President-elect of the American Neurological Association.[9]

Selected publications

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  • Wong Y.C., Ysselstein, D. and Krainc, D (2018). Mitochondria-lysosome contacts regulate mitochondrial fission via Rab7 hydrolysis. Nature, 15;554(7692):382-386[10]
  • Burbulla, L.F., Song, P., Mazzulli, J.R., Zampese, E., Wong, Y.C., Jeon, S., Santos, D.P., Blanz, J., Obermaier, C., Strojny, C., Savas, J., Kiskinis, E., Zhuang, X., Krüger, R., Surmeier, J.D., Krainc, D. (2017) Dopamine oxidation mediates mitochondrial and lysosomal dysfunction in Parkinson's disease. Science, 357(6357):1255-1261[11]
  • Song, P, Peng, W., Sauve V., Fakih R., Xie Z., Ysselstein, Y, Krainc, T, Wong, YC,   Mencacci N. Savas J.N., Surmeier D.J., Gehring K. and Krainc, D: Parkinson’s disease linked parkin mutation disrupts recycling of synaptic vesicles in human dopaminergic neurons. Neuron, 2023[12]
  • Burbulla, L., Jeon, S., Zheng, J, Song, P, Silverman, R.B. and Krainc, D.(2019) Direct targeting of wild type glucocerebrosidase improves pathogenic phenotypes in multiple forms of Parkinson’s disease. Science Translational Medicine, 16; 11(514)[13]
  • Ysselstein, D., Nguyen, M., Young, T, Severino, A., Schwake, M., Merchant, K., Krainc, D. LRRK2 kinase activity regulates lysosomal glucocerebrosidase in Parkinson’s Disease pathogenesis. Nature Communications, 2019[14]
  • Jeong, H., Cohen, D.E., Cui, L., Supinski, A., Bordone, L., Guarente, L.P., and Krainc, D. (2011) Sirt1 mediates neuroprotection from mutant huntingtin by activation of TORC1 and CREB transcriptional pathway. Nature Medicine, 18(1):159-65.[15]
  • Mazzulli, J.R., Sun, Y., Knight, A.L., McLean, P.J., Caldwell, G, Sidransky, E, Grabowski, G.A. and Krainc, D. (2011) Gaucher disease glucocerebrosidase and alpha-synuclein form a bidirectional pathogenic loop in synucleinopathies. Cell, 146(1):37-52.[16]
  • Jeong H., Then F., Mazzulli JR., Melia, T. Savas J., Voisine C., Tanese, N., Hart C.A., Yamamoto A. and Krainc D. (2009) Acetylation targets mutant huntingtin to autophagosomes for degradation. Cell, 137(1):60-72.[17]
  • Cui L., Jeong H., Borovecki F. Parkhurst C., Tanese, N. and Krainc D. (2006) Transcriptional Repression of PGC-1alpha by Mutant Huntingtin Leads to Mitochondrial Dysfunction and Neurodegeneration. Cell, 126, 59-69.[18]
  • Zhai, Jeong H., Cui L, Krainc D, and Tjian R. (2005). In vitro Analysis of Huntingtin Mediated Transcriptional Repression Reveals Novel Target and Mechanism, Cell, 123, 1241-53.[19]
  • Dunah A.W., Jeong H., Griffin A., Kim M.J., Standaert D.G., Hersch S.M., Mouradian M.M., Young A.B., Tanese N., and Krainc D.(2002) Sp1 and TAF130 transcriptional activity disrupted in early Huntington’s Disease. Science, 296(5576):2238-43.[20]

References

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  1. ^ "Faculty Profile". www.neurology.northwestern.edu. Retrieved 2022-10-11.
  2. ^ Medicine, Northwestern. "Dimitri Krainc, MD, PhD". Northwestern Medicine. Retrieved 2022-10-11.
  3. ^ "Dimitri Krainc | National Institute of Neurological Disorders and Stroke". www.ninds.nih.gov. Retrieved 2022-10-11.
  4. ^ "Krainc to Receive $9 Million, 8-Year NIH Grant". Breakthroughs for Physicians. Retrieved 2022-10-11.
  5. ^ Dimmer, Olivia (2023-12-12). "Krainc Elected to National Academy of Inventors". News Center. Retrieved 2023-12-13.
  6. ^ "HAZU – Hrvatska akademija znanosti i umjetnosti". www.info.hazu.hr. Retrieved 2024-08-26.
  7. ^ "Dimitri Krainc, MD, Ph.D." Vanqua Bio. Retrieved 2022-10-11.
  8. ^ "Leadership | OrbiMed". Retrieved 2023-01-09.
  9. ^ Dimmer, Olivia (2023-08-22). "Krainc Elected President of American Neurological Association". News Center. Retrieved 2023-08-23.
  10. ^ Wong, Yvette C.; Ysselstein, Daniel; Krainc, Dimitri (2018-02-15). "Mitochondria-lysosome contacts regulate mitochondrial fission via RAB7 GTP hydrolysis". Nature. 554 (7692): 382–386. Bibcode:2018Natur.554..382W. doi:10.1038/nature25486. ISSN 1476-4687. PMC 6209448. PMID 29364868.
  11. ^ Burbulla, Lena F.; Song, Pingping; Mazzulli, Joseph R.; Zampese, Enrico; Wong, Yvette C.; Jeon, Sohee; Santos, David P.; Blanz, Judith; Obermaier, Carolin D.; Strojny, Chelsee; Savas, Jeffrey N.; Kiskinis, Evangelos; Zhuang, Xiaoxi; Krüger, Rejko; Surmeier, D. James (2017-09-22). "Dopamine oxidation mediates mitochondrial and lysosomal dysfunction in Parkinson's disease". Science. 357 (6357): 1255–1261. Bibcode:2017Sci...357.1255B. doi:10.1126/science.aam9080. ISSN 1095-9203. PMC 6021018. PMID 28882997.
  12. ^ Song, Pingping; Peng, Wesley; Sauve, Veronique; Fakih, Rayan; Xie, Zhong; Ysselstein, Daniel; Krainc, Talia; Wong, Yvette C.; Mencacci, Niccolò E.; Savas, Jeffrey N.; Surmeier, D. James; Gehring, Kalle; Krainc, Dimitri (2023-12-06). "Parkinson's disease-linked parkin mutation disrupts recycling of synaptic vesicles in human dopaminergic neurons". Neuron. 111 (23): 3775–3788.e7. doi:10.1016/j.neuron.2023.08.018. ISSN 1097-4199. PMID 37716354.
  13. ^ Burbulla, Lena F.; Zheng, Jianbin; Song, Pingping; Jiang, Weilan; Johnson, Michaela E.; Brundin, Patrik; Krainc, Dimitri (2021-10-08). "Direct targeting of wild-type glucocerebrosidase by antipsychotic quetiapine improves pathogenic phenotypes in Parkinson's disease models". JCI Insight. 6 (19): e148649. doi:10.1172/jci.insight.148649. ISSN 2379-3708. PMC 8525588. PMID 34622801.
  14. ^ Ysselstein, Daniel; Nguyen, Maria; Young, Tiffany J.; Severino, Alex; Schwake, Michael; Merchant, Kalpana; Krainc, Dimitri (2019-12-05). "LRRK2 kinase activity regulates lysosomal glucocerebrosidase in neurons derived from Parkinson's disease patients". Nature Communications. 10 (1): 5570. Bibcode:2019NatCo..10.5570Y. doi:10.1038/s41467-019-13413-w. ISSN 2041-1723. PMC 6895201. PMID 31804465.
  15. ^ Jeong, Hyunkyung; Cohen, Dena E.; Cui, Libin; Supinski, Andrea; Savas, Jeffrey N.; Mazzulli, Joseph R.; Yates, John R.; Bordone, Laura; Guarente, Leonard; Krainc, Dimitri (2011-12-18). "Sirt1 mediates neuroprotection from mutant huntingtin by activation of the TORC1 and CREB transcriptional pathway". Nature Medicine. 18 (1): 159–165. doi:10.1038/nm.2559. ISSN 1546-170X. PMC 3509213. PMID 22179316.
  16. ^ Mazzulli, Joseph R.; Xu, You-Hai; Sun, Ying; Knight, Adam L.; McLean, Pamela J.; Caldwell, Guy A.; Sidransky, Ellen; Grabowski, Gregory A.; Krainc, Dimitri (2011-07-08). "Gaucher disease glucocerebrosidase and α-synuclein form a bidirectional pathogenic loop in synucleinopathies". Cell. 146 (1): 37–52. doi:10.1016/j.cell.2011.06.001. ISSN 1097-4172. PMC 3132082. PMID 21700325.
  17. ^ Jeong, Hyunkyung; Then, Florian; Melia, Thomas J.; Mazzulli, Joseph R.; Cui, Libin; Savas, Jeffrey N.; Voisine, Cindy; Paganetti, Paolo; Tanese, Naoko; Hart, Anne C.; Yamamoto, Ai; Krainc, Dimitri (2009-04-03). "Acetylation targets mutant huntingtin to autophagosomes for degradation". Cell. 137 (1): 60–72. doi:10.1016/j.cell.2009.03.018. ISSN 1097-4172. PMC 2940108. PMID 19345187.
  18. ^ Cui, Libin; Jeong, Hyunkyung; Borovecki, Fran; Parkhurst, Christopher N.; Tanese, Naoko; Krainc, Dimitri (2006-10-06). "Transcriptional repression of PGC-1alpha by mutant huntingtin leads to mitochondrial dysfunction and neurodegeneration". Cell. 127 (1): 59–69. doi:10.1016/j.cell.2006.09.015. ISSN 0092-8674. PMID 17018277. S2CID 15656723.
  19. ^ Zhai, Weiguo; Jeong, Hyunkyung; Cui, Libin; Krainc, Dimitri; Tjian, Robert (2005-12-29). "In vitro analysis of huntingtin-mediated transcriptional repression reveals multiple transcription factor targets". Cell. 123 (7): 1241–1253. doi:10.1016/j.cell.2005.10.030. ISSN 0092-8674. PMID 16377565. S2CID 15700502.
  20. ^ Dunah, Anthone W.; Jeong, Hyunkyung; Griffin, April; Kim, Yong-Man; Standaert, David G.; Hersch, Steven M.; Mouradian, M. Maral; Young, Anne B.; Tanese, Naoko; Krainc, Dimitri (2002-06-21). "Sp1 and TAFII130 transcriptional activity disrupted in early Huntington's disease". Science. 296 (5576): 2238–2243. Bibcode:2002Sci...296.2238D. doi:10.1126/science.1072613. ISSN 1095-9203. PMID 11988536. S2CID 21849663.
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