Craig
Blackstone M.D., Ph.D., InvestigatorDr. Blackstone received B.S. and M.S. degrees in 1987 from the University of Chicago and M.D. and Ph.D. degrees in 1994 from
Johns Hopkins University. His graduate studies, in the laboratory of Richard Huganir, were on the structure and regulation
of glutamate receptors, for which he received the David Israel Macht Award. After a neurology residency at the Harvard-Longwood
Neurology Program, Dr. Blackstone completed a fellowship in clinical movement disorders at the Massachusetts General Hospital.
During this time he also conducted postdoctoral research with Morgan Sheng at Harvard Medical School, investigating the functions
of proteins implicated in hereditary dystonias. Dr. Blackstone joined the NINDS as an investigator in 2001. His laboratory
investigates the cellular and molecular mechanisms underlying hereditary movement disorders.
Laboratory StaffJoanna Bakowska, Ph.D. Special Volunteer
301-451-
9682
Chuang-Rung Chang, Ph.D. Postdoctoral Fellow
301-451-
9684
Michael Hanna, Ph.D. Research Fellow
301-451-
9686
Henri Jupille, B.S. Post baccalaureate Fellow
301-451-
9683
Benoit Renvoise, Ph.D. Visiting Fellow
301-451-
9682
Neggy Rismanchi, Ph.D. Postdoctoral Fellow
301-496-
0284
Cynthia Soderblom, B.S. Predoctoral Fellow
301-451-
9683
Julia Stadler, B.A. Research Assistant
301-451-
9685
Peng-Peng Zhu, M.D. Staff Scientist
301-451-
9687
Research InterestsResearch in the Cellular Neurology Unit emphasizes two major disease-related aims. The first focuses on understanding the
cellular pathogenesis of a group of disorders known as the hereditary spastic paraplegias (HSPs), whose cardinal feature is
a length-dependent axonopathy of corticospinal motor neurons. A particular advantage in piecing together the molecular and
cellular pathogenesis underlying the HSPs is that well over 30 genetic loci (SPG1-33) have been mapped, with 16 gene products
already identified that segregate into a smaller number of functional groups. Many of these proteins are suspected to be
involved in protein and membrane trafficking, and we are currently studying HSP disease proteins involved in both secretory
and endocytic pathways.
Selected Recent PublicationsRismanchi N, Soderblom C, Stadler J, Zhu P-P, Blackstone CAtlastin GTPases are required for Golgi apparatus and ER morphogenesis - Hum Molec Genet
17 1591-1604 2008
Bakowska JC, Wang H, Xin B, Sumner CJ, Blackstone CLoss of spartin protein in Troyer syndrome: a loss-of-function disease mechanism? - Arch Neurol
65 520-524 2008
Bakowska J, Jupille H, Fatheddin P, Puertollano R, Blackstone CTroyer syndrome protein spartin is mono-ubiquitinated and functions in EGF receptor trafficking - Mol Biol Cell
18 1683-1692 2007
Chang C-R, Blackstone CCyclic-AMP-dependent phosphorylation of Drp1 regulates its GTPase activity and mitochondrial morphology - J Biol Chem
282 21583-21587 2007
Soderblom C, Blackstone CTraffic accidents: molecular genetic insights into the pathogenesis of the hereditary spastic paraplegias - Pharmacol Ther
109 42-56 2006
Zhu P-P, Soderblom C, Tao-Cheng J-H, Stadler J, Blackstone CSPG3A protein atlastin-1 is enriched in growth cones and promotes axon elongation during neuronal development - Hum Mol Genet
15 1343-1353 2006
Selected Earlier Publications
Contact InformationCellular Neurology Unit, NINDS Porter Neuroscience Research Center
Building 35, Room 2C-913
35 Convent Drive, MSC 3704 Bethesda MD
20892-3704
Telephone:
301-451-
9680 (office), -
- (laboratory),
301-480-
4888 (fax), Email:
blackstc@ninds.nih.gov