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 StaffUma Goyal, B.S., HHMI Scholar
, 301-451-
9683
Seong-hee Park, Ph.D., Postdoctoral Fellow
Benoit Renvoise, Ph.D., Postdoctoral Fellow
, 301-451-
9682
Cynthia Soderblom, B.S., Predoctoral Fellow
, 301-451-
9683
Julia Stadler, B.A., Research Assistant
, 301-451-
9685
Yuko Tagami, Ph.D., Postdoctoral Fellow
, 301-451-
9684
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 PublicationsBlackstone CInfantile parkinsonism-dystonia: a dopamine 'transportopathy' - J Clin Invest
119 1455-1458 2009
Hu J, Shibata Y, Zhu P-P, Voss C, Rismanchi N, Prinz WA, Rapoport TA, Blackstone CA class of dynamin-like GTPases involved in the generation of the tubular ER network - Cell
138 549-561 2009
Rismanchi 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
Yang D, Rismanchi N, Renvoise B, Lippincott-Schwartz J, Blackstone C, Hurley JHStructural basis for midbody targeting of spastin by the ESCRT-III protein CHMP1B - Nat Struct Mol Biol
15 1278-1286 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
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