Harvard Catalyst Profiles

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David Christopher Stoppel, Ph.D.

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Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.
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  1. Stoppel DC, Anderson MP. Hypersociability in the Angelman syndrome mouse model. Exp Neurol. 2017 07; 293:137-143. PMID: 28411125.
    View in: PubMed
  2. Krishnan V, Stoppel DC, Nong Y, Johnson MA, Nadler MJ, Ozkaynak E, Teng BL, Nagakura I, Mohammad F, Silva MA, Peterson S, Cruz TJ, Kasper EM, Arnaout R, Anderson MP. Autism gene Ube3a and seizures impair sociability by repressing VTA Cbln1. Nature. 2017 03 23; 543(7646):507-512. PMID: 28297715.
    View in: PubMed
  3. Tata A, Stoppel DC, Hong S, Ben-Zvi A, Xie T, Gu C. An image-based RNAi screen identifies SH3BP1 as a key effector of Semaphorin 3E-PlexinD1 signaling. J Cell Biol. 2014 May 26; 205(4):573-90. PMID: 24841563; PMCID: PMC4033773.
  4. Smith SE, Zhou YD, Zhang G, Jin Z, Stoppel DC, Anderson MP. Increased gene dosage of Ube3a results in autism traits and decreased glutamate synaptic transmission in mice. Sci Transl Med. 2011 Oct 05; 3(103):103ra97. PMID: 21974935; PMCID: PMC3356696.
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Funded by the NIH/NCATS Clinical and Translational Science Award (CTSA) program, grant number UL1TR001102, and through institutional support from Harvard University, Harvard Medical School, Harvard T.H. Chan School of Public Health, Beth Israel Deaconess Medical Center, Boston Children's Hospital, Brigham and Women's Hospital, Massachusetts General Hospital and the Dana Farber Cancer Institute.