D
Daniel A. Mordes
Researcher at Harvard University
Publications - 42
Citations - 3023
Daniel A. Mordes is an academic researcher from Harvard University. The author has contributed to research in topics: Amyotrophic lateral sclerosis & Neurodegeneration. The author has an hindex of 20, co-authored 38 publications receiving 2436 citations. Previous affiliations of Daniel A. Mordes include Duke University & Vanderbilt University.
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Journal ArticleDOI
Evidence for α-synuclein prions causing multiple system atrophy in humans with parkinsonism
Stanley B. Prusiner,Amanda L. Woerman,Daniel A. Mordes,Joel C. Watts,Ryan Rampersaud,David B. Berry,Smita S. Patel,Abby Oehler,Jennifer K. Lowe,Stephanie N Kravitz,Daniel H. Geschwind,David V. Glidden,Glenda M. Halliday,Lefkos T. Middleton,Steve M. Gentleman,Lea T. Grinberg,Kurt Giles +16 more
TL;DR: The findings argue that MSA is caused by a unique strain of α-synuclein prions, which is different from the putative prions causing PD and from those causing spontaneous neurodegeneration in TgM83+/+ mice.
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TopBP1 activates ATR through ATRIP and a PIKK regulatory domain
TL;DR: The data indicate that the DNA-PKcs (DNA-dependent protein kinase catalytic subunit) PRD is important for DNA- PKcs regulation, and divergent amino acid sequences within the PRD and a unique protein partner allow each of these PIK kinases to respond to distinct cellular events.
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ALS-implicated protein TDP-43 sustains levels of STMN2, a mediator of motor neuron growth and repair
Joseph R. Klim,Luis A. Williams,Francesco Limone,Irune Guerra San Juan,Brandi N. Davis-Dusenbery,Daniel A. Mordes,Aaron Burberry,Michael J. Steinbaugh,Kanchana K. Gamage,Rory Kirchner,Rob Moccia,Seth H. Cassel,Kuchuan Chen,Brian J. Wainger,Brian J. Wainger,Clifford J. Woolf,Kevin Eggan +16 more
TL;DR: In this paper, the authors report transcripts whose abundances in human motor neurons are sensitive to TDP-43 depletion, and they propose that restoring STMN2 expression warrants examination as a therapeutic strategy for ALS.
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Loss-of-function mutations in the C9ORF72 mouse ortholog cause fatal autoimmune disease
Aaron Burberry,Aaron Burberry,Naoki Suzuki,Naoki Suzuki,Jin Yuan Wang,Jin Yuan Wang,Rob Moccia,Rob Moccia,Daniel A. Mordes,Daniel A. Mordes,Morag Stewart,Morag Stewart,Satomi Suzuki-Uematsu,Satomi Suzuki-Uematsu,Sulagna Ghosh,Sulagna Ghosh,Ajay K. Singh,Ajay K. Singh,Florian T. Merkle,Florian T. Merkle,Kathryn Koszka,Kathryn Koszka,Quan Zhen Li,Leonard I. Zon,Derrick J. Rossi,Derrick J. Rossi,Jennifer J. Trowbridge,Luigi D. Notarangelo,Luigi D. Notarangelo,Kevin Eggan,Kevin Eggan +30 more
TL;DR: It is shown that mice harboring loss-of-function mutations in the ortholog of C9ORF72 develop splenomegaly, neutrophilia, thrombocytopenia, increased expression of inflammatory cytokines, and severe autoimmunity, ultimately leading to a high mortality rate.
Journal ArticleDOI
Propagation of prions causing synucleinopathies in cultured cells
Amanda L. Woerman,Jan Stöhr,Atsushi Aoyagi,Ryan Rampersaud,Zuzana Krejciova,Joel C. Watts,Takao Ohyama,Smita S. Patel,Kartika Widjaja,Abby Oehler,David W. Sanders,Marc I. Diamond,William W. Seeley,Lefkos T. Middleton,Steve M. Gentleman,Daniel A. Mordes,Thomas C. Südhof,Kurt Giles,Stanley B. Prusiner +18 more
TL;DR: Improved bioassay using selective precipitation of tau prions from human PSP brain homogenates before infection of the HEK cells is reported, providing compelling evidence that PSP and MSA are prion diseases and that MSA is caused by several distinct prion strains.