L
Luis A. Williams
Researcher at Harvard University
Publications - 26
Citations - 2938
Luis A. Williams is an academic researcher from Harvard University. The author has contributed to research in topics: Induced pluripotent stem cell & Motor neuron. The author has an hindex of 15, co-authored 21 publications receiving 2401 citations. Previous affiliations of Luis A. Williams include University of California, Davis & University of Minnesota.
Papers
More filters
Journal ArticleDOI
Intrinsic Membrane Hyperexcitability of Amyotrophic Lateral Sclerosis Patient-Derived Motor Neurons
Brian J. Wainger,Evangelos Kiskinis,Cassidy Mellin,Ole Wiskow,Steve S.W. Han,Jackson Sandoe,Numa P. Perez,Luis A. Williams,Seungkyu Lee,Gabriella L. Boulting,James D. Berry,Robert H. Brown,Merit Cudkowicz,Bruce P. Bean,Kevin Eggan,Kevin Eggan,Clifford J. Woolf,Clifford J. Woolf +17 more
TL;DR: It is shown that hyperexcitability detected by clinical neurophysiological studies of ALS patients is recapitulated in induced pluripotent stem cell-derived motor neurons from patients harboring superoxide dismutase 1 (SOD1), C9orf72, and fused-in-sarcoma mutations.
Journal ArticleDOI
Axonal Transport of TDP-43 mRNA Granules Is Impaired by ALS-Causing Mutations
Nael H. Alami,Rebecca B. Smith,Monica A. Carrasco,Luis A. Williams,Christina S. Winborn,Steve S.W. Han,Evangelos Kiskinis,Brett J. Winborn,Brian D. Freibaum,Anderson P. Kanagaraj,Alison J. Clare,Nisha M. Badders,Bilada Bilican,Edward Chaum,Siddharthan Chandran,Christopher Shaw,Kevin Eggan,Tom Maniatis,J. Paul Taylor +18 more
TL;DR: It is shown that TDP-43 forms cytoplasmic mRNP granules that undergo bidirectional, microtubule-dependent transport in neurons in-vitro and in vivo and facilitate delivery of target mRNA to distal neuronal compartments, and that TSP-43 mutations that cause ALS lead to partial loss of a novel cytopLasmic function of T DP-43.
Journal ArticleDOI
Pathways disrupted in human ALS motor neurons identified through genetic correction of mutant SOD1.
Evangelos Kiskinis,Evangelos Kiskinis,Evangelos Kiskinis,Jackson Sandoe,Jackson Sandoe,Jackson Sandoe,Luis A. Williams,Luis A. Williams,Luis A. Williams,Gabriella L. Boulting,Gabriella L. Boulting,Rob Moccia,Rob Moccia,Rob Moccia,Brian J. Wainger,Brian J. Wainger,Steve S.W. Han,Steve S.W. Han,Steve S.W. Han,Theodore Peng,Theodore Peng,Theodore Peng,Sebastian Thams,Shravani Mikkilineni,Shravani Mikkilineni,Shravani Mikkilineni,Cassidy Mellin,Florian T. Merkle,Florian T. Merkle,Florian T. Merkle,Brandi N. Davis-Dusenbery,Brandi N. Davis-Dusenbery,Brandi N. Davis-Dusenbery,Michael J. Ziller,Derek H. Oakley,Justin K. Ichida,Justin K. Ichida,Stefania Di Costanzo,Stefania Di Costanzo,Nick Atwater,Nick Atwater,Nick Atwater,Morgan L. Maeder,Mathew J. Goodwin,James Nemesh,James Nemesh,James Nemesh,Robert E. Handsaker,Robert E. Handsaker,Robert E. Handsaker,Daniel Paull,Scott Noggle,Steven A. McCarroll,Steven A. McCarroll,Steven A. McCarroll,J. Keith Joung,Clifford J. Woolf,Robert H. Brown,Kevin Eggan,Kevin Eggan,Kevin Eggan +60 more
TL;DR: Reprogramming and stem cell differentiation approaches with genome engineering and RNA sequencing are combined to define the transcriptional and functional changes that are induced in human motor neurons by mutant SOD1, indicating that at least a subset of these changes are more broadly conserved in ALS.
Journal ArticleDOI
KEEP ON GOING, a RING E3 Ligase Essential for Arabidopsis Growth and Development, Is Involved in Abscisic Acid Signaling
TL;DR: The observations that KEG accumulates high levels of ABSCISIC ACID-INSENSITIVE5 (ABI5) without exogenous ABA, interacts with ABA5 in vitro, and that loss of ABI5 rescues the growth-arrest phenotype of keg mutant seedlings indicate that K EG is required for ABI 5 degradation.
Journal ArticleDOI
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.