M
Matthew B. Harms
Researcher at Washington University in St. Louis
Publications - 51
Citations - 7488
Matthew B. Harms is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Amyotrophic lateral sclerosis & C9orf72. The author has an hindex of 33, co-authored 46 publications receiving 6550 citations. Previous affiliations of Matthew B. Harms include Stanford University & University of Washington.
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Journal ArticleDOI
Exome sequencing in amyotrophic lateral sclerosis identifies risk genes and pathways
Elizabeth T. Cirulli,Brittany N. Lasseigne,Slavé Petrovski,Peter C. Sapp,Patrick A. Dion,Claire S. Leblond,Julien Couthouis,Yi-Fan Lu,Quanli Wang,Brian J. Krueger,Zhong-fa Ren,Jonathan E. M. Keebler,Yujun Han,Shawn Levy,Braden E. Boone,Jack R. Wimbish,Lindsay L. Waite,Angela Jones,John P. Carulli,Aaron G. Day-Williams,John F. Staropoli,Winnie Xin,Alessandra Chesi,Alya R. Raphael,Diane McKenna-Yasek,Janet Cady,J. M. B. Vianney de Jong,Kevin P. Kenna,Bradley N. Smith,Simon Topp,Jack W. Miller,Athina-Soragia Gkazi,Ammar Al-Chalabi,Leonard H. van den Berg,Jan H. Veldink,Vincenzo Silani,Nicola Ticozzi,Christopher Shaw,Robert H. Baloh,Stanley H. Appel,Ericka Simpson,Clotilde Lagier-Tourenne,Stefan M. Pulst,Summer Gibson,John Q. Trojanowski,Lauren Elman,Leo McCluskey,Murray Grossman,Neil A. Shneider,Wendy K. Chung,John Ravits,Jonathan D. Glass,Katherine B. Sims,Vivianna M. Van Deerlin,Tom Maniatis,Sebastian D. Hayes,Alban Ordureau,Sharan Swarup,John Landers,Frank Baas,Andrew S. Allen,Richard Bedlack,J. Wade Harper,Aaron D. Gitler,Guy A. Rouleau,Robert H. Brown,Matthew B. Harms,Gregory M. Cooper,Tim Harris,Richard M. Myers,David Goldstein +70 more
TL;DR: A moderate-scale sequencing study aimed at increasing the number of genes known to contribute to predisposition for ALS found several known ALS genes were found to be associated, and TBK1 (the gene encoding TANK-binding kinase 1) was identified as an ALS gene.
Journal ArticleDOI
Small GTPases Rac and Rho in the Maintenance of Dendritic Spines and Branches in Hippocampal Pyramidal Neurons
TL;DR: It is found that expression of dominant-negative Rac1 results in a progressive elimination of dendritic spines, whereas hyperactivation of RhoA causes a drastic simplification of dENDritic branch patterns that is dependent on the activity of a downstream kinase ROCK.
Journal ArticleDOI
RAN proteins and RNA foci from antisense transcripts in C9ORF72 ALS and frontotemporal dementia
Tao Zu,Yuanjing Liu,Monica Banez-Coronel,Tammy Reid,Olga Pletnikova,Jada Lewis,Timothy M. Miller,Matthew B. Harms,Annet E. Falchook,S. H. Subramony,Lyle W. Ostrow,Jeffrey D. Rothstein,Juan C. Troncoso,Laura P.W. Ranum +13 more
TL;DR: It is shown that C9ORF72 antisense transcripts are elevated in the brains of C9 ORF72 expansion-positive [C9(+)] patients, and antisense GGCCCC (G2C4) repeat-expansion RNAs accumulate in nuclear foci in brain and are potential biomarkers of the disease.
Journal ArticleDOI
Targeting RNA Foci in iPSC-Derived Motor Neurons from ALS Patients with a C9ORF72 Repeat Expansion
Dhruv Sareen,Jacqueline G. O’Rourke,Pratap Meera,A. K. M. G. Muhammad,Sharday Grant,Megan Simpkinson,Shaughn Bell,Sharon Carmona,Loren Ornelas,Anais Sahabian,Tania F. Gendron,Leonard Petrucelli,Michael Baughn,John Ravits,Matthew B. Harms,Frank Rigo,C. Frank Bennett,Thomas S. Otis,Clive N. Svendsen,Robert H. Baloh +19 more
TL;DR: Findings support the idea that the buildup of “toxic” RNA containing the GGGGCC repeat contributes to the death of motor neurons in ALS, and suggest that antisense oligonucleotides targeting this transcript may be a strategy for treating ALS patients with the C9ORF72 repeat expansion.
Journal ArticleDOI
Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration
Clotilde Lagier-Tourenne,Michael Baughn,Frank Rigo,Shuying Sun,Patrick Liu,Hairi Li,Jie Jiang,Andrew T. Watt,Seung J. Chun,Melanie Katz,Jinsong Qiu,Ying Sun,Shuo-Chien Ling,Qiang Zhu,Magdalini Polymenidou,Kevin Drenner,Jonathan W. Artates,Melissa McAlonis-Downes,Sebastian Markmiller,Kasey R. Hutt,Donald P. Pizzo,Janet Cady,Matthew B. Harms,Robert H. Baloh,Scott R. VandenBerg,Gene W. Yeo,Xiang-Dong Fu,C. Frank Bennett,Don W. Cleveland,John Ravits +29 more
TL;DR: Sustained ASO-mediated lowering of C9orf72 RNAs throughout the CNS of mice is demonstrated to be well tolerated, producing no behavioral or pathological features characteristic of ALS/FTD and only limited RNA expression alterations.