R
Robert H. Baloh
Researcher at Cedars-Sinai Medical Center
Publications - 97
Citations - 14636
Robert H. Baloh is an academic researcher from Cedars-Sinai Medical Center. The author has contributed to research in topics: Amyotrophic lateral sclerosis & Glial cell line-derived neurotrophic factor. The author has an hindex of 52, co-authored 97 publications receiving 12619 citations. Previous affiliations of Robert H. Baloh include Washington University in St. Louis & Helmholtz Association of German Research Centres.
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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.
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TDP-43 mutant transgenic mice develop features of ALS and frontotemporal lobar degeneration
TL;DR: The results indicate that the cellular and molecular substrates for selective vulnerability in FTLD-U and ALS are shared between mice and humans, and suggest that altered DNA/RNA-binding protein function, rather than toxic aggregation, is central to TDP-43-related neurodegeneration.
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Artemin, a Novel Member of the GDNF Ligand Family, Supports Peripheral and Central Neurons and Signals through the GFRα3–RET Receptor Complex
Robert H. Baloh,Malú G. Tansey,Patricia A. Lampe,Timothy J. Fahrner,Hideki Enomoto,Kelli S. Simburger,Melanie L. Leitner,Toshiyuki Araki,Eugene M. Johnson,Jeffrey Milbrandt +9 more
TL;DR: Artemin is a survival factor for sensory and sympathetic neurons in culture and its expression pattern suggests that it also influences these neurons in vivo, indicating that like GDNF and NTN, Artemin has a preferred receptor (GFRalpha3-RET) but that alternative receptor interactions also occur.
Journal ArticleDOI
TDP-43 A315T mutation in familial motor neuron disease.
Michael A. Gitcho,Robert H. Baloh,Sumi Chakraverty,Kevin Mayo,Joanne Norton,Denise Levitch,Kimmo J. Hatanpaa,Charles L. White,Eileen H. Bigio,Richard J. Caselli,Matt Baker,Muhammad Al-Lozi,John C. Morris,Alan Pestronk,Rosa Rademakers,Alison Goate,Nigel J. Cairns +16 more
TL;DR: The discovery of a missense mutation in TDP‐43 in a family with dominantly inherited motor neuron disease provides evidence of a direct link between altered T DP‐43 function and neurodegeneration.
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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.