Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Amandeep Girdhar *Department of Biochemistry and Molecular Biology, Thomas Jefferson University, Philadelphia, PA, USA.
Maria E Cicardi *Jefferson Weinberg ALS Center, Vickie and Jack Farber Institute for Neuroscience, Department of Neuroscience, Thomas Jefferson University, Philadelphia, PA, USA.ORCID http://orcid.org/0000-0001-9490-303X
Vaishnavi KankateJefferson Weinberg ALS Center, Vickie and Jack Farber Institute for Neuroscience, Department of Neuroscience, Thomas Jefferson University, Philadelphia, PA, USA.
Davide TrottiJefferson Weinberg ALS Center, Vickie and Jack Farber Institute for Neuroscience, Department of Neuroscience, Thomas Jefferson University, Philadelphia, PA, USA. Davide.Trotti@jefferson.edu.ORCID http://orcid.org/0000-0001-6338-6404
Lin GuoDepartment of Biochemistry and Molecular Biology, Thomas Jefferson University, Philadelphia, PA, USA. Lin.Guo@jefferson.edu.ORCID http://orcid.org/0000-0002-2589-9513
Funding
STRUCTURAL BIOLOGY TRAINING PROGRAMT32GM008275 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI WAND, A. JOSHUA · 1988 to 2018
$6.0M
Defining the mechanistic basis of a prion disaggregaseR01GM099836 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI SHORTER, JAMES · 2013 to 2024
$3.9M
Exosome-mediated propagation of disease linked poly-dipeptides in C9orf72-FTD/ALSRF1AG057882 · NIA · THOMAS JEFFERSON UNIVERSITY · PI TROTTI, DAVIDE, YANG, YONGJIE · 2018 to 2018
$3.6M
Mechanism of Viral Genome Delivery into CellsR35GM140733 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CINGOLANI, GINO · 2021 to 2025
$2.8M
Elucidating the Mechanism in the Regulation of RNA-binding Protein Phase SeparationR35GM138109 · NIGMS · THOMAS JEFFERSON UNIVERSITY · PI Lin Guo · 2020 to 2026
$2.6M
Developing RNA Oligonucleotides to Mitigate Abberant FUS Phase Transition in FTD/ALSRF1NS121143 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI GUO, LIN · 2021 to 2021
$1.2M
Developing RNA Oligonucleotides to Mitigate Abberant FUS Phase Transition in FTD/ALSR01NS121143 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI GUO, LIN · 2024 to 2025
$741k
Protein therapeutics inspired by importinsR21NS128396 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CINGOLANI, GINO · 2022 to 2022
$429k
Development of a mouse model of C9ORF72 ALS/FTD expressing RAN translated peptideR21NS090912 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI TROTTI, DAVIDE · 2014 to 2015
$428k
Engineering KapB2 to Disaggregate Disease-Linked ProteinsF31NS111870 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI FARE, CHARLOTTE MIRIAM · 2019 to 2021
$137k
Muscular Dystrophy Association (Muscular Dystrophy Association Inc.) 628389NIA NIH HHS RF1 AG057882NIGMS NIH HHS R01 GM099836NIGMS NIH HHS R35 GM138109NIGMS NIH HHS R35 GM140733NIGMS NIH HHS T32 GM008275NINDS NIH HHS F31 NS111870NINDS NIH HHS R01 NS121143NINDS NIH HHS R21 NS090912NINDS NIH HHS R21 NS128396NINDS NIH HHS RF1 NS121143U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R01GM099836U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R35GM138109U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R35GM140733U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) T32GM008275U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) F31NS111870U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) R21-NS090912U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) R21NS128396U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) RF1NS121143
6 · The paper itself
Abstract
Arginine-rich dipeptide repeat proteins (R-DPRs) are highly toxic proteins found in patients with C9orf72-linked amyotrophic lateral sclerosis and frontotemporal dementia (C9-ALS/FTD). R-DPRs can cause toxicity by disrupting the natural phase behavior of RNA-binding proteins (RBPs). Mitigating this abnormal phase behavior is, therefore, crucial to reduce R-DPR-induced toxicity. Here, we use FUS as a model RBP to investigate the mechanism of R-DPR-induced aberrant RBP phase transition. We find that this phase transition can be mitigated by Kapβ2. However, as a nuclear import receptor and phase modifier for PY-NLS-containing RBPs, the function of WT Kapβ2 could lead to undesired interaction with its native substrates when used as therapeutics for C9-ALS/FTD. To address this issue, it is crucial to devise effective strategies that allow Kapβ2 to selectively target its binding to the R-DPRs, instead of the RBPs. We show that NLS-binding deficient Kapβ2
Indexed as
Amyotrophic Lateral SclerosisC9orf72 ProteinDipeptidesFrontotemporal Dementiabeta KaryopherinsHEK293 CellsHumansProtein BindingRNA-Binding Protein FUSbeta KaryopherinsC9orf72 ProteinC9orf72 protein, humanDipeptidesFUS protein, humanRNA-Binding Protein FUS
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
NLS-binding deficient Kapβ2 reduces neurotoxicity via selective interaction with C9orf72-ALS/FTD dipeptide repeats. · full record | OpenQuestion