Evidence map›Paper›PMID 30120199›Full record

ArticleThe Journal of biological chemistry2018

Identification and characterization of ubiquitinylation sites in TAR DNA-binding protein of 43 kDa (TDP-43).

Friederike Hans, Marita Eckert, Felix von Zweydorf, Christian Johannes Gloeckner, Philipp J Kahle

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.1field-weighted citation impact, top 9% of its field
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.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 59 citations in OpenAlex.

  1. TDP-43: [GU]-ardian of the transcriptome.Molecular neurodegeneration · 2026
    Review
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  4. TDP-43: unveiling the hidden key to cellular fate decisions.Cell communication and signaling : CCS · 2025
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  19. TDP-43 Pathology in Alzheimer's Disease.Molecular neurodegeneration · 2021
    Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Friederike HansFrom the German Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen and.
Marita EckertFrom the German Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen and.
Felix von ZweydorfFrom the German Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen and.
Christian Johannes GloecknerFrom the German Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen and.ORCID 0000-0001-6494-6944
Philipp J KahleFrom the German Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen and philipp.kahle@uni-tuebingen.de.
German Center for Neurodegenerative Diseases · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TAR DNA-binding protein of 43 kDa (TDP-43) forms pathological aggregates in neurodegenerative diseases, particularly in certain forms of frontotemporal dementia and amyotrophic lateral sclerosis. Pathological modifications of TDP-43 include proteolytic fragmentation, phosphorylation, and ubiquitinylation. A pathognomonic TDP-43 C-terminal fragment (CTF) spanning amino acids 193-414 contains only four lysine residues that could be potentially ubiquitinylated. Here, serial mutagenesis of these four lysines to arginine revealed that not a single residue is responsible for the ubiquitinylation of mCherry-tagged CTF. Removal of all four lysines was necessary to suppress ubiquitinylation. Interestingly, Lys-408 substitution enhanced the pathological phosphorylation of the immediately adjacent serine residues 409/410 in the context of mCherry-CTF. Thus, Lys-408 ubiquitinylation appears to hinder Ser-409/410 phosphorylation in TDP-43 CTF. However, we did not observe the same effect for full-length TDP-43. We extended the mutagenesis study to full-length TDP-43 and performed MS. Ubiquitinylated lysine residues were identified in the nuclear localization sequence (NLS; Lys-84 and Lys-95) and RNA-binding region (mostly Lys-160, Lys-181, and Lys-263). Mutagenesis of Lys-84 confirmed its importance as the major determinant for nuclear import, whereas Lys-95 mutagenesis did not significantly affect TDP-43's nucleo-cytoplasmic distribution, solubility, aggregation, and RNA-processing activities. Nevertheless, the K95A mutant had significantly reduced Ser-409/410 phosphorylation, emphasizing the suspected interplay between TDP-43 ubiquitinylation and phosphorylation. Collectively, our analysis of TDP-43 ubiquitinylation sites indicates that the NLS residues Lys-84 and Lys-95 have more prominent roles in TDP-43 function than the more C-terminal lysines and suggests a link between specific ubiquitinylation events and pathological TDP-43 phosphorylation.

Indexed as

Active Transport, Cell NucleusCell NucleusDNA-Binding ProteinsHEK293 CellsHumansLysineMutagenesis, Site-DirectedMutationPhosphorylationProtein Processing, Post-TranslationalSolubilityUbiquitinDNA-Binding ProteinsLysineTARDBP protein, humanUbiquitinamyotrophic lateral sclerosis (ALS) (Lou Gehrig disease)frontotemporal dementiamass spectrometry (MS)neurodegenerationproteasomeprotein aggregationprotein phosphorylationsite-directed mutagenesisTDP-43ubiquitylation (ubiquitination)

Identifiers

PMID30120199
PMCPMC6187624
OpenAlexW2885114943

What OpenQuestion holds

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Registered trials

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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.