Evidence map›Paper›PMID 38728009›Full record

ArticleJournal of neuropathology and experimental neurology2024

Production and characterization of novel monoclonal antibodies against pathological human TDP-43 proteins.

Xiaojing Zheng, Mengtian Wang, Qiongyan He, Shuyu Chen, Dilihumaer Simayi, Xia Ma, Junli Zhao, Xiaohong Sun, Peiyan Yang, Qinwen Mao and 1 more

Abstract read
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2024. 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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Review
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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

11 authors.

Xiaojing ZhengLaboratory of Gene Therapy, Department of Biochemistry, College of Life Sciences, Shaanxi Normal University, Shaanxi, P.R. China.
Mengtian WangLaboratory of Gene Therapy, Department of Biochemistry, College of Life Sciences, Shaanxi Normal University, Shaanxi, P.R. China.
Qiongyan HeLaboratory of Gene Therapy, Department of Biochemistry, College of Life Sciences, Shaanxi Normal University, Shaanxi, P.R. China.
Shuyu ChenLaboratory of Gene Therapy, Department of Biochemistry, College of Life Sciences, Shaanxi Normal University, Shaanxi, P.R. China.
Dilihumaer SimayiLaboratory of Gene Therapy, Department of Biochemistry, College of Life Sciences, Shaanxi Normal University, Shaanxi, P.R. China.
Xia MaLaboratory of Gene Therapy, Department of Biochemistry, College of Life Sciences, Shaanxi Normal University, Shaanxi, P.R. China.
Junli ZhaoLaboratory of Gene Therapy, Department of Biochemistry, College of Life Sciences, Shaanxi Normal University, Shaanxi, P.R. China.
Xiaohong SunLaboratory of Gene Therapy, Department of Biochemistry, College of Life Sciences, Shaanxi Normal University, Shaanxi, P.R. China.
Peiyan YangLaboratory of Gene Therapy, Department of Biochemistry, College of Life Sciences, Shaanxi Normal University, Shaanxi, P.R. China.
Qinwen MaoDepartment of Pathology, University of Utah, Salt Lake City, Utah, USA.ORCID 0000-0001-7876-2046
Haibin XiaLaboratory of Gene Therapy, Department of Biochemistry, College of Life Sciences, Shaanxi Normal University, Shaanxi, P.R. China.

Funding

Fundamental Research Funds for the Central Universities GK202007023Key Research and Development Plan of Shaanxi Province 2018SF-106National Natural Science Foundation of China 81773265Natural Science Foundation 2023-JC-YB-642Natural Science Foundation of Shaanxi Province 2023-JC-YB-642
6 · The paper itself

Abstract

The RNA/DNA-binding protein TDP-43 plays a pivotal role in the ubiquitinated inclusions characteristic of TDP-43 proteinopathies, including most cases of frontotemporal lobar degeneration (FTLD-TDP) and Alzheimer disease (AD). To understand the mechanisms of pathological TDP-43 processing and identify potential biomarkers, we generated novel phosphorylation-independent monoclonal antibodies (MAbs) using bacteria-expressed human full-length recombinant TDP-43. Remarkably, we identified a distinctive MAb, No. 9, targeting an epitope in amino acid (aa) region 311-360 of the C-terminus. This antibody showed preferential reactivity for pathological TDP-43 inclusions, with only mild reactivity for normal nuclear TDP-43. MAb No. 9 revealed more pathology in FTLD-TDP type A and type B brains and in AD brains compared to the commercial p409/410 MAb. Using synthetic phosphorylated peptides, we also obtained MAbs targeting the p409/410 epitope. Interestingly, MAb No. 14 was found to reveal additional pathology in AD compared to the commercial p409/410 MAb, specifically, TDP-43-immunopositive deposits with amyloid plaques in AD brains. These unique immunopositivities observed with MAbs No. 9 and No. 14 are likely attributed to their conformation-dependent binding to TDP-43 inclusions. We expect that this novel set of MAbs will prove valuable as tools for future patient-oriented investigations into TDP-43 proteinopathies.

Indexed as

Antibodies, MonoclonalDNA-Binding ProteinsAgedAlzheimer DiseaseAnimalsBrainFemaleFrontotemporal Lobar DegenerationHumansMaleAntibodies, MonoclonalDNA-Binding ProteinsTARDBP protein, humanAlzheimer diseaseFrontotemporal lobar degenerationPhosphorylation-dependent antibodyPhosphorylation-independent antibodyProteinopathyTDP-43

Identifiers

PMID38728009
PMCPMC11258413

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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.