Evidence map›Paper›PMID 29899114›Full record

ArticleThe Journal of biological chemistry2018

Directed evolution of a picomolar-affinity, high-specificity antibody targeting phosphorylated tau.

Dan Li, Lei Wang, Brandon F Maziuk, Xudong Yao, Benjamin Wolozin, Yong Ku Cho

Abstract 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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
  2. Nanobodies targeting hnRNPA2/B1 and tau.bioRxiv : the preprint server for biology · 2025
    Article
  3. Article
  4. Yeast biopanning against site-specific phosphorylations in tau.Protein engineering, design & selection : PEDS · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. 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

6 authors.

Dan LiDepartment of Biomedical Engineering, University of Connecticut, Storrs, Connecticut 06269.
Lei WangDepartment of Chemistry, University of Connecticut, Storrs, Connecticut 06269.
Brandon F MaziukDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, Massachusetts 02118.
Xudong YaoDepartment of Chemistry, University of Connecticut, Storrs, Connecticut 06269; Department of Institute for Systems Genomics, University of Connecticut, Storrs, Connecticut 06269.
Benjamin WolozinDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, Massachusetts 02118.
Yong Ku ChoDepartment of Biomedical Engineering, University of Connecticut, Storrs, Connecticut 06269; Department of Institute for Systems Genomics, University of Connecticut, Storrs, Connecticut 06269; Department of Chemical and Biomolecular Engineering, University of Connecticut, Storrs, Connecticut 06269. Electronic address: cho@uconn.edu.

Funding

Neuropathology CoreP30AG013846 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KOWALL, NEIL W. · 1996 to 2020
$29.1M
Capturing the molecular complexity of Alzheimer's disease through the lens of RNA binding proteinsRF1AG056318 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LI, HU, WOLOZIN, BENJAMIN L · 2018 to 2020
$4.4M
Stress Granules and the Biology of TDP-43R01ES020395 · NIEHS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WOLOZIN, BENJAMIN L · 2012 to 2016
$4.1M
Genetic Modifiers of Protein Interaction Networks in TauopathyR01AG064932 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI EMILI, ANDREW, WOLOZIN, BENJAMIN L · 2019 to 2023
$3.2M
RNA binding proteins as novel targets in Alzheimer's diseaseR01AG050471 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WOLOZIN, BENJAMIN L · 2015 to 2019
$2.9M
The role of acetylation in regulating pathophysiology of tauR01NS089544 · NINDS · MAYO CLINIC JACKSONVILLE · PI PETRUCELLI, LEONARD, WOLOZIN, BENJAMIN L · 2014 to 2018
$1.9M
EARLY DETECTION OF TAU ACETYLATION USING ULTRA-HIGH AFFINITY ANTIBODIESR03NS099903 · NINDS · UNIVERSITY OF CONNECTICUT STORRS · PI CHO, YONGKU PETER · 2016 to 2017
$149k
Dysfunction of mRNA metabolism in tauopathyF31NS106751 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MAZIUK, BRANDON FRANCIS · 2018 to 2019
$85k
NIA NIH HHS P30 AG013846NIA NIH HHS R01 AG050471NIA NIH HHS R01 AG064932NIA NIH HHS RF1 AG056318NIEHS NIH HHS R01 ES020395NINDS NIH HHS F31 NS106751NINDS NIH HHS R01 NS089544NINDS NIH HHS R03 NS099903
6 · The paper itself

Abstract

Antibodies are essential biochemical reagents for detecting protein post-translational modifications (PTMs) in complex samples. However, recent efforts in developing PTM-targeting antibodies have reported frequent nonspecific binding and limited affinity of such antibodies. To address these challenges, we investigated whether directed evolution could be applied to improve the affinity of a high-specificity antibody targeting phosphothreonine 231 (pThr-231) of the human microtubule-associated protein tau. On the basis of existing structural information, we hypothesized that improving antibody affinity may come at the cost of loss in specificity. To test this hypothesis, we developed a novel approach using yeast surface display to quantify the specificity of PTM-targeting antibodies. When we affinity-matured the single-chain variable antibody fragment through directed evolution, we found that its affinity can be improved >20-fold over that of the WT antibody, reaching a picomolar range. We also discovered that most of the high-affinity variants exhibit cross-reactivity toward the nonphosphorylated target site but not to the phosphorylation site with a scrambled sequence. However, systematic quantification of the specificity revealed that such a tradeoff between the affinity and specificity did not apply to all variants and led to the identification of a picomolar-affinity variant that has a matching high specificity of the original phosphotau antibody. In cell- and tissue-imaging experiments, the high-affinity variant gave significantly improved signal intensity while having no detectable nonspecific binding. These results demonstrate that directed evolution is a viable approach for obtaining high-affinity PTM-specific antibodies and highlight the importance of assessing the specificity in the antibody engineering process.

Indexed as

Protein Processing, Post-TranslationalAmino Acid SequenceAntibody AffinityAntibody SpecificityBinding SitesCell Surface Display TechniquesCross ReactionsDirected Molecular EvolutionGene ExpressionHumansModels, MolecularPhosphorylationPhosphothreonineProtein BindingProtein Conformation, alpha-HelicalProtein Conformation, beta-StrandMAPT protein, humanPhosphothreonineRecombinant ProteinsSingle-Chain Antibodiestau Proteinsaffinityantibodyantibody specificityanti-PTM antibodyimmunochemistryneurodegenerationphospho-specificpost-translational modificationprotein phosphorylationtau protein (tau)

Identifiers

PMID29899114
PMCPMC6078456

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.