Engineering Murine Cross-Reactivity Into an Affibody to Human Death Receptor 5.

Tse-Han Kuo, Nagamani Vunnam, Jonathan N Sachs, Benjamin J Hackel

Abstract read

In one paragraph

Article in Biotechnology and bioengineering, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed

–field-weighted citation impact

1 · What the graph read from it

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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

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3 · Its place in the literature

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Tse-Han KuoDepartment of Chemical Engineering and Materials Science, University of Minnesota - Twin Cities, Minneapolis, Minnesota, USA.

Nagamani VunnamDepartment of Biomedical Engineering, University of Minnesota - Twin Cities, Minneapolis, Minnesota, USA.

Jonathan N SachsDepartment of Biomedical Engineering, University of Minnesota - Twin Cities, Minneapolis, Minnesota, USA.

Benjamin J HackelDepartment of Chemical Engineering and Materials Science, University of Minnesota - Twin Cities, Minneapolis, Minnesota, USA.

Funding

Engineering synthetic ligands with potent allosteric inhibition of tumornecrosis factor receptorsR01EB028274 · NIBIB · UNIVERSITY OF MINNESOTA · PI HACKEL, BENJAMIN, SACHS, JONATHAN N · 2019 to 2022

$1.5M

Engineering protein developabilityR01GM146372 · NIGMS · UNIVERSITY OF MINNESOTA · PI HACKEL, BENJAMIN · 2022 to 2025

$1.4M

NIBIB NIH HHS R01 EB028274NIGMS NIH HHS R01 GM146372NIH HHS R01 EB028274

6 · The paper itself

Abstract

Interspecies cross-reactive protein therapeutics that target conserved epitopes across species are critical for translational research. The present study showcases the engineering of an affibody molecule, originally discovered for binding to human death receptor 5 (hDR5) with 94 nM affinity, to simultaneously acquire cross-reactivity to murine DR5 and enhance its binding affinity to human DR5. DR5 plays a pivotal role in metabolic dysfunction-associated steatohepatitis (MASH) by mediating hepatocyte apoptosis and inflammation. Utilizing a rationally designed library guided by enrichment information and a helix-walking mutagenesis strategy, combined with alternating binding selections between human and murine DR5, we evolved affibody variants exhibiting significantly improved binding to both receptors. Deep sequencing revealed amino acid preferences in the paratope, and the dominant variant, ABY

Indexed as

Protein EngineeringReceptors, TNF-Related Apoptosis-Inducing LigandRecombinant Fusion ProteinsAnimalsCross ReactionsHumansMiceProtein BindingReceptors, TNF-Related Apoptosis-Inducing LigandRecombinant Fusion ProteinsTNFRSF10B protein, human

Identifiers

PMID42087709

DOI10.1002/bit.70216

PMCPMC13245200

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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.