Evidence map›Paper›PMID 32573202›Full record

ArticleACS sensors2020

Genetically Encoded Split-Luciferase Biosensors to Measure Endosome Disruption Rapidly in Live Cells.

Kameron V Kilchrist, John William Tierney, Craig L Duvall

Open access · greenAbstract read
In one paragraph

Article in ACS sensors, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Endosomal Mechanisms in Heart Failure Pathophysiology.Current heart failure reports · 2025
    Review
  4. Article
  5. Review
  6. Endosomal escape: A bottleneck for LNP-mediated therapeutics.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
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

3 authors at 1 institution in 1 country.

Kameron V KilchristDepartment of Biomedical Engineering, Vanderbilt University, Nashville, Tennessee 37235, United States.ORCID 0000-0002-2391-9488
John William TierneyDepartment of Biomedical Engineering, Vanderbilt University, Nashville, Tennessee 37235, United States.
Craig L DuvallDepartment of Biomedical Engineering, Vanderbilt University, Nashville, Tennessee 37235, United States.ORCID 0000-0003-3979-0620
Vanderbilt University · US

Funding

Substrate Mediated siRNA Delivery from Scaffolds to Promote Wound RepairR01EB019409 · NIBIB · VANDERBILT UNIVERSITY · PI Craig Lewis Duvall · 2014 to 2026
$4.0M
NextGen RNAi Delivery to Breast Tumors for Selective mTORC2 BlockadeR01CA224241 · NCI · VANDERBILT UNIVERSITY · PI BRANTLEY-SIEDERS, DANA M, COOK, REBECCA SARA · 2018 to 2022
$2.5M
MK2 Inhibitory Nanoplexes to Enhance Long-Term Vascular Graft PatencyR01HL122347 · NHLBI · VANDERBILT UNIVERSITY · PI DUVALL, CRAIG LEWIS · 2016 to 2020
$2.2M
NCI NIH HHS R01 CA224241NHLBI NIH HHS R01 HL122347NIBIB NIH HHS R01 EB019409
6 · The paper itself

Abstract

Endosomal escape is a critical step in the intracellular delivery of biomacromolecular drugs, but a quantitative, high-throughput study of endosomal-vesicle disruption remains elusive. We designed two genetically encoded split-luciferase turn-on reporter assays that can be measured rapidly in well plates on live cells using a luminometer. Both systems use nonluminescent N-terminal and C-terminal luciferase fragments that can reconstitute a functional luminescent enzyme when they are colocalized by their fusion partners. The first system uses luciferase-fragment fusion to Galectin 8 (Gal8) and CALCOCO2. Gal8 and CALCOCO2 interact following endosomal-vesicle disruption to facilitate luciferase complementation into the active enzyme, enabling a luminescence readout (G8C2 system). The second system expresses the N-terminal carbohydrate recognition domain (N-CRD) of Gal8 fused to each luciferase fragment (G8G8 system). Following endosome disruption, G8-NCRD binds to exposed glycans inside endosomes, concentrating both fragments in close proximity and reconstituting active luciferase. The G8G8 system emerged as the lead reporter candidate and was further characterized by comparing it to previously reported Gal8-YFP tracking using microscopy. We also characterized the G8G8 system response to several commercial and research drug-delivery reagents: DOTAP lipid, JetPEI, Lipofectamine 2000, and a library of polymers with known endosomal-escape activity, revealing dose-dependent increases in luminescence due to endosomal disruption. These new reporters provide a first-in-class luminescent assay to rapidly detect endosome disruption in a high-throughput format while excluding toxic formulations. Endosome-disruption screening with these turn-on assays has the potential to accelerate and to improve the rigor of programs focused on the discovery and development of intracellular biologic drug-delivery formulations.

Indexed as

Biosensing TechniquesEndosomesLuciferasesLuminescent MeasurementsLuciferasesendosomal escapeendosome disruptionhigh-throughput screeningintracellular drug deliverysplit luciferase

Identifiers

PMID32573202
PMCPMC8191826
OpenAlexW3037926128

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.