Evidence map›Paper›PMID 36246165›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2021

Synthetic Artificial Apoptosis-Inducing Receptor for On-Demand Deactivation of Engineered Cells.

Pere Monge, Kaja Borup Løvschall, Ane Bretschneider Søgaard, Raoul Walther, Thaddeus W Golbek, Lars Schmüser, Tobias Weidner, Alexander N Zelikin

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Pere MongeDepartment of Chemistry and iNano Interdisciplinary Nanoscience Centre Aarhus University Aarhus 8000 Denmark.
Kaja Borup LøvschallDepartment of Chemistry and iNano Interdisciplinary Nanoscience Centre Aarhus University Aarhus 8000 Denmark.
Ane Bretschneider SøgaardDepartment of Chemistry and iNano Interdisciplinary Nanoscience Centre Aarhus University Aarhus 8000 Denmark.
Raoul WaltherDepartment of Chemistry and iNano Interdisciplinary Nanoscience Centre Aarhus University Aarhus 8000 Denmark.
Thaddeus W GolbekDepartment of Chemistry and iNano Interdisciplinary Nanoscience Centre Aarhus University Aarhus 8000 Denmark.
Lars SchmüserDepartment of Chemistry and iNano Interdisciplinary Nanoscience Centre Aarhus University Aarhus 8000 Denmark.
Tobias WeidnerDepartment of Chemistry and iNano Interdisciplinary Nanoscience Centre Aarhus University Aarhus 8000 Denmark.
Alexander N ZelikinDepartment of Chemistry and iNano Interdisciplinary Nanoscience Centre Aarhus University Aarhus 8000 Denmark.ORCID 0000-0002-9864-321X
Aarhus University · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The design of a fully synthetic, chemical "apoptosis-inducing receptor" (AIR) molecule is reported that is anchored into the lipid bilayer of cells, is activated by the incoming biological input, and responds with the release of a secondary messenger-a highly potent toxin for cell killing. The AIR molecule has four elements, namely, an exofacial trigger group, a bilayer anchor, a toxin as a secondary messenger, and a self-immolative scaffold as a mechanism for signal transduction. Receptor installation into cells is established via a robust protocol with minimal cell handling. The synthetic receptor remains dormant in the engineered cells, but is effectively triggered externally by the addition of an activating biomolecule (enzyme) or in a mixed cell population through interaction with the surrounding cells. In 3D cell culture (spheroids), receptor activation is accessible for at least 5 days, which compares favorably with other state of the art receptor designs.

Indexed as

Lipid BilayersReceptors, ArtificialApoptosisSignal TransductionLipid BilayersReceptors, Artificialartificial receptorsglucuronideprodrugsself‐immolative linkerssignal transduction

Identifiers

PMID36246165
PMCPMC9539725
OpenAlexW3157238595

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.