Mutational Analysis of RIP Type I Dianthin-30 Suggests a Role for Arg24 in Endocytosis.

Louisa Schlaak, Christoph Weise, Benno Kuropka, Alexander Weng

Abstract read

In one paragraph

Article in Toxins, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing 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

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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

1 citing paper in PubMed.

Potentiation of Gelonin Cytotoxicity by Pulsed Electric Fields.International journal of molecular sciences · 2025
Article

4 · The record

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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

4 authors.

Louisa SchlaakInstitute of Pharmacy, Freie Universität Berlin, Königin-Luise-Str. 2+4, 14195 Berlin, Germany.

Christoph WeiseInstitute of Chemistry and Biochemistry, Freie Universität Berlin, Thielallee 63, 14195 Berlin, Germany.ORCID 0000-0002-5507-4694

Benno KuropkaInstitute of Chemistry and Biochemistry, Freie Universität Berlin, Thielallee 63, 14195 Berlin, Germany.ORCID 0000-0001-5088-6346

Alexander WengInstitute of Pharmacy, Freie Universität Berlin, Königin-Luise-Str. 2+4, 14195 Berlin, Germany.ORCID 0000-0003-1640-2189

Funding

Deutsche Forschungsgemeinschaft 422686308

6 · The paper itself

Abstract

Saponin-mediated endosomal escape is a mechanism that increases the cytotoxicity of type I ribosome-inactivating proteins (type I RIPs). In order to actualize their cytotoxicity, type I RIPs must be released into the cytosol after endocytosis. Without release from the endosomes, type I RIPs are largely degraded and cannot exert their cytotoxic effects. Certain triterpene saponins are able to induce the endosomal escape of these type I RIPs, thus increasing their cytotoxicity. However, the molecular mechanism underlying the endosomal escape enhancement of type I RIPs by triterpene saponins has not been fully elucidated. In this report, we investigate the involvement of the basic amino acid residues of dianthin-30, a type I RIP isolated from the plant

Indexed as

EndocytosisRibosome Inactivating ProteinsAnimalsArginineCell Line, TumorCell SurvivalDianthusDNA Mutational AnalysisEndosomesMiceMutationSaponinsArginineRibosome Inactivating ProteinsSaponinsbasic amino acid residuesendocytosisendosomal escape enhancerN-glycosylaseribosome-inactivating proteinstriterpene saponinstype I RIP

Identifiers

PMID38787071

DOI10.3390/toxins16050219

PMCPMC11125672

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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.