Evidence map›Paper›PMID 38753874›Full record

ArticlePLoS computational biology2024

Liebig's law of the minimum in the TGF-β/SMAD pathway.

Yuchao Li, Difan Deng, Chris Tina Höfer, Jihye Kim, Won Do Heo, Quanbin Xu, Xuedong Liu, Zhike Zi

Abstract read
In one paragraph

Article in PLoS computational biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Molecular Engineering of the Helminth TGF-β Mimetics, TGM1 and TGM4, Reveals a Novel Antagonist of TGF-β Signaling in Fibroblasts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. 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

8 authors.

Yuchao LiMax Planck Institute for Molecular Genetics, Otto Warburg Laboratory, Berlin, Germany.
Difan DengGerman Federal Institute for Risk Assessment, Department of Experimental Toxicology and ZEBET, Berlin, Germany.
Chris Tina HöferGerman Federal Institute for Risk Assessment, Department of Experimental Toxicology and ZEBET, Berlin, Germany.
Jihye KimDepartment of Biological Sciences, KAIST Institute for the BioCentury, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.
Won Do HeoDepartment of Biological Sciences, KAIST Institute for the BioCentury, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.
Quanbin XuDepartment of Biochemistry, University of Colorado Boulder, Boulder, Colorado, United States of America.
Xuedong LiuDepartment of Biochemistry, University of Colorado Boulder, Boulder, Colorado, United States of America.
Zhike ZiMax Planck Institute for Molecular Genetics, Otto Warburg Laboratory, Berlin, Germany.ORCID 0000-0002-7601-915X

Funding

Programmable Microvesicles for Intracellular Macromolecule DeliveryR01GM144749 · NIGMS · UNIVERSITY OF COLORADO · PI XUEDONG LIU · 2022 to 2026
$3.2M
NIGMS NIH HHS R01 GM144749
6 · The paper itself

Abstract

Cells use signaling pathways to sense and respond to their environments. The transforming growth factor-β (TGF-β) pathway produces context-specific responses. Here, we combined modeling and experimental analysis to study the dependence of the output of the TGF-β pathway on the abundance of signaling molecules in the pathway. We showed that the TGF-β pathway processes the variation of TGF-β receptor abundance using Liebig's law of the minimum, meaning that the output-modifying factor is the signaling protein that is most limited, to determine signaling responses across cell types and in single cells. We found that the abundance of either the type I (TGFBR1) or type II (TGFBR2) TGF-β receptor determined the responses of cancer cell lines, such that the receptor with relatively low abundance dictates the response. Furthermore, nuclear SMAD2 signaling correlated with the abundance of TGF-β receptor in single cells depending on the relative expression levels of TGFBR1 and TGFBR2. A similar control principle could govern the heterogeneity of signaling responses in other signaling pathways.

Indexed as

Signal TransductionTransforming Growth Factor betaCell Line, TumorComputational BiologyHumansModels, BiologicalReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IReceptor, Transforming Growth Factor-beta Type IISmad2 ProteinSmad ProteinsReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IReceptor, Transforming Growth Factor-beta Type IISmad2 ProteinSmad ProteinsTGFBR1 protein, humanTransforming Growth Factor beta

Identifiers

PMID38753874
PMCPMC11135686

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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.