Evidence map›Paper›PMID 40913769›Full record

ArticleCell reports2025

Chemogenetic tuning reveals optimal MAPK signaling for cell-fate programming.

Brittany A Lende-Dorn, Jane C Atkinson, Yunbeen Bae, Kate E Galloway

Abstract read
In one paragraph

Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Programmable nanobody circuits for cell selection.bioRxiv : the preprint server for biology · 2026
    Article
  6. 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

4 authors.

Brittany A Lende-DornDepartment of Chemical Engineering, MIT, Cambridge, MA 02139, USA.
Jane C AtkinsonDepartment of Chemical Engineering, MIT, Cambridge, MA 02139, USA.
Yunbeen BaeDepartment of Chemical Engineering, MIT, Cambridge, MA 02139, USA.
Kate E GallowayDepartment of Chemical Engineering, MIT, Cambridge, MA 02139, USA. Electronic address: katiegal@mit.edu.

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI Jacqueline A. Lees · 1985 to 2026
$93.9M
Multiscale tools and approaches for understanding and engineering cell-fate transitionsR35GM143033 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI GALLOWAY, KATE ELIZABETH · 2021 to 2025
$1.9M
NCI NIH HHS P30 CA014051NIGMS NIH HHS R35 GM143033
6 · The paper itself

Abstract

Cell states evolve through the combined activity of signaling pathways and gene networks. While transcription factors can direct cell fate, these factors rely on a receptive cell state. How signaling levels contribute to the emergence of receptive cell states remains poorly defined. Using a well-defined model of direct conversion, we examined how levels of the mitogen-activated protein kinase (MAPK)-activating oncogene HRAS

Indexed as

MAP Kinase Signaling SystemMitogen-Activated Protein KinasesAnimalsCell DifferentiationCell ProliferationCellular SenescenceChemogeneticsFibroblastsHumansMiceMotor NeuronsProto-Oncogene Proteins p21(ras)Mitogen-Activated Protein KinasesProto-Oncogene Proteins p21(ras)cell fateCP: Developmental biologydirect conversionMAPKNgn2p53proliferationRASsenescencetransdifferentiation

Identifiers

PMID40913769
PMCPMC12571515

What OpenQuestion holds

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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.