Evidence mapPaperPMID 40161657Full record

ArticlebioRxiv : the preprint server for biology2025

Activation of a Src-JNK pathway in unscheduled endocycling cells of the

Yi-Ting Huang, Brian R Calvi

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Yi-Ting HuangDepartment of Biology, Indiana University, Bloomington, Indiana, 47405 USA.ORCID 0009-0007-7796-6021
Brian R CalviDepartment of Biology, Indiana University, Bloomington, Indiana, 47405 USA.ORCID 0000-0001-5304-0047

Funding

Cell cycle and checkpoint variations in development and diseaseR35GM152255 · NIGMS · TRUSTEES OF INDIANA UNIVERSITY · PI BRIAN R CALVI · 2024 to 2026
$1.3M
NIGMS NIH HHS R35 GM152255
6 · The paper itself

Abstract

The endocycle is a specialized cell cycle during which cells undergo repeated G / S phases to replicate DNA without division, leading to large polyploid cells. The transition from a mitotic cycle to an endocycle can be triggered by various stresses, which results in unscheduled, or induced endocycling cells (iECs). While iECs can be beneficial for wound healing, they can also be detrimental by impairing tissue growth or promoting cancer. However, the regulation of endocycling and its role in tissue growth remain poorly understood. Using the

Indexed as

chronic woundEndocycleJNKpolyploidsenescenceSrc42Atissue closuretumorigenesiswound response

Identifiers

PMID40161657
PMCPMC11952448

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.