Evidence map›Paper›PMID 40765797›Full record

ReviewNagoya journal of medical science2025

Calcineurin in cancer signaling networks.

Honoka Haba, Shoma Tsubota, Midori Shimada

Abstract readReview
In one paragraph

Review in Nagoya journal of medical science, 2025. 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

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

1 citing paper in PubMed.

  1. Review
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

3 authors.

Honoka HabaDepartment of Molecular Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Shoma TsubotaDepartment of Molecular Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Midori ShimadaDepartment of Molecular Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcium/calcineurin/nuclear factor of activated T-cell signaling is a vital regulator of the development and function of immune, nervous, cardiovascular, and musculoskeletal systems. The dysregulation of calcineurin activity has been implicated in various pathological conditions, including certain cancers, cardiac hypertrophy, and neurodegenerative disorders. Calcineurin is highly expressed in certain cancers and stabilizes and activates factors that promote cancer cell proliferation. Research has shown that protein dephosphorylation by calcineurin contributes to tumor formation and progression. Thus, elucidating molecular mechanisms of calcineurin-mediated tumorigenesis and tumor cell growth and targeting signaling pathways downstream of calcineurin may lead to new cancer therapies. This study reviewed the multiple roles of calcineurin in cell cycle progression and its potential as a target for cancer treatment.

Indexed as

CalcineurinNeoplasmsSignal TransductionAnimalsHumansNFATC Transcription FactorsCalcineurinNFATC Transcription Factorscalcineurincalciumcell proliferationdephosphorylationprognosis in cancer

Identifiers

PMID40765797
PMCPMC12320341

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.