Evidence map›Paper›PMID 29892481›Full record

ArticleSignal transduction and targeted therapy

Transcriptional cofactors Ski and SnoN are major regulators of the TGF-β/Smad signaling pathway in health and disease.

Angeles C Tecalco-Cruz, Diana G Ríos-López, Genaro Vázquez-Victorio, Reyna E Rosales-Alvarez, Marina Macías-Silva

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 2 pooled it
4.3field-weighted citation impact, top 5% of its field
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

78 citing papers in PubMed, 2 syntheses or guidelines pooled it, 117 citations in OpenAlex.

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  17. JunB-HBZ nuclear translocation by TGF-β is a key driver in HTLV-1-mediated leukemogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  18. Cancer innovation · 2025
    Article
  19. Article
  20. Transcriptomic Analysis Reveals Key Pathways Influenced by HIV-2 Vpx.International journal of molecular sciences · 2025
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18 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Angeles C Tecalco-Cruz1Instituto de Investigaciones Biomédicas at Universidad Nacional Autónoma de México, Mexico city, 04510 Mexico.
Diana G Ríos-López2Instituto de Fisiología Celular at Universidad Nacional Autónoma de México, Mexico city, 04510 Mexico.
Genaro Vázquez-Victorio3Facultad de Ciencias at Universidad Nacional Autónoma de México, Mexico city, 04510 Mexico.
Reyna E Rosales-Alvarez2Instituto de Fisiología Celular at Universidad Nacional Autónoma de México, Mexico city, 04510 Mexico.
Marina Macías-Silva2Instituto de Fisiología Celular at Universidad Nacional Autónoma de México, Mexico city, 04510 Mexico.ORCID 0000-0002-3972-0983
Universidad Nacional Autónoma de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transforming growth factor-β (TGF-β) family plays major pleiotropic roles by regulating many physiological processes in development and tissue homeostasis. The TGF-β signaling pathway outcome relies on the control of the spatial and temporal expression of >500 genes, which depend on the functions of the Smad protein along with those of diverse modulators of this signaling pathway, such as transcriptional factors and cofactors. Ski (Sloan-Kettering Institute) and SnoN (Ski novel) are Smad-interacting proteins that negatively regulate the TGF-β signaling pathway by disrupting the formation of R-Smad/Smad4 complexes, as well as by inhibiting Smad association with the p300/CBP coactivators. The Ski and SnoN transcriptional cofactors recruit diverse corepressors and histone deacetylases to repress gene transcription. The TGF-β/Smad pathway and coregulators Ski and SnoN clearly regulate each other through several positive and negative feedback mechanisms. Thus, these cross-regulatory processes finely modify the TGF-β signaling outcome as they control the magnitude and duration of the TGF-β signals. As a result, any alteration in these regulatory mechanisms may lead to disease development. Therefore, the design of targeted therapies to exert tight control of the levels of negative modulators of the TGF-β pathway, such as Ski and SnoN, is critical to restore cell homeostasis under the specific pathological conditions in which these cofactors are deregulated, such as fibrosis and cancer.

Identifiers

PMID29892481
PMCPMC5992185
OpenAlexW2805654943

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.