Evidence map›Paper›PMID 31407020›Full record

ReviewCellular and molecular life sciences : CMLS2020

Smad linker region phosphorylation is a signalling pathway in its own right and not only a modulator of canonical TGF-β signalling.

Danielle Kamato, Bich Hang Do, Narin Osman, Benjamin P Ross, Raafat Mohamed, Suowen Xu, Peter J Little

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
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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

7 authors at 6 institutions in 5 countries.

Danielle KamatoPharmacy Australia Centre of Excellence, School of Pharmacy, The University of Queensland, 20 Cornwall Street, Woolloongabba, QLD, 4102, Australia. d.kamato@uq.edu.au.ORCID http://orcid.org/0000-0002-1089-2829
Bich Hang DoFaculty of Pharmacy, Ton Duc Thang University, Ho Chi Minh City, 700000, Vietnam.
Narin OsmanSchool of Medical Sciences, RMIT University, Bundoora, VIC, 3083, Australia.
Benjamin P RossPharmacy Australia Centre of Excellence, School of Pharmacy, The University of Queensland, 20 Cornwall Street, Woolloongabba, QLD, 4102, Australia.
Raafat MohamedPharmacy Australia Centre of Excellence, School of Pharmacy, The University of Queensland, 20 Cornwall Street, Woolloongabba, QLD, 4102, Australia.
Suowen XuDepartment of Medicine, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.
Peter J LittlePharmacy Australia Centre of Excellence, School of Pharmacy, The University of Queensland, 20 Cornwall Street, Woolloongabba, QLD, 4102, Australia.
The University of Queensland · AUMonash University · AUSun Yat-sen University · CNTon Duc Thang University · VNUniversity of Mosul · IQUniversity of Rochester · US

Funding

National Health and Medical Research Council 1160925National Heart Foundation of Australia 102129
6 · The paper itself

Abstract

Transforming growth factor (TGF)-β signalling pathways are intensively investigated because of their diverse association with physiological and pathophysiological states. Smad transcription factors are the key mediators of TGF-β signalling. Smads can be directly phosphorylated in the carboxy terminal by the TGF-β receptor or in the linker region via multiple intermediate serine/threonine kinases. Growth factors in addition to hormones and TGF-β can activate many of the same kinases which can phosphorylate the Smad linker region. Historically, Smad linker region phosphorylation was shown to prevent nuclear translocation of Smads and inhibit TGF-β signalling pathways; however, it was subsequently shown that Smad linker region phosphorylation can be a driver of gene expression. This review will cover the signalling pathways of Smad linker region phosphorylation that drive the expression of genes involved in pathology and pathophysiology. The role of Smad signalling in cell biology is expanding rapidly beyond its role in TGF-β signalling and many signalling paradigms need to be re-evaluated in terms of Smad involvement.

Indexed as

AnimalsGene ExpressionHumansPhosphorylationSignal TransductionSmad ProteinsTransforming Growth Factor betaSmad ProteinsTransforming Growth Factor betaAlk 5CancerCell signallingG protein coupled receptorsNuclear translocationSerine/threonine kinase receptors

Identifiers

PMID31407020
PMCPMC11104920
OpenAlexW2968078373

What OpenQuestion holds

Textmetadata
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.