Evidence map›Paper›PMID 32235336›Full record

ArticleBiomolecules2020

Activins as Dual Specificity TGF-β Family Molecules: SMAD-Activation via Activin- and BMP-Type 1 Receptors.

Oddrun Elise Olsen, Hanne Hella, Samah Elsaadi, Carsten Jacobi, Erik Martinez-Hackert, Toril Holien

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 47 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Context-dependent TGFβ family signalling in cell fate regulation.Nature reviews. Molecular cell biology · 2023
    Review
  18. Article
  19. Article
  20. 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

6 authors at 3 institutions in 3 countries.

Oddrun Elise OlsenDepartment of Clinical and Molecular Medicine, NTNU - Norwegian University of Science and Technology, 7491 Trondheim, Norway.
Hanne HellaDepartment of Clinical and Molecular Medicine, NTNU - Norwegian University of Science and Technology, 7491 Trondheim, Norway.
Samah ElsaadiDepartment of Clinical and Molecular Medicine, NTNU - Norwegian University of Science and Technology, 7491 Trondheim, Norway.
Carsten JacobiNovartis Institutes for BioMedical Research Basel, Musculoskeletal Disease Area, Novartis Pharma AG, CH-4056 Basel, Switzerland.
Erik Martinez-HackertDepartment of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI 48824, USA.
Toril HolienDepartment of Clinical and Molecular Medicine, NTNU - Norwegian University of Science and Technology, 7491 Trondheim, Norway.ORCID 0000-0002-2051-5824
Norwegian University of Science and Technology · NOMichigan State University · USNovartis (Switzerland) · CH

Funding

TGF-β signaling and regulation: Elucidating molecular mechanisms and pathogenic functions of the ‘co-receptor’ Cripto-1 and the receptor BMPRIIR01GM121499 · NIGMS · MICHIGAN STATE UNIVERSITY · PI MARTINEZ HACKERT, ERIK MATTHIAS · 2018 to 2022
$1.5M
NIGMS NIH HHS R01 GM121499
6 · The paper itself

Abstract

Activins belong to the transforming growth factor (TGF)-β family of multifunctional cytokines and signal via the activin receptors ALK4 or ALK7 to activate the SMAD2/3 pathway. In some cases, activins also signal via the bone morphogenetic protein (BMP) receptor ALK2, causing activation of the SMAD1/5/8 pathway. In this study, we aimed to dissect how activin A and activin B homodimers, and activin AB and AC heterodimers activate the two main SMAD branches. We compared the activin-induced signaling dynamics of ALK4/7-SMAD2/3 and ALK2-SMAD1/5 in a multiple myeloma cell line. Signaling via the ALK2-SMAD1/5 pathway exhibited greater differences between ligands than signaling via ALK4/ALK7-SMAD2/3. Interestingly, activin B and activin AB very potently activated SMAD1/5, resembling the activation commonly seen with BMPs. As SMAD1/5 was also activated by activins in other cell types, we propose that dual specificity is a general mechanism for activin ligands. In addition, we found that the antagonist follistatin inhibited signaling by all the tested activins, whereas the antagonist cerberus specifically inhibited activin B. Taken together, we propose that activins may be considered dual specificity TGF-β family members, critically affecting how activins may be considered and targeted clinically.

Indexed as

Activin Receptors, Type IActivinsBone Morphogenetic Protein Receptors, Type ICell Line, TumorHumansProtein MultimerizationProtein Structure, QuaternarySmad ProteinsSubstrate SpecificityTransforming Growth Factor betaactivin Aactivin BActivin Receptors, Type IActivinsACVR1 protein, humanBone Morphogenetic Protein Receptors, Type ISmad ProteinsTransforming Growth Factor betaactivinACVR1ALK2BMPsignal transductionSMAD

Identifiers

PMID32235336
PMCPMC7225989
OpenAlexW3014008006

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.