Evidence map›Paper›PMID 27992407›Full record

ArticleNature cell biology2017

LIN28 phosphorylation by MAPK/ERK couples signalling to the post-transcriptional control of pluripotency.

Kaloyan M Tsanov, Daniel S Pearson, Zhaoting Wu, Areum Han, Robinson Triboulet, Marc T Seligson, John T Powers, Jihan K Osborne, Susan Kane, Steven P Gygi and 2 more

Open access · greenAbstract read
In one paragraph

Article in Nature cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. TheCurrent pharmaceutical biotechnology · 2023
    Article
  16. Article
  17. Article
  18. Review
  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

12 authors at 6 institutions in 1 country.

Kaloyan M TsanovStem Cell Transplantation Program, Division of Hematology/Oncology, Manton Center for Orphan Disease Research, Boston Children's Hospital and Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.
Daniel S PearsonStem Cell Transplantation Program, Division of Hematology/Oncology, Manton Center for Orphan Disease Research, Boston Children's Hospital and Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.
Zhaoting WuStem Cell Transplantation Program, Division of Hematology/Oncology, Manton Center for Orphan Disease Research, Boston Children's Hospital and Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.
Areum HanStem Cell Transplantation Program, Division of Hematology/Oncology, Manton Center for Orphan Disease Research, Boston Children's Hospital and Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.
Robinson TribouletDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Stem Cell Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.
Marc T SeligsonStem Cell Transplantation Program, Division of Hematology/Oncology, Manton Center for Orphan Disease Research, Boston Children's Hospital and Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.
John T PowersStem Cell Transplantation Program, Division of Hematology/Oncology, Manton Center for Orphan Disease Research, Boston Children's Hospital and Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.
Jihan K OsborneStem Cell Transplantation Program, Division of Hematology/Oncology, Manton Center for Orphan Disease Research, Boston Children's Hospital and Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.
Susan KaneCell Signaling Technology, Inc., Danvers, Massachusetts 01923, USA.
Steven P GygiDepartment of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Richard I GregoryDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Stem Cell Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.
George Q DaleyStem Cell Transplantation Program, Division of Hematology/Oncology, Manton Center for Orphan Disease Research, Boston Children's Hospital and Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.
Harvard University · USBoston Children's Hospital · USHoward Hughes Medical Institute · USCell Signaling Technology (United States) · USDana-Farber Cancer Institute · USHarvard Stem Cell Institute · US

Funding

Medical Scientist Training ProgramT32GM007753 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WALENSKY, LOREN DAVID · 1985 to 2021
$50.0M
SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2M
Regulation of microRNA Biogenesis in Stem CellsR01GM086386 · NIGMS · BOSTON CHILDREN'S HOSPITAL · PI GREGORY, RICHARD I. · 2009 to 2018
$3.1M
Understanding the role of the lin28 paralogs and branching morphogenesisR01GM107536 · NIGMS · BOSTON CHILDREN'S HOSPITAL · PI DALEY, GEORGE Q · 2014 to 2017
$1.9M
NICHD NIH HHS P30 HD018655NIGMS NIH HHS R01 GM086386NIGMS NIH HHS R01 GM107536NIGMS NIH HHS T32 GM007753
6 · The paper itself

Abstract

Signalling and post-transcriptional gene control are both critical for the regulation of pluripotency, yet how they are integrated to influence cell identity remains poorly understood. LIN28 (also known as LIN28A), a highly conserved RNA-binding protein, has emerged as a central post-transcriptional regulator of cell fate through blockade of let-7 microRNA biogenesis and direct modulation of mRNA translation. Here we show that LIN28 is phosphorylated by MAPK/ERK in pluripotent stem cells, which increases its levels via post-translational stabilization. LIN28 phosphorylation had little impact on let-7 but enhanced the effect of LIN28 on its direct mRNA targets, revealing a mechanism that uncouples LIN28's let-7-dependent and -independent activities. We have linked this mechanism to the induction of pluripotency by somatic cell reprogramming and the transition from naive to primed pluripotency. Collectively, our findings indicate that MAPK/ERK directly impacts LIN28, defining an axis that connects signalling, post-transcriptional gene control, and cell fate regulation.

Indexed as

MAP Kinase Signaling SystemTranscription, GeneticAmino Acid SequenceAnimalsBlotting, WesternHeLa CellsHumansImmunoprecipitationMass SpectrometryMiceMice, TransgenicMicroRNAsMouse Embryonic Stem CellsPhosphorylationPluripotent Stem CellsProtein DomainsLin-28 protein, mouseMicroRNAsmirnlet7 microRNA, mouseRNA-Binding Proteins

Identifiers

PMID27992407
PMCPMC5182091
OpenAlexW2563522092

What OpenQuestion holds

Textmetadata
LicenceTDM
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.