Evidence map›Paper›PMID 28238764›Full record

ArticleJournal of molecular biology2017

Cullin E3 Ligase Activity Is Required for Myoblast Differentiation.

Jordan Blondelle, Paige Shapiro, Andrea A Domenighetti, Stephan Lange

Abstract read
In one paragraph

Article in Journal of molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Altered contractility, CaAmerican journal of physiology. Heart and circulatory physiology · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
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

4 authors at 2 institutions in 1 country.

Jordan BlondelleDivision of Cardiology, University of California San Diego, La Jolla, CA-92093 USA.
Paige ShapiroDivision of Cardiology, University of California San Diego, La Jolla, CA-92093 USA.
Andrea A DomenighettiRehabilitation Institute of Chicago, Chicago, IL-60611 USA; Department of Physical Medicine and Rehabilitation, Northwestern University, Chicago, IL-60611, USA.
Stephan LangeDivision of Cardiology, University of California San Diego, La Jolla, CA-92093 USA. Electronic address: slange@ucsd.edu.
University of California San Diego · USNorthwestern University · US

Funding

U of Calif, San Diego Neuroscience Microscopy ImagingP30NS047101 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLEESON, JOSEPH G, ZHENG, BINHAI · 2003 to 2022
$9.0M
Signaling Pathways in Dilated CardiomyopathyR01HL128457 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LANGE, STEPHAN · 2015 to 2019
$1.9M
Cullin mediated protein turnover in skeletal and cardiac musclesR00HL107744 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LANGE, STEPHAN · 2013 to 2015
$726k
Cullin mediated protein turnover in skeletal and cardiac musclesK99HL107744 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LANGE, STEPHAN · 2011 to 2012
$178k
NHLBI NIH HHS K99 HL107744NHLBI NIH HHS R00 HL107744NHLBI NIH HHS R01 HL128457NINDS NIH HHS P30 NS047101
6 · The paper itself

Abstract

The role of cullin E3-ubiquitin ligases for muscle homeostasis is best known during muscle atrophy, as the cullin-1 substrate adaptor atrogin-1 is among the most well-characterized muscle atrogins. We investigated whether cullin activity was also crucial during terminal myoblast differentiation and aggregation of acetylcholine receptors for the establishment of neuromuscular junctions in vitro. The activity of cullin E3-ligases is modulated through post-translational modification with the small ubiquitin-like modifier nedd8. Using either the Nae1 inhibitor MLN4924 (Pevonedistat) or siRNA against nedd8 in early or late stages of differentiation on C2C12 myoblasts, and primary satellite cells from mouse and human, we show that cullin E3-ligase activity is necessary for each step of the muscle cell differentiation program in vitro. We further investigate known transcriptional repressors for terminal muscle differentiation, namely ZBTB38, Bhlhe41, and Id1. Due to their identified roles for terminal muscle differentiation, we hypothesize that the accumulation of these potential cullin E3-ligase substrates may be partially responsible for the observed phenotype. MLN4924 is currently undergoing clinical trials in cancer patients, and our experiments highlight concerns on the homeostasis and regenerative capacity of muscles in these patients who often experience cachexia.

Indexed as

Cell DifferentiationAnimalsCells, CulturedHumansMiceMyoblastsUbiquitin-Protein LigasesUbiquitin-Protein LigasescullinE3-ubiquitin ligaseMLN4924muscle development

Identifiers

PMID28238764
PMCPMC5395100
OpenAlexW2590769547

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.