Evidence map›Paper›PMID 21293188›Full record

ArticleCell cycle (Georgetown, Tex.)2011

Post-translational control of Myc function during differentiation.

Maralice Conacci-Sorrell, Robert N Eisenman

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. ACYP2 contributes to malignant progression of glioma through promoting CaJournal of experimental & clinical cancer research : CR · 2020
    Article
  5. MYC leads the way.Small GTPases · 2020
    Review
  6. MYC-nick promotes cell migration by inducing fascin expression and Cdc42 activation.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  7. Article
  8. Review
  9. Article
  10. Fam65b is important for formation of the HDAC6-dysferlin protein complex during myogenic cell differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
    Article
  11. Article
  12. MYC degradation.Cold Spring Harbor perspectives in medicine · 2014
    Review
  13. Article
  14. Control of vertebrate development by MYC.Cold Spring Harbor perspectives in medicine · 2013
    Review
  15. Correct timing of proliferation and differentiation is necessary for normal inner ear development and auditory hair cell viability.Developmental dynamics : an official publication of the American Association of Anatomists · 2013
    Article
  16. 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

2 authors at 1 institution in 2 countries.

Maralice Conacci-SorrellDivision of Basic Sciences, Fred Hutchinson Cancer Research Center; Seattle, WA USA. mconacci@fhcrc.org
Robert N Eisenman
Cape Town HVTN Immunology Laboratory / Hutchinson Centre Research Institute of South Africa · ZA

Funding

Regulation of cell growth and proliferation by MycR01CA020525 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI EISENMAN, ROBERT NEIL · 1985 to 2018
$10.7M
CONTROL MECHANISMS IN AVIAN ONCORNAVIRUS REPLICATIONR37CA020525 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI EISENMAN, ROBERT NEIL · 1990 to 1999
–
NCI NIH HHS CA20525NCI NIH HHS R01 CA020525NCI NIH HHS R37 CA020525
6 · The paper itself

Abstract

Myc proteins are deeply involved in multiple biological processes including cell proliferation, growth, metabolism, apoptosis, differentiation, and tumorigenesis. Paradoxically, Myc proteins have been found to be capable of both inhibiting and facilitating differentiation depending on the biological context. Recently we identified a new mode of Myc regulation in differentiating muscle cells in which c-Myc protein is proteolytically cleaved by calcium-dependent calpains in the cytoplasm. This cleavage serves two purposes. First, it inactivates the transcriptional function of Myc by removing its C-terminus, a region responsible for the interaction of Myc with Max and DNA. Second, it alters cytoskeletal architecture and accelerates muscle differentiation through the activity of the remaining N-terminal cleavage product (termed Myc-nick). Here we discuss the roles and regulation of full-length Myc and Myc-nick in terminal differentiation and propose a model in which calpain-mediated cleavage of Myc operates as a functional switch.

Indexed as

Protein Processing, Post-TranslationalCalciumCalpainCell DifferentiationCytoplasmCytoskeletonDNADNA-Binding ProteinsGene Expression Regulation, DevelopmentalGenes, mycHumansMicrotubulesMuscle CellsProto-Oncogene Proteins c-mycSignal TransductionTranscription, GeneticCalciumCalpainDNADNA-Binding ProteinsProto-Oncogene Proteins c-myc

Identifiers

PMID21293188
PMCPMC3173997
OpenAlexW2080766313

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.