Evidence map›Paper›PMID 18032916›Full record

ReviewCell cycle (Georgetown, Tex.)2007

Feedback regulation of c-Myc by ribosomal protein L11.

Mu-Shui Dai, Rosalie Sears, Hua Lu

Open access · greenAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

45 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Ribosome specialization by cancer-associated ribosomal protein mutations: progress made and open questions.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. The Interplay Between theInternational journal of molecular sciences · 2024
    Review
  9. Article
  10. Article
  11. RNA-binding motif protein 10 inactivates c-Myc by partnering with ribosomal proteins uL18 and uL5.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Hallmarks of ribosomopathies.Nucleic acids research · 2020
    Review
  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

3 authors at 2 institutions in 1 country.

Mu-Shui DaiDepartment of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
Rosalie Sears
Hua Lu
Indiana University Bloomington · USIndiana University School of Medicine

Funding

The Role of Ribosomal Proteins in the P53-MDM2 PathwayR01CA095441 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2002 to 2021
$5.1M
Cellular Mechanisms Controlling Myc Protein StabilityR01CA100855 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI SEARS, ROSALIE C · 2003 to 2014
$3.6M
MOLECULAR DISSECTION OF A NOVEL P53 LIKE PROTEINR01CA079721 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI LU, HUA · 1999 to 2006
$1.8M
Study of a FACTp140-SSRP1-associated p53 KinaseR01CA093614 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI LU, HUA · 2002 to 2006
$1.5M
Dissection of the feedback inhibition of c-Myc by L11R00CA127134 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI DAI, MU-SHUI · 2009 to 2011
$740k
Integration of Ras, Myc and E2F Signaling PathwaysK01CA086957 · NCI · OREGON HEALTH AND SCIENCE UNIVERSITY · PI SEARS, ROSALIE C · 2001 to 2005
$700k
Dissection of the feedback inhibition of c-Myc by L11K99CA127134 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI DAI, MU-SHUI · 2007 to 2008
$186k
NCI NIH HHS CA 079721NCI NIH HHS CA095441NCI NIH HHS CA93614NCI NIH HHS K01 CA086957NCI NIH HHS K01-CA086957NCI NIH HHS K990CA127134NCI NIH HHS K99 CA127134NCI NIH HHS R00 CA127134NCI NIH HHS R01 CA079721NCI NIH HHS R01 CA093614NCI NIH HHS R01 CA095441NCI NIH HHS R01 CA100855NCI NIH HHS R01-CA100855
6 · The paper itself

Abstract

Several ribosomal proteins including L11 have been shown to activate p53 by inhibiting oncoprotein MDM2, leading to inhibition of cell cycle progression. Our recent study showed that L11 also inhibits oncoprotein c-Myc. Overexpression of L11 inhibits c-Myc-induced transcription and cell proliferation, while reduction of endogenous L11 increases these c-Myc activities. Interestingly, L11 is a transcriptional target of c-Myc, thus forming a negative feedback loop. We further showed that L11 competes with coactivator TRRAP for binding to c-Myc through the Myc box II (MB II) and reduces histone H4 acetylation at c-Myc target gene promoters. In addition, L11 appears to regulate c-Myc levels. Knocking down L11 markedly increases the mRNA and protein levels of endogenous c-Myc. These results suggest that L11 also inhibits cell cycle progression by regulating the c-Myc pathway. Here we further discuss the implications of this regulation and questions that this finding raises.

Indexed as

AnimalsFeedback, PhysiologicalGene Expression Regulation, NeoplasticGrowth InhibitorsHumansProtein BindingProto-Oncogene Proteins c-mycRibosomal ProteinsGrowth InhibitorsProto-Oncogene Proteins c-mycribosomal protein L11Ribosomal Proteins

Identifiers

PMID18032916
PMCPMC2694724
OpenAlexW2055078106

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.