Evidence map›Paper›PMID 16705184›Full record

ArticleMolecular and cellular biology2006

E Proteins and Id2 converge on p57Kip2 to regulate cell cycle in neural cells.

Gerson Rothschild, Xudong Zhao, Antonio Iavarone, Anna Lasorella

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.6field-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

46 citing papers in PubMed, 80 citations in OpenAlex.

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  2. HNRNPH1-mediated splicing events regulatebioRxiv : the preprint server for biology · 2025
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  7. The small molecule kobusone can stimulate islet β-cell replicationThe Journal of international medical research · 2021
    Article
  8. Review
  9. Functional Versatility of the CDK Inhibitor p57Frontiers in cell and developmental biology · 2020
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Retinoic acid signaling and neuronal differentiation.Cellular and molecular life sciences : CMLS · 2015
    Review
  16. Article
  17. 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

4 authors at 2 institutions in 1 country.

Gerson RothschildInstitute for Cancer Genetics, 1150 St. Nicholas Ave., Columbia University, New York, NY 10032, USA.
Xudong Zhao
Antonio Iavarone
Anna Lasorella
Cancer Genetics (United States) · USColumbia University · US

Funding

ID2 IN CELL CYCLE REGULATION AND CANCERR01CA085628 · NCI · YESHIVA UNIVERSITY · PI IAVARONE, ANTONIO · 2000 to 2010
$3.8M
The role of Id proteins in tumor development and angiogenesis in the brainR01CA101644 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LASORELLA, ANNA · 2003 to 2013
$3.5M
NCI NIH HHS R01 CA085628NCI NIH HHS R01 CA101644NCI NIH HHS R01-CA101644PHS HHS R01-A85628
6 · The paper itself

Abstract

A precise balance between proliferation and differentiation must be maintained during neural development to obtain the correct proportion of differentiated cell types in the adult nervous system. The basic helix-loop-helix (bHLH) transcription factors known as E proteins and their natural inhibitors, the Id proteins, control the timing of differentiation and terminal exit from the cell cycle. Here we show that progression into S phase of human neuroblastoma cells is prevented by E proteins and promoted by Id2. Cyclin-dependent kinase inhibitors (CKI) have been identified as key effectors of cell cycle arrest in differentiating cells. However, p57Kip2 is the only CKI that is absolutely required for normal development. Through the use of global gene expression analysis in neuroblastoma cells engineered to acutely express the E protein E47 and Id2, we find that p57Kip2 is a target of E47. Consistent with the role of Id proteins, Id2 prevents activation of p57Kip2 expression, and the retinoblastoma tumor suppressor protein, a known Id2 inhibitor, counters this activity. The strong E47-mediated inhibition of entry into S phase is entirely reversed in cells in which expression of p57Kip2 is silenced by RNA interference. During brain development, expression of p57Kip2 is opposite that of Id2. Our findings identify p57Kip2 as a functionally relevant target recruited by bHLH transcription factors to induce cell cycle arrest in developing neuroblasts and suggest that deregulated expression of Id proteins may be an epigenetic mechanism to silence expression of this CKI in neural tumors.

Indexed as

Cell CycleGene Expression Regulation, NeoplasticAdenoviridaeBasic Helix-Loop-Helix ProteinsCell ProliferationChromosomes, Human, Pair 11Cyclin-Dependent Kinase Inhibitor p57HumansInhibitor of Differentiation Protein 2Microarray AnalysisNeuroblastomaNeuronsRetinoblastoma ProteinTCF Transcription FactorsTranscription Factor 7-Like 1 ProteinTranscription, GeneticBasic Helix-Loop-Helix ProteinsCyclin-Dependent Kinase Inhibitor p57ID2 protein, humanInhibitor of Differentiation Protein 2Retinoblastoma ProteinTCF7L1 protein, humanTCF Transcription FactorsTranscription Factor 7-Like 1 Protein

Identifiers

PMID16705184
PMCPMC1489106
OpenAlexW2151806406

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.