Evidence map›Paper›PMID 10449746›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Immortalization of primary human keratinocytes by the helix-loop-helix protein, Id-1.

R M Alani, J Hasskarl, M Grace, M C Hernandez, M A Israel, K Münger

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 140 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. The Role of p16International journal of molecular sciences · 2017
    Review
  6. Article
  7. ID proteins regulate diverse aspects of cancer progression and provide novel therapeutic opportunities.Molecular therapy : the journal of the American Society of Gene Therapy · 2014
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Regulation of senescence in cancer and aging.Journal of aging research · 2011
    Article
  14. Article
  15. Article
  16. Tumor suppression by p53: making cells senescent.Histology and histopathology · 2010
    Review
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 3 institutions in 1 country.

R M AlaniDepartment of Pathology, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA.
J Hasskarl
M Grace
M C Hernandez
M A Israel
K Münger
University of California, San Francisco · USHarvard University · USMassachusetts General Hospital · US

Funding

DERMATOLOGY TRAINING GRANTT32AR007098 · NIAMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI THOMAS S. KUPPER · 1986 to 2026
$8.1M
BIOLOGICAL ACTIVITY OF HPV E7 IN HUMAN EPITHELIAL CELLSR01CA066980 · NCI · TUFTS UNIVERSITY BOSTON · PI MUNGER, KARL · 1996 to 2019
$7.4M
Virus discovery in cutaneous T cell lymphomaP30AR042689 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI KUPPER, THOMAS S. · 1994 to 2010
$6.8M
MECHANISMS OF HUMAN KERATINOCYTE DIFFERENTIATIONK08AR001975 · NIAMS · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI ALANI, RHODA M · 1996 to 2000
$126k
NCI NIH HHS CA66980NCI NIH HHS R01 CA066980NIAMS NIH HHS K08 AR01975-01A1NIAMS NIH HHS P30 AR042689NIAMS NIH HHS T32 AR007098NIAMS NIH HHS T32 AR07098-21
6 · The paper itself

Abstract

Basic helix-loop-helix (bHLH) DNA-binding proteins have been demonstrated to regulate tissue-specific transcription within multiple cell lineages. The Id family of helix-loop-helix proteins does not possess a basic DNA-binding domain and functions as a negative regulator of bHLH proteins. Overexpression of Id proteins within a variety of cell types has been shown to inhibit their ability to differentiate under appropriate conditions. We demonstrate that ectopic expression of Id-1 leads to activation of telomerase activity and immortalization of primary human keratinocytes. These immortalized cells have a decreased capacity to differentiate as well as activate phosphorylation of the retinoblastoma protein. Additionally, these cells acquire an impaired p53-mediated DNA-damage response as a late event in immortalization. We conclude that bHLH proteins play a pivotal role in regulating normal keratinocyte growth and differentiation, which can be disrupted by the immortalizing functions of Id-1 through activation of telomerase activity and inactivation of the retinoblastoma protein.

Indexed as

Helix-Loop-Helix MotifsRepressor ProteinsRNACatalytic DomainCells, CulturedCellular SenescenceDNA-Binding ProteinsDNA DamageEnzyme ActivationHumansInhibitor of Differentiation Protein 1KeratinocytesPhosphorylationRetinoblastoma ProteinTelomeraseTranscription FactorsDNA-Binding ProteinsID1 protein, humanInhibitor of Differentiation Protein 1Repressor ProteinsRetinoblastoma ProteinRNATelomerasetelomerase RNATranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID10449746
PMCPMC22262
OpenAlexW4244341972

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.