Evidence map›Paper›PMID 11486031›Full record

ArticleMolecular and cellular biology2001

Induction of cyclin D1 transcription and CDK2 activity by Notch(ic): implication for cell cycle disruption in transformation by Notch(ic).

C Ronchini, A J Capobianco

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers.

0numbers the graph read from it
0cells of the map it votes in
176citing papers in PubMed
6.0field-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

176 citing papers in PubMed, 425 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Targeting CDK4 and CDK6 in cancer.Nature reviews. Cancer · 2022
    Review
  18. Article
  19. Article
  20. Review

116 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

C RonchiniDepartment of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati, College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267-0524, USA.
A J Capobianco
Sabin Vaccine Institute · USUniversity of Cincinnati · US

Funding

MOLECULAR MECHANISMS OF NOTCH SIGNALING IN NEOPLASIAR01CA083736 · NCI · WISTAR INSTITUTE · PI CAPOBIANCO, ANTHONY JOHN · 2000 to 2016
$4.0M
NCI NIH HHS R01 CA083736NCI NIH HHS R01 CA 83736
6 · The paper itself

Abstract

Notch genes encode a family of transmembrane proteins that are involved in many cellular processes such as differentiation, proliferation, and apoptosis. Although it is well established that all four Notch genes can act as oncogenes, the mechanism by which Notch proteins transform cells remains unknown. Previously, we have shown that transformation of RKE cells can be conditionally induced by hormone activation of Notch(ic)-estrogen receptor (ER) chimeras. Using this inducible system, we show that Notch(ic) activates transcription of the cyclin D1 gene with rapid kinetics. Transcriptional activation of cyclin D1 is independent from serum-derived growth factors and de novo synthesis of secondary transcriptional activators. Moreover, hormone activation of Notch(ic)-ER proteins induces CDK2 activity in the absence of serum. Upregulation of cyclin D1 and activation of CDK2 by Notch(ic) result in the promotion of S-phase entry. These data demonstrate the first evidence that Notch(ic) proteins can directly regulate factors involved in cell cycle control and affect cellular proliferation. Furthermore, nontransforming Notch(ic) proteins do not induce cyclin D1 expression, indicating that the mechanism of transformation involves cell cycle deregulation through constitutive expression of cyclin D1. Finally, we have identified a CSL [stands for CBF1, Su(H), and Lag-1] binding site within the human and rat cyclin D1 promoters, suggesting that Notch(ic) proteins activate cyclin D1 transcription through a CSL-dependent pathway.

Indexed as

CDC2-CDC28 KinasesDrosophila ProteinsNuclear ProteinsTranscriptional ActivationCell CycleCell Line, TransformedChemokine CCL4Chemokines, CCCyclin D1Cyclin-Dependent Kinase 2Cyclin-Dependent KinasesDNA-Binding ProteinsEnzyme ActivationHumansImmunoglobulin J Recombination Signal Sequence-Binding ProteinMacrophage Inflammatory ProteinsafimoxifeneCCL4 protein, humanCDC2-CDC28 KinasesCDK2 protein, humanChemokine CCL4Chemokines, CCCyclin D1Cyclin-Dependent Kinase 2Cyclin-Dependent KinasesDNA-Binding ProteinsDrosophila ProteinsImmunoglobulin J Recombination Signal Sequence-Binding ProteinMacrophage Inflammatory ProteinsMembrane ProteinsNuclear ProteinsProteinsProtein Serine-Threonine KinasesRBPJ protein, humanReceptors, Cell SurfaceReceptors, EstrogenReceptors, NotchRecombinant Fusion ProteinsRepressor ProteinsRNA, MessengerSu(H) protein, DrosophilaTamoxifen

Identifiers

PMID11486031
PMCPMC87311
OpenAlexW2147135997

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.