Evidence map›Paper›PMID 10698498›Full record

ArticleOncogene2000

v-Abl utilizes multiple mechanisms to drive G1/S progression in fibroblasts.

M Coutts, X Zou, K Calame

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

3 authors at 1 institution in 1 country.

M CouttsDepartment of Microbiology, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.
X Zou
K Calame
Columbia University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transformation of 3T3 fibroblasts by the v-Abl tyrosine kinase replaces mitogenic and adhesion signals normally required for cell cycle progression. A 3T3 cell line conditionally transformed with v-Abl has been used to study v-Abl's effects on cell cycle in the context of either serum depletion or absence of adhesion signals. We show that E2F-dependent mRNAs, encoding proteins required for cell cycle progression, are induced by v-Abl. In addition, we identify two previously unknown targets of v-Abl signaling: (1) cyclin D1 and D2 mRNAs are induced upon v-Abl activation; and (2) the CDK inhibitor p27 is decreased upon v-Abl activation.

Indexed as

Carrier ProteinsCell Cycle ProteinsDNA-Binding ProteinsGene Expression Regulation, NeoplasticSignal TransductionTumor Suppressor Proteins3T3 CellsAnimalsCell Transformation, NeoplasticCulture Media, Serum-FreeCyclin ACyclin D1Cyclin D2Cyclin D3Cyclin-Dependent Kinase Inhibitor p27Cyclin EArid4a protein, mouseCarrier ProteinsCcnd2 protein, mouseCcnd3 protein, mouseCdkn1b protein, mouseCell Cycle ProteinsCulture Media, Serum-FreeCyclin ACyclin D1Cyclin D2Cyclin D3Cyclin-Dependent Kinase Inhibitor p27Cyclin ECyclinsDNA-Binding ProteinsE2F Transcription FactorsMicrotubule-Associated ProteinsOncogene Proteins v-ablRecombinant Fusion ProteinsRetinoblastoma-Binding Protein 1Ribonucleotide ReductasesRNA, MessengerTetrahydrofolate DehydrogenaseTranscription Factor DP1Transcription FactorsTumor Suppressor Proteins

Identifiers

PMID10698498
OpenAlexW2329179743

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.