Evidence map›Paper›PMID 15601862›Full record

ArticleMolecular and cellular biology2005

Growth inhibition by the tumor suppressor p33ING1 in immortalized and primary cells: involvement of two silencing domains and effect of Ras.

Frauke Goeman, Dorit Thormeyer, Maria Abad, Manuel Serrano, Oliver Schmidt, Ignacio Palmero, Aria Baniahmad

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Review
  3. Altered endocytosis in cellular senescence.Ageing research reviews · 2021
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  8. Adenovirus-mediated expression of p33(ING1b) induces apoptosis and inhibits proliferation in gastric adenocarcinoma cells in vitro.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2012
    Article
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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

7 authors at 2 institutions in 2 countries.

Frauke GoemanGenetic Institute, Justus-Liebig-University, Heinrich-Buff-Ring 58-62, 35392 Giessen, Germany.
Dorit Thormeyer
Maria Abad
Manuel Serrano
Oliver Schmidt
Ignacio Palmero
Aria Baniahmad
University of Giessen · DECentro Nacional de Epidemiología · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ING1 was identified as an inhibitor of growth and has been described as a tumor suppressor. Furthermore, the expression of ING1 is induced in senescent cells and antisense ING1 extends the proliferative life span of primary human fibroblasts. Cooperation of p33ING1 with p53 has been suggested to be an important function of ING1 in cell cycle control. Intriguingly, it has been shown that p33ING1 is associated with histone acetylation as well as with histone deacetylation function. Here we show that p33ING1 is a potent transcriptional silencer in various cell types. However, the silencing function is independent of the presence of p53. By use of deletion mutants two potent autonomous and transferable silencing domains were identified, but no evidence of an activation domain was found. The amino (N)-terminal silencing domain is sensitive to the histone deacetylase inhibitor trichostatin A (TSA) whereas the carboxy-terminal silencing function is resistant to TSA, suggesting that p33ING1 confers gene silencing through both HDAC-dependent and -independent mechanisms. Interestingly, the presence of oncogenic Ras, which is able to induce premature senescence, increases the p33ING1-mediated silencing function. Moreover, ING1-mediated silencing was reduced by coexpressing dominant-negative Ras or by treatment with the mitogen-activated protein kinase inhibitor PD98059 but not by treatment with SB203580, an inhibitor of the p38 pathway. In addition, we show that both silencing domains of ING1 are involved in cell cycle control, as measured by inhibition of colony formation of immortalized cells and by thymidine incorporation of primary human diploid fibroblasts (HDF). Interestingly, p33ING1 expression induces features of cellular senescence in HDFs.

Indexed as

Gene SilencingAnimalsCell CycleCell Cycle ProteinsCell LineChickensDNA-Binding ProteinsEnzyme InhibitorsFibroblastsFlavonoidsGene DeletionGenes, Tumor SuppressorHumansHydroxamic AcidsImidazolesInhibitor of Growth Protein 12-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneCell Cycle ProteinsDNA-Binding ProteinsEnzyme InhibitorsFlavonoidsHydroxamic AcidsImidazolesING1 protein, humanIng1 protein, mouseInhibitor of Growth Protein 1Intracellular Signaling Peptides and ProteinsNuclear ProteinsProteinsPyridinesras ProteinsSB 203580Thymidinetrichostatin ATumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID15601862
PMCPMC538761
OpenAlexW2071792548

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.