Evidence map›Paper›PMID 23814485›Full record

ArticleNeoplasia (New York, N.Y.)2013

A new p53 target gene, RKIP, is essential for DNA damage-induced cellular senescence and suppression of ERK activation.

Su-Jin Lee, Sun-Hye Lee, Min-Ho Yoon, Bum-Joon Park

Abstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2013. 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
–field-weighted citation impact
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.

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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

4 authors.

Su-Jin LeeDepartment of Molecular Biology, College of Natural Science, Pusan National University, Pusan, Republic of Korea.
Sun-Hye Lee
Min-Ho Yoon
Bum-Joon Park

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p53, a strong tumor suppressor protein, is known to be involved in cellular senescence, particularly premature cellular senescence. Oncogenic stresses, such as Ras activation, can initiate p53-mediated senescence, whereas activation of the Ras-mitogen-activated protein kinase (MAPK) pathway can promote cell proliferation. These conflicting facts imply that there is a regulatory mechanism for balancing p53 and Ras-MAPK signaling. To address this, we evaluated the effects of p53 on the extracellular signal-regulated kinase (ERK) activation and found that p53 could suppress ERK activation through de novo synthesis. Through several molecular biologic analyses, we found that RKIP, an inhibitor of Raf kinase, is responsible for p53-mediated ERK suppression and senescence. Overexpression of RKIP can induce cellular senescence in several types of cell lines, including p53-deficient cells, whereas the elimination of RKIP by siRNA or forced expression of ERK blocks p53-mediated cellular senescence. These results suggested that RKIP is an essential protein for cellular senescence. Moreover, modification of the p53 serine 46 residue was critical for RKIP induction and ERK suppression as well as cellular senescence. These results indicated that RKIP is a novel p53 target gene that is responsible for p53-mediated cellular senescence and tumor suppressor protein expression.

Indexed as

DNA DamageAntineoplastic AgentsCell Line, TumorCellular SenescenceDoxorubicinEnzyme ActivationEtoposideExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, NeoplasticHumansNeoplasmsPhosphatidylethanolamine Binding ProteinPhosphorylationSignal TransductionTopoisomerase II InhibitorsTumor Suppressor Protein p53Antineoplastic AgentsDoxorubicinEtoposideExtracellular Signal-Regulated MAP KinasesPEBP1 protein, humanPhosphatidylethanolamine Binding ProteinTopoisomerase II InhibitorsTumor Suppressor Protein p53

Identifiers

PMID23814485
PMCPMC3689236

What OpenQuestion holds

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Registered trials

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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.