Evidence map›Paper›PMID 31635420›Full record

ReviewInternational journal of molecular sciences2019

Mathematical Modeling of p53 Pathways.

Eunjung Kim, Jae-Young Kim, Joo-Yong Lee

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Systematic comparison of temporal hepatotoxicant-induced gene network responses across 3 liver test systems.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Mathematical Models of Death Signaling Networks.Entropy (Basel, Switzerland) · 2022
    Review
  7. Article
  8. Review
  9. p53: A Key Protein That Regulates Pulmonary Fibrosis.Oxidative medicine and cellular longevity · 2020
    Review
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.

Eunjung KimGraduate School of Analytical Science and Technology (GRAST), Chungnam National University, Daejeon 34134, Korea. eunjung.kim@cnu.ac.kr.
Jae-Young KimGraduate School of Analytical Science and Technology (GRAST), Chungnam National University, Daejeon 34134, Korea. jaeyoung@cnu.ac.kr.
Joo-Yong LeeGraduate School of Analytical Science and Technology (GRAST), Chungnam National University, Daejeon 34134, Korea. leejooyong@cnu.ac.kr.ORCID 0000-0003-1049-6006

Funding

Chungnam National University .Korea Basic Science Institute T39643National Research Foundation of Korea NRF-2016M3A9E1918329, NRF-2019R1A2C1005334, NRF-2019H1D3A2A02057475
6 · The paper itself

Abstract

Cells have evolved balanced systems that ensure an appropriate response to stress. The systems elicit repair responses in temporary or moderate stress but eliminate irreparable cells via apoptosis in detrimental conditions of prolonged or severe stress. The tumor suppressor p53 is a central player in these stress response systems. When activated under DNA damage stress, p53 regulates hundreds of genes that are involved in DNA repair, cell cycle, and apoptosis. Recently, increasing studies have demonstrated additional regulatory roles of p53 in metabolism and mitochondrial physiology. Due to the inherent complexity of feedback loops between p53 and its target genes, the application of mathematical modeling has emerged as a novel approach to better understand the multifaceted functions and dynamics of p53. In this review, we discuss several mathematical modeling approaches in exploring the p53 pathways.

Indexed as

Models, BiologicalSignal TransductionAlgorithmsAnimalsApoptosisCarrier ProteinsCell CycleDNA DamageDNA RepairGene Expression RegulationHumansMitochondriaProtein BindingTumor Suppressor Protein p53Carrier ProteinsTumor Suppressor Protein p53DNA damage responsemathematical modelingmetabolismp53 dynamics

Identifiers

PMID31635420
PMCPMC6834204

What OpenQuestion holds

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LicenceCC BY
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.