Evidence map›Paper›PMID 28617078›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2018

Interplay between Notch and p53 promotes neuronal cell death in ischemic stroke.

Priyanka Balaganapathy, Sang-Ha Baik, Karthik Mallilankaraman, Christopher G Sobey, Dong-Gyu Jo, Thiruma V Arumugam

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

40 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
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  3. Suppression of Nr1d1/Bnip3-dependent mitophagy by notch signaling aggravates inflammatory response in RSV-infected mice lungs.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  19. The regulatory role of Pin1 in neuronal death.Neural regeneration research · 2023
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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

6 authors at 3 institutions in 3 countries.

Priyanka Balaganapathy1 Department of Physiology, Yong Loo Lin School Medicine, National University of Singapore, Singapore, Singapore.
Sang-Ha Baik1 Department of Physiology, Yong Loo Lin School Medicine, National University of Singapore, Singapore, Singapore.
Karthik Mallilankaraman1 Department of Physiology, Yong Loo Lin School Medicine, National University of Singapore, Singapore, Singapore.
Christopher G Sobey3 Department of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora, Victoria, Australia.
Dong-Gyu Jo2 School of Pharmacy, Sungkyunkwan University, Suwon, Republic of Korea.
Thiruma V Arumugam1 Department of Physiology, Yong Loo Lin School Medicine, National University of Singapore, Singapore, Singapore.
National University of Singapore · SGLa Trobe University · AUSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stroke is the world's second leading cause of mortality, with a high incidence of morbidity. Numerous neuronal membrane receptors are activated by endogenous ligands and may contribute to infarct development. Notch is a well-characterized membrane receptor involved in cell differentiation and proliferation, and now shown to play a pivotal role in cell death during ischemic stroke. Blockade of Notch signaling by inhibition of γ-secretase, an enzyme that generates the active form of Notch, is neuroprotective following stroke. We have also identified that Pin1, a peptidyl-prolyl isomerase that regulates p53 transactivation under stress, promotes the pathogenesis of ischemic stroke via Notch signaling. Moreover, Notch can also mediate cell death through a p53-dependent pathway, resulting in apoptosis of neural progenitor cells. The current study has investigated the interplay between Notch and p53 under ischemic stroke conditions. Using pharmacological inhibitors, we have demonstrated that a Notch intracellular domain (NICD)/p53 interaction is involved in transcriptional regulation of genes downstream of p53 and NICD to modify stroke severity. Furthermore, the NICD/p53 interaction confers stability to p53 by rescuing it from ubiquitination. Together, these results indicate that Notch contributes to the pathogenesis of ischemic stroke by promoting p53 stability and signaling.

Indexed as

AnimalsApoptosisBrain IschemiaGene Expression RegulationHEK293 CellsHumansMiceNerve DegenerationNeuronsReceptors, NotchSignal TransductionStrokeTumor Suppressor Protein p53Receptors, NotchTumor Suppressor Protein p53Cell deathIschemic strokeNeuroprotectionNotchp53

Identifiers

PMID28617078
PMCPMC6168918
OpenAlexW2626821877

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.