Evidence map›Paper›PMID 23348590›Full record

ArticleCell death & disease2013

Cooperative role of RanBP9 and P73 in mitochondria-mediated apoptosis.

T Liu, S E Roh, J A Woo, H Ryu, D E Kang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

46 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
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  6. The p53 reactivator PRIMA-1Investigational new drugs · 2023
    Article
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  9. Structural and Functional Insights into GID/CTLH E3 Ligase Complexes.International journal of molecular sciences · 2022
    Review
  10. Article
  11. Review
  12. EGCG Promotes Neurite Outgrowth through the IntegrinEvidence-based complementary and alternative medicine : eCAM · 2021
    Article
  13. Article
  14. Article
  15. Review
  16. RANBP9 as potential therapeutic target in non-small cell lung cancer.Journal of cancer metastasis and treatment · 2020
    Article
  17. The plant pathology journal · 2019
    Article
  18. Article
  19. Article
  20. 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

5 authors at 1 institution in 2 countries.

T LiuWCU-Neurocytomics Program, Seoul National University College of Medicine, Seoul, Korea.
S E Roh
J A Woo
H Ryu
D E Kang
Seoul National University · KR

Funding

Epigenetic Regulation of Heterochromatin Condensation in Huntington's DiseaseR01NS067283 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI RYU, HOON · 2011 to 2015
$1.2M
Novel Mechanisms of RanBP9 in APP PathogenesisR01AG033055 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI KANG, DAVID E · 2009 to 2012
$1.2M
LRP/RanBP9 Pathway in Alzheiimer's Disease PathogenesisK02AG031920 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI KANG, DAVID E · 2009 to 2011
$341k
NIA NIH HHS 1K02AG031920-10A1NIA NIH HHS 1R01AG033055-01A1NIA NIH HHS K02 AG031920NIA NIH HHS R01 AG033055NINDS NIH HHS R01 NS067283
6 · The paper itself

Abstract

Mitochondrial dysfunction and synaptic damage are critical early features of Alzheimer's disease (AD) associated with amyloid β (Aβ) and τ. We previously reported that the scaffolding protein RanBP9, which is overall increased in AD, simultaneously promotes Aβ generation and focal adhesion disruption by accelerating the endocytosis of APP and β1-integrin, respectively. Moreover, RanBP9 induces neurodegeneration in vitro and in vivo and mediates Aβ-induced neurotoxicity. However, little is known regarding the mechanisms underlying such neurotoxic processes. Here, we show that RanBP9 induces the loss of mitochondrial membrane potential and increase in mitochondrial superoxides associated with decrease in Bcl-2, increase in Bax protein and oligomerization, fragmentation of mitochondria, and cytochrome c release. RanBP9-induced neurotoxic changes are significantly prevented by the mitochondrial fission inhibitor Mdivi-1 and by classical inhibitors of the mitochondrial apoptosis, XIAP, Bcl-2, and Bcl-xl. RanBP9 physically interacts with the tumor suppressor p73 and increases endogenous p73α levels at both transcriptional and post-translational levels;moreover, the knockdown of endogenous p73 by siRNA effectively blocks RanBP9 and Aβ1-42-induced mitochondria-mediated cell death. Conversely, siRNA knockdown of endogenous RanBP9 also suppresses p73-induced apoptosis, suggesting that RanBP9 and p73 have cooperative roles in inducing cell death. Taken together, these finding implicate the RanBP9/p73 complex in mitochondria-mediated apoptosis in addition to its role in enhancing Aβ generation.

Indexed as

ApoptosisAdaptor Proteins, Signal TransducingAmyloid beta-PeptidesAnimalsbcl-2-Associated X Proteinbcl-X ProteinCaspasesCells, CulturedCyclin D1Cytochromes cCytoskeletal ProteinsDNA-Binding ProteinsHippocampusMembrane Potential, MitochondrialMiceMice, Transgenic3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinoneAdaptor Proteins, Signal TransducingAmyloid beta-Peptidesamyloid beta-protein (1-42)bcl-2-Associated X Proteinbcl-X ProteinCaspasesCyclin D1Cytochromes cCytoskeletal ProteinsDNA-Binding ProteinsNuclear ProteinsPeptide FragmentsQuinazolinonesRan binding protein 9RNA, Small InterferingSuperoxidesTrp73 protein, mouseTumor Protein p73Tumor Suppressor ProteinsX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID23348590
PMCPMC3563991
OpenAlexW2037386201

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.