Evidence map›Paper›PMID 19278624›Full record

ArticleBiochimie2009

Hydrogen peroxide-induced Akt phosphorylation regulates Bax activation.

Mahdieh Sadidi, Stephen I Lentz, Eva L Feldman

Open access · greenAbstract read
In one paragraph

Article in Biochimie, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Effects ofPharmaceuticals (Basel, Switzerland) · 2024
    Article
  5. AKT-dependent nuclear localization of EPRS1 activates PARP1 in breast cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Mangostanin, a Xanthone Derived fromPharmaceuticals (Basel, Switzerland) · 2022
    Article
  11. Article
  12. Hydrogen peroxide (HScientific reports · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

3 authors at 1 institution in 1 country.

Mahdieh SadidiDepartment of Neurology, University of Michigan, Ann Arbor, MI 48109-2200, USA.
Stephen I Lentz
Eva L Feldman
University of Michigan–Ann Arbor · US

Funding

PUBLIC HEALTH DEMONSTRATIONP60DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MYERS, MARTIN G · 1985 to 2012
$26.5M
Research BaseP30DK092926 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MARY ELLEN MICHELE HEISLER, ADESUWA B OLOMU · 2011 to 2026
$10.0M
Mitochondrial SOD as a Target for Diabetic NeuropathyU01DK076160 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FELDMAN, EVA LUCILLE · 2006 to 2010
$1.2M
GLUCOTOXICITY MEDIATES APOPTOSIS IN DIABETIC NEUROPATHYR01NS038849 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FELDMAN, EVA LUCILLE · 1998 to 2005
$854k
IGFS MEDIATE MOTILITY IN HUMAN NEUROBLASTOMA CELLSR01NS036778 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FELDMAN, EVA L · 1998 to 2002
$636k
NIDDK NIH HHS 5P60 DK20572NIDDK NIH HHS DK 076160NIDDK NIH HHS P30 DK092926NIDDK NIH HHS P60 DK020572NIDDK NIH HHS U01 DK076160NINDS NIH HHS NS36778NINDS NIH HHS NS38849NINDS NIH HHS R01 NS036778NINDS NIH HHS R01 NS038849
6 · The paper itself

Abstract

Reactive oxygen species such as hydrogen peroxide (H(2)O(2)) are involved in many cellular processes that positively and negatively regulate cell fate. H(2)O(2), acting as an intracellular messenger, activates phosphatidylinositol-3 kinase (PI3K) and its downstream target Akt, and promotes cell survival. The aim of the current study was to understand the mechanism by which PI3K/Akt signaling promotes survival in SH-SY5Y neuroblastoma cells. We demonstrate that PI3K/Akt mediates phosphorylation of the pro-apoptotic Bcl-2 family member Bax. This phosphorylation suppresses apoptosis and promotes cell survival. Increased survival in the presence of H(2)O(2) was blocked by LY294002, an inhibitor of PI3K activation. LY294002 prevented Bax phosphorylation and resulted in Bax translocation to the mitochondria, cytochrome c release, caspase-3 activation, and cell death. Collectively, these findings reveal a mechanism by which H(2)O(2)-induced activation of PI3K/Akt influences post-translational modification of Bax and inactivates a key component of the cell death machinery.

Indexed as

bcl-2-Associated X ProteinBlotting, WesternCell DeathCell Line, TumorChromonesFlow CytometryGene Expression Regulation, NeoplasticHumansHydrogen PeroxideImmunohistochemistryImmunoprecipitationMitochondriaMorpholinesPhosphoinositide-3 Kinase InhibitorsPhosphorylationProto-Oncogene Proteins c-akt2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-onebcl-2-Associated X ProteinChromonesHydrogen PeroxideMorpholinesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-akt

Identifiers

PMID19278624
PMCPMC2697849
OpenAlexW2026674344

What OpenQuestion holds

Textmetadata
LicenceTDM
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.