Evidence map›Paper›PMID 21454573›Full record

ArticleThe Journal of biological chemistry2011

Developmental control of apoptosis by the immunophilin aryl hydrocarbon receptor-interacting protein (AIP) involves mitochondrial import of the survivin protein.

Byoung Heon Kang, Fang Xia, Ramona Pop, Takehiko Dohi, Merav Socolovsky, Dario C Altieri

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Toxics · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Byoung Heon KangProstate Cancer Discovery and Development Program, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.
Fang Xia
Ramona Pop
Takehiko Dohi
Merav Socolovsky
Dario C Altieri
Prostate Cancer Foundation · USUniversity of Massachusetts Chan Medical School · USThe Wistar Institute · US

Funding

Role of Runx2 in prostate tumorigenesis and metastasisP01CA140043 · NCI · WISTAR INSTITUTE · PI ALTIERI, DARIO C · 2010 to 2021
$12.2M
CONTROL OF APOPTOSIS IN CANCER BY SURVIVINR01CA078810 · NCI · YALE UNIVERSITY · PI ALTIERI, DARIO C · 1998 to 2017
$5.5M
Molecular Pathology of Vascular InjuryR37HL054131 · NHLBI · WISTAR INSTITUTE · PI ALTIERI, DARIO C · 2004 to 2013
$3.1M
Molecular Analysis of the Erythropoietic Stress Response in vivoR01HL084168 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SOCOLOVSKY, MERAV · 2006 to 2010
$2.1M
Rational Design and Clinical Development of Shepherdin: A Novel Anti-Cancer AgentR01CA118005 · NCI · WISTAR INSTITUTE · PI ALTIERI, DARIO C · 2009 to 2013
$1.7M
MOLECULAR PATHOLOGY OF VASCULAR INJURYR01HL054131 · NHLBI · YALE UNIVERSITY · PI ALTIERI, DARIO C. · 1994 to 2003
$1.0M
NCI NIH HHS CA118005NCI NIH HHS CA140043NCI NIH HHS CA78810NCI NIH HHS P01 CA140043NCI NIH HHS R01 CA078810NCI NIH HHS R01 CA118005NHLBI NIH HHS HL084168NHLBI NIH HHS HL54131NHLBI NIH HHS R01 HL054131NHLBI NIH HHS R01 HL084168NHLBI NIH HHS R37 HL054131
6 · The paper itself

Abstract

Survivin is a multifunctional protein with essential roles in cell division and inhibition of apoptosis, but the molecular underpinnings of its cytoprotective properties are poorly understood. Here we show that homozygous deletion of the aryl hydrocarbon receptor-interacting protein (AIP), a survivin-associated immunophilin, causes embryonic lethality in mice by embryonic day 13.5-14, increased apoptosis of Ter119(-)/CD71(-) early erythropoietic progenitors, and loss of survivin expression in its cytosolic and mitochondrial compartments in vivo. In import assays using recombinant proteins, AIP directly mediated the import of survivin to mitochondria, thus enabling its anti-apoptotic function, whereas a survivin 1-141 mutant that does not bind AIP was not imported to mitochondria and failed to inhibit apoptosis. AIP-directed mitochondrial import of survivin did not affect cell division, was independent of the organelle transmembrane potential, did not require the chaperone Heat Shock Protein 90 (Hsp90), and was inhibited by cytosolic factor(s) present in normal cells. shRNA knockdown of the mitochondrial import receptor Tom20 abolished mitochondrial import of survivin and sensitized tumor cells to apoptosis, whereas silencing of Tom70 had no effect. Therefore, an AIP-Tom20 recognition contributes to cell survival in development and cancer by mediating the mitochondrial import of survivin.

Indexed as

ApoptosisAnimalsBiological TransportCytosolGene Expression Regulation, DevelopmentalGene SilencingHeLa CellsHomozygoteHSP90 Heat-Shock ProteinsHumansInhibitor of Apoptosis ProteinsIntracellular Signaling Peptides and ProteinsMiceMice, KnockoutMitochondriaMitochondrial Membrane Transport Proteinsaryl hydrocarbon receptor-interacting proteinBIRC5 protein, humanBirc5 protein, mouseHSP90 Heat-Shock ProteinsInhibitor of Apoptosis ProteinsIntracellular Signaling Peptides and ProteinsMitochondrial Membrane Transport ProteinsMitochondrial Precursor Protein Import Complex ProteinsRepressor ProteinsSurvivinTom70 protein, mouseTOMM70 protein, human

Identifiers

PMID21454573
PMCPMC3089518
OpenAlexW2057654390

What OpenQuestion holds

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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.