Evidence map›Paper›PMID 24903482›Full record

ArticleLeukemia2015

Survivin modulates genes with divergent molecular functions and regulates proliferation of hematopoietic stem cells through Evi-1.

S Fukuda, J Hoggatt, P Singh, M Abe, J M Speth, P Hu, E M Conway, G Nucifora, S Yamaguchi, L M Pelus

Open access · bronzeAbstract read
In one paragraph

Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  16. Article
  17. Survivin: a unique target for tumor therapy.Cancer cell international · 2016
    Review
  18. Article
  19. Survivin - The inconvenient IAP.Seminars in cell & developmental biology · 2015
    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

10 authors at 5 institutions in 3 countries.

S FukudaDepartment of Pediatrics, Shimane University School of Medicine, Izumo, Japan.
J Hoggatt1] Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA [2] Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.
P SinghDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA.
M AbeDepartment of Pediatrics, Shimane University School of Medicine, Izumo, Japan.
J M SpethDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA.
P HuDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA.
E M ConwayCentre for Blood Research, University of British Columbia, Vancouver, British Columbia, Canada.
G NuciforaDepartment of Pathology, University of Chicago, Chicago, IL, USA.
S YamaguchiDepartment of Pediatrics, Shimane University School of Medicine, Izumo, Japan.
L M PelusDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA.
Indiana University – Purdue University Indianapolis · USShimane University · JPIndiana University School of MedicineUniversity of British Columbia · CAUniversity of Chicago · US

Funding

Role of PGE2 and other eicosanoids in hematopoietic stem cell functionR01HL096305 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI PELUS, LOUIS M · 2010 to 2018
$3.5M
Chemokine Induced Hematopoietic Stem Cell MobilizationR01HL069669 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI PELUS, LOUIS M · 2001 to 2009
$2.8M
Role of Survivin in Blood Stem Cell Cycle and ApoptosisR01HL079654 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI PELUS, LOUIS M · 2004 to 2007
$1.3M
NHLBI NIH HHS HL079654NHLBI NIH HHS HL096305NHLBI NIH HHS HL69669,NHLBI NIH HHS R01 HL069669NHLBI NIH HHS R01 HL079654NHLBI NIH HHS R01 HL096305
6 · The paper itself

Abstract

The inhibitor of apoptosis protein Survivin regulates hematopoiesis, although its mechanisms of regulation of hematopoietic stem cells (HSCs) remain largely unknown. While investigating conditional Survivin deletion in mice, we found that Survivin was highly expressed in phenotypically defined HSCs, and Survivin deletion in mice resulted in significantly reduced total marrow HSCs and hematopoietic progenitor cells. Transcriptional analysis of Survivin(-/-) HSCs revealed altered expression of multiple genes not previously linked to Survivin activity. In particular, Survivin deletion significantly reduced expression of the Evi-1 transcription factor indispensable for HSC function, and the downstream Evi-1 target genes Gata2, Pbx1 and Sall2. The loss of HSCs following Survivin deletion and impaired long-term HSC repopulating function could be partially rescued by ectopic Evi-1 expression in Survivin -/- HSCs. These data demonstrate that Survivin partially regulates HSC function by modulating the Evi-1 transcription factor and its downstream targets and identify new genetic pathways in HSCs regulated by Survivin.

Indexed as

Gene Expression Regulation, LeukemicAllelesAnimalsBone Marrow CellsCell CycleCell ProliferationDNA-Binding ProteinsFemaleGATA2 Transcription FactorGene DeletionHematopoiesisHematopoietic Stem CellsHomeodomain ProteinsHumansInhibitor of Apoptosis ProteinsIntracellular Signaling Peptides and ProteinsBirc5 protein, mouseDNA-Binding ProteinsGata2 protein, mouseGATA2 Transcription FactorHomeodomain ProteinsInhibitor of Apoptosis ProteinsIntracellular Signaling Peptides and ProteinsMDS1 and EVI1 Complex Locus ProteinMECOM protein, humanMecom protein, mousePbx1 protein, mousePre-B-Cell Leukemia Transcription Factor 1Repressor ProteinsSall2 protein, mouseSurvivinTranscription Factors

Identifiers

PMID24903482
PMCPMC4258188
OpenAlexW1996346417

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.