Evidence map›Paper›PMID 18349318›Full record

ArticleBlood2008

EPO receptor circuits for primary erythroblast survival.

Pradeep Sathyanarayana, Arvind Dev, Jing Fang, Estelle Houde, Olga Bogacheva, Oleg Bogachev, Madhu Menon, Sarah Browne, Anamika Pradeep, Christine Emerson and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing 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

42 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
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  7. Review
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  12. Development and differentiation of the erythroid lineage in mammals.Developmental and comparative immunology · 2016
    Review
  13. Article
  14. Article
  15. Article
  16. BH3-only protein Noxa contributes to apoptotic control of stress-erythropoiesis.Apoptosis : an international journal on programmed cell death · 2013
    Article
  17. Article
  18. Article
  19. Review
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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

11 authors at 2 institutions in 1 country.

Pradeep SathyanarayanaStem and Progenitor Cell Biology Program, Molecular Medicine Division, Maine Medical Center Research Institute, Scarborough, ME 04074, USA.
Arvind Dev
Jing Fang
Estelle Houde
Olga Bogacheva
Oleg Bogachev
Madhu Menon
Sarah Browne
Anamika Pradeep
Christine Emerson
Don M Wojchowski
Maine Medical Center Research Institute · USMaine Medical Center · US

Funding

Transcriptional Decisions in Endothelial Cell DifferentiationP20RR015555 · NCRR · MAINE MEDICAL CENTER · PI PRUDOVSKY, IGOR · 2000 to 2009
$21.4M
WNT SIGNALING IN PREIMPLANTATION EMBRYOP20RR018789 · NCRR · MAINE MEDICAL CENTER · PI WANG, ZACK Z. · 2003 to 2011
$18.9M
IN VITRO STUDIES OF ERYTHROPOIETIN ACTIONR01HL044491 · NHLBI · UNIVERSITY OF NEW HAMPSHIRE · PI WOJCHOWSKI, DON MICHAEL · 1991 to 2020
$4.8M
NCRR NIH HHS P20 RR015555NCRR NIH HHS P20-RR015555NCRR NIH HHS P20 RR018789NCRR NIH HHS P20-RR018789NHLBI NIH HHS R01 HL044491NHLBI NIH HHS R01-HL44491
6 · The paper itself

Abstract

EPO functions primarily as an erythroblast survival factor, and its antiapoptotic actions have been proposed to involve predominantly PI3-kinase and BCL-X pathways. Presently, the nature of EPO-regulated survival genes has been investigated through transcriptome analyses of highly responsive, primary bone marrow erythroblasts. Two proapoptotic factors, Bim and FoxO3a, were rapidly repressed not only via the wild-type EPOR, but also by PY-deficient knocked-in EPOR alleles. In parallel, Pim1 and Pim3 kinases and Irs2 were induced. For this survival gene set, induction failed via a PY-null EPOR-HM allele, but was restored upon reconstitution of a PY343 STAT5-binding site within a related EPOR-H allele. Notably, EPOR-HM supports erythropoiesis at steady state but not during anemia, while EPOR-H exhibits near wild-type EPOR activities. EPOR-H and the wild-type EPOR (but not EPOR-HM) also markedly stimulated the expression of Trb3 pseudokinase, and intracellular serpin, Serpina-3G. For SERPINA-3G and TRB3, ectopic expression in EPO-dependent progenitors furthermore significantly inhibited apoptosis due to cytokine withdrawal. BCL-XL and BCL2 also were studied, but in highly responsive Kit(pos)CD71(high)Ter119(neg) erythroblasts, neither was EPO modulated. EPOR survival circuits therefore include the repression of Bim plus FoxO3a, and EPOR/PY343/STAT5-dependent stimulation of Pim1, Pim3, Irs2 plus Serpina-3G, and Trb3 as new antiapoptotic effectors.

Indexed as

AnimalsApoptosisCell SurvivalErythroblastsFlow CytometryGene ExpressionGene Expression ProfilingGene Expression RegulationMiceReceptors, ErythropoietinReverse Transcriptase Polymerase Chain ReactionReceptors, Erythropoietin

Identifiers

PMID18349318
PMCPMC2396729
OpenAlexW2030219313

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.