Evidence map›Paper›PMID 25188417›Full record

ArticlePloS one2014

LIN28A expression reduces sickling of cultured human erythrocytes.

Jaira F de Vasconcellos, Ross M Fasano, Y Terry Lee, Megha Kaushal, Colleen Byrnes, Emily R Meier, Molly Anderson, Antoinette Rabel, Raul Braylan, David F Stroncek and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Physiological and Aberrant γ-Globin Transcription During Development.Frontiers in cell and developmental biology · 2021
    Review
  5. Article
  6. Article
  7. The RNA-binding protein LIN28 controls progenitor and neuronal cell fate during postnatal neurogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
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 4 institutions in 1 country.

Jaira F de VasconcellosMolecular Genomics and Therapeutics Section, Molecular Medicine Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Ross M FasanoCenter for Cancer and Blood Disorders, Children's National Medical Center, Washington, District of Columbia, United States of America.
Y Terry LeeMolecular Genomics and Therapeutics Section, Molecular Medicine Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Megha KaushalMolecular Genomics and Therapeutics Section, Molecular Medicine Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America; Center for Cancer and Blood Disorders, Children's National Medical Center, Washington, District of Columbia, United States of America.
Colleen ByrnesMolecular Genomics and Therapeutics Section, Molecular Medicine Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Emily R MeierMolecular Genomics and Therapeutics Section, Molecular Medicine Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America; Center for Cancer and Blood Disorders, Children's National Medical Center, Washington, District of Columbia, United States of America.
Molly AndersonMolecular Genomics and Therapeutics Section, Molecular Medicine Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Antoinette RabelMolecular Genomics and Therapeutics Section, Molecular Medicine Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Raul BraylanDepartment of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland, United States of America.
David F StroncekCell Processing Section, Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland, United States of America.
Jeffery L MillerMolecular Genomics and Therapeutics Section, Molecular Medicine Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
National Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · USNational Institutes of Health Clinical Center · USChildren's National · US

Funding

Regulation of Fetal Hemoglobin Production in Humans.ZIADK025101 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI MILLER, JEFFERY · 2009 to 2016
$3.4M
Rationale for the Pediatric Hematology and Transfusion Medicine Multidisciplinary Research Training Award (PHTMMRT) at Children?s NationalT32HL110841 · NHLBI · CHILDREN'S RESEARCH INSTITUTE · PI Catherine M. Bollard, NAOMI L LUBAN · 2012 to 2026
$2.0M
Develop novel assays for assessing cellular and gene therapiesZIACL002119 · CLC · CLINICAL CENTER · PI STRONCEK, DAVID · 2010 to 2025
$0k
Development of novel cell and gene therapiesZIACL002120 · CLC · CLINICAL CENTER · PI STRONCEK, DAVID · 2009 to 2025
$0k
Collaboration with Investigators from the Multiple Myeloma Section, Medical Oncology Branch, NCI and of the Molecular Medicine Branch, Molecular Genomics & Therapeutics Section, NIDDKZIACL060089 · CLC · CLINICAL CENTER · PI BRAYLAN, RAUL · 2014 to 2015
$0k
Intramural NIH HHSNHLBI NIH HHS T32 HL110841
6 · The paper itself

Abstract

Induction of fetal hemoglobin (HbF) has therapeutic importance for patients with sickle cell disease (SCD) and the beta-thalassemias. It was recently reported that increased expression of LIN28 proteins or decreased expression of its target let-7 miRNAs enhances HbF levels in cultured primary human erythroblasts from adult healthy donors. Here LIN28A effects were studied further using erythrocytes cultured from peripheral blood progenitor cells of pediatric subjects with SCD. Transgenic expression of LIN28A was accomplished by lentiviral transduction in CD34(+) sickle cells cultivated ex vivo in serum-free medium. LIN28A over-expression (LIN28A-OE) increased HbF, reduced beta (sickle)-globin, and strongly suppressed all members of the let-7 family of miRNAs. LIN28A-OE did not affect erythroblast differentiation or prevent enucleation, but it significantly reduced or ameliorated the sickling morphologies of the enucleated erythrocytes.

Indexed as

AdolescentAnemia, Sickle Cellbeta-GlobinsCell DifferentiationCell ShapeChildErythroblastsErythrocytes, AbnormalErythrocyte TransfusionFetal HemoglobinGene Expression RegulationGenetic VectorsHumansLentivirusMaleMicroRNAsbeta-GlobinsFetal HemoglobinLIN28B protein, humanMicroRNAsmirnlet7 microRNA, humanRNA-Binding Proteins

Identifiers

PMID25188417
PMCPMC4154803
OpenAlexW2031042502

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.