Evidence map›Paper›PMID 19179303›Full record

ArticleBlood2009

Novel roles for erythroid Ankyrin-1 revealed through an ENU-induced null mouse mutant.

Gerhard Rank, Rosemary Sutton, Vikki Marshall, Rachel J Lundie, Jacinta Caddy, Tony Romeo, Kate Fernandez, Matthew P McCormack, Brian M Cooke, Simon J Foote and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 48 citations in OpenAlex.

  1. Host-pathogen interactions involved in erythrocyte invasion byFrontiers in cellular and infection microbiology · 2025
    Article
  2. Article
  3. Article
  4. Forward Genetics in Apicomplexa Biology: The Host Side of the Story.Frontiers in cellular and infection microbiology · 2022
    Review
  5. Characterization ofBlood advances · 2018
    Article
  6. Host genetics in malaria: lessons from mouse studies.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Characterization of ENU-induced Mutations in Red Blood Cell Structural Proteins.Computational and structural biotechnology journal · 2013
    Article
  20. 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

15 authors at 4 institutions in 1 country.

Gerhard RankRotary Bone Marrow Research Laboratory, Melbourne Health Research Directorate, Parkville, Australia.
Rosemary Sutton
Vikki Marshall
Rachel J Lundie
Jacinta Caddy
Tony Romeo
Kate Fernandez
Matthew P McCormack
Brian M Cooke
Simon J Foote
Brendan S Crabb
David J Curtis
Douglas J Hilton
Benjamin T Kile
Stephen M Jane
Melbourne Health · AUWalter and Eliza Hall Institute of Medical Research · AUMonash University · AUUniversity of Sydney · AU

Funding

VIROSOME/PROTEOLIPOSOME MEDIATED GENE TRANSFERP01HL053749 · NHLBI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI WEISS, MITCHELL J · 1994 to 2022
$43.6M
NHLBI NIH HHS P01 HL053749NHLBI NIH HHS P01 HL53749-03
6 · The paper itself

Abstract

Insights into the role of ankyrin-1 (ANK-1) in the formation and stabilization of the red cell cytoskeleton have come from studies on the nb/nb mice, which carry hypomorphic alleles of Ank-1. Here, we revise several paradigms established in the nb/nb mice through analysis of an N-ethyl-N-nitrosourea (ENU)-induced Ank-1-null mouse. Mice homozygous for the Ank-1 mutation are profoundly anemic in utero and most die perinatally, indicating that Ank-1 plays a nonredundant role in erythroid development. The surviving pups exhibit features of severe hereditary spherocytosis (HS), with marked hemolysis, jaundice, compensatory extramedullary erythropoiesis, and tissue iron overload. Red cell membrane analysis reveals a complete loss of ANK-1 protein and a marked reduction in beta-spectrin. As a consequence, the red cells exhibit total disruption of cytoskeletal architecture and severely altered hemorheologic properties. Heterozygous mutant mice, which have wild-type levels of ANK-1 and spectrin in their RBC membranes and normal red cell survival and ultrastructure, exhibit profound resistance to malaria, which is not due to impaired parasite entry into RBC. These findings provide novel insights into the role of Ank-1, and define an ideal model for the study of HS and malarial resistance.

Indexed as

EthylnitrosoureaAnimalsAnimals, NewbornAnkyrinsBase SequenceCarcinogensCytoskeletonDNA Mutational AnalysisErythrocytesErythrocytes, AbnormalErythroid CellsErythropoiesisHematologic NeoplasmsHemolysisMalariaMiceAnk1 protein, mouseAnkyrinsCarcinogensEthylnitrosourea

Identifiers

PMID19179303
PMCPMC2665900
OpenAlexW2014702882

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.