Evidence map›Paper›PMID 21553221›Full record

ArticleMammalian genome : official journal of the International Mammalian Genome Society2011

Generation of N-ethyl-N-nitrosourea-induced mouse mutants with deviations in hematological parameters.

Bernhard Aigner, Birgit Rathkolb, Martina Klempt, Sibylle Wagner, Dian Michel, Matthias Klaften, Jürgen Laufs, Boris Schneider, Reinhard Sedlmeier, Martin Hrabé de Angelis and 1 more

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In one paragraph

Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. New C3H KitScientific reports · 2022
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Viable EdnraMammalian genome : official journal of the International Mammalian Genome Society · 2016
    Article
  12. Article
  13. Article
  14. Review
  15. New mouse models for metabolic bone diseases generated by genome-wide ENU mutagenesis.Mammalian genome : official journal of the International Mammalian Genome Society · 2012
    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 3 institutions in 2 countries.

Bernhard AignerDepartment of Veterinary Sciences, Chair for Molecular Animal Breeding and Biotechnology, and Laboratory for Functional Genome Analysis (LAFUGA), Gene Center, LMU Munich, Moorversuchsgut, Hackerstr. 27, 85764, Oberschleiβheim, Munich, Germany. b.aigner@gen.vetmed.uni-muenchen.de
Birgit Rathkolb
Martina Klempt
Sibylle Wagner
Dian Michel
Matthias Klaften
Jürgen Laufs
Boris Schneider
Reinhard Sedlmeier
Martin Hrabé de Angelis
Eckhard Wolf
Helmholtz Zentrum München · DELudwig-Maximilians-Universität München · DEIngenium (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Research on hematological disorders relies on suitable animal models. We retrospectively evaluated the use of the hematological parameters hematocrit (HCT), hemoglobin (HGB), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), mean corpuscular volume (MCV), red blood cell count (RBC), white blood cell count (WBC), and platelet count (PLT) in the phenotype-driven Munich N-ethyl-N-nitrosourea (ENU) mouse mutagenesis project as parameters for the generation of novel animal models for human diseases. The analysis was carried out on more than 16,000 G1 and G3 offspring of chemically mutagenized inbred C3H mice to detect dominant and recessive mutations leading to deviations in the levels of the chosen parameters. Identification of animals exhibiting altered values and transmission of the phenotypic deviations to the subsequent generations led to the successful establishment of mutant lines for the parameters MCV, RBC, and PLT. Analysis of the causative mutation was started in selected lines, thereby revealing a novel mutation in the transferrin receptor gene (Tfrc) in one line. Thus, novel phenotype-driven mouse models were established to analyze the genetic components of hematological disorders.

Indexed as

Disease Models, AnimalMutagenesisMutationAnimalsBase SequenceEthylnitrosoureaFemaleGenetic LinkageGenotypeHematologic DiseasesHematologic TestsMaleMiceMice, Inbred C3HMice, Inbred C57BLMutagensEthylnitrosoureaMutagensReceptors, TransferrinTfrc protein, mouse

Identifiers

PMID21553221
OpenAlexW2033835099

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.