Evidence map›Paper›PMID 26830229›Full record

ArticleMolecular and cellular biology2016

Arrested Hematopoiesis and Vascular Relaxation Defects in Mice with a Mutation in Dhfr.

Julie A I Thoms, Kathy Knezevic, Jia Jenny Liu, Elias N Glaros, Thuan Thai, Qiao Qiao, Heather Campbell, Deborah Packham, Yizhou Huang, Peter Papathanasiou and 11 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

21 authors at 4 institutions in 1 country.

Julie A I ThomsAdult Cancer Program, Prince of Wales Clinical School, Lowy Cancer Research Centre, University of New South Wales, Sydney, NSW, Australia.
Kathy KnezevicAdult Cancer Program, Prince of Wales Clinical School, Lowy Cancer Research Centre, University of New South Wales, Sydney, NSW, Australia.
Jia Jenny LiuAdult Cancer Program, Prince of Wales Clinical School, Lowy Cancer Research Centre, University of New South Wales, Sydney, NSW, Australia.
Elias N GlarosSchool of Medical Sciences, University of New South Wales, Sydney, NSW, Australia.
Thuan ThaiSchool of Medical Sciences, University of New South Wales, Sydney, NSW, Australia.
Qiao QiaoAdult Cancer Program, Prince of Wales Clinical School, Lowy Cancer Research Centre, University of New South Wales, Sydney, NSW, Australia.
Heather CampbellAdult Cancer Program, Prince of Wales Clinical School, Lowy Cancer Research Centre, University of New South Wales, Sydney, NSW, Australia.
Deborah PackhamAdult Cancer Program, Prince of Wales Clinical School, Lowy Cancer Research Centre, University of New South Wales, Sydney, NSW, Australia.
Yizhou HuangAdult Cancer Program, Prince of Wales Clinical School, Lowy Cancer Research Centre, University of New South Wales, Sydney, NSW, Australia.
Peter PapathanasiouAustralian Phenomics Facility, John Curtin School of Medical Research, Australian National University, Acton, ACT, Australia.
Robert TunningleyAustralian Phenomics Facility, John Curtin School of Medical Research, Australian National University, Acton, ACT, Australia.
Belinda WhittleAustralian Phenomics Facility, John Curtin School of Medical Research, Australian National University, Acton, ACT, Australia.
Amanda W S YeungSchool of Medical Sciences, University of New South Wales, Sydney, NSW, Australia.
Vashe ChandrakanthanAdult Cancer Program, Prince of Wales Clinical School, Lowy Cancer Research Centre, University of New South Wales, Sydney, NSW, Australia.
Luke HessonAdult Cancer Program, Prince of Wales Clinical School, Lowy Cancer Research Centre, University of New South Wales, Sydney, NSW, Australia.
Vivien ChenAdult Cancer Program, Prince of Wales Clinical School, Lowy Cancer Research Centre, University of New South Wales, Sydney, NSW, Australia Haematology, Concord Repatriation and General Hospital, Concord, NSW, Australia.
Jason W H WongAdult Cancer Program, Prince of Wales Clinical School, Lowy Cancer Research Centre, University of New South Wales, Sydney, NSW, Australia.
Louise E PurtonStem Cell Regulation Unit, St. Vincent's Institute of Medical Research and Department of Medicine at St. Vincent's Hospital, The University of Melbourne, Fitzroy, Victoria, Australia.
Robyn L WardAdult Cancer Program, Prince of Wales Clinical School, Lowy Cancer Research Centre, University of New South Wales, Sydney, NSW, Australia.
Shane R ThomasSchool of Medical Sciences, University of New South Wales, Sydney, NSW, Australia shane.thomas@unsw.edu.au pimanda@unsw.edu.au.
John E PimandaAdult Cancer Program, Prince of Wales Clinical School, Lowy Cancer Research Centre, University of New South Wales, Sydney, NSW, Australia Department of Haematology, Prince of Wales Hospital, Sydney, NSW, Australia shane.thomas@unsw.edu.au pimanda@unsw.edu.au.
UNSW Sydney · AUAustralian National University · AUPrince of Wales Hospital · AUSt Vincents Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dihydrofolate reductase (DHFR) is a critical enzyme in the folate metabolism pathway and also plays a role in regulating nitric oxide (NO) signaling in endothelial cells. Although both coding and noncoding mutations with phenotypic effects have been identified in the human DHFR gene, no mouse model is currently available to study the consequences of perturbing DHFR in vivo In order to identify genes involved in definitive hematopoiesis, we performed a forward genetic screen and produced a mouse line, here referred to as Orana, with a point mutation in the Dhfr locus leading to a Thr136Ala substitution in the DHFR protein. Homozygote Orana mice initiate definitive hematopoiesis, but expansion of progenitors in the fetal liver is compromised, and the animals die between embryonic day 13.5 (E13.5) and E14.5. Heterozygote Orana mice survive to adulthood but have tissue-specific alterations in folate abundance and distribution, perturbed stress erythropoiesis, and impaired endothelium-dependent relaxation of the aorta consistent with the role of DHFR in regulating NO signaling. Orana mice provide insight into the dual roles of DHFR and are a useful model for investigating the role of environmental and dietary factors in the context of vascular defects caused by altered NO signaling.

Indexed as

Amino Acid SubstitutionHematopoiesisAmino Acid SequenceAnimalsAortaBase SequenceCell LineFolic AcidHomozygoteHumansLiverMiceMice, Inbred C57BLModels, MolecularNitric OxideTetrahydrofolate DehydrogenaseFolic AcidNitric OxideTetrahydrofolate Dehydrogenase

Identifiers

PMID26830229
PMCPMC4836279
OpenAlexW2260544907

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.