Evidence map›Paper›PMID 30024025›Full record

ArticleThe Journal of physiology2018

Abnormal folate metabolism causes age-, sex- and parent-of-origin-specific haematological defects in mice.

Nisha Padmanabhan, Katerina Menelaou, Jiali Gao, Alexander Anderson, Georgina E T Blake, Tanya Li, B Nuala Daw, Erica D Watson

Open access · hybridAbstract read
In one paragraph

Article in The Journal of physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

7 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  7. Molecular genetics and metabolism reports · 2020
    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

8 authors at 1 institution in 1 country.

Nisha PadmanabhanDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.ORCID 0000-0003-1253-2162
Katerina MenelaouDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
Jiali GaoDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
Alexander AndersonDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
Georgina E T BlakeDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
Tanya LiDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
B Nuala DawDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
Erica D WatsonDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.ORCID 0000-0003-4496-2271
University of Cambridge · GB

Funding

Wellcome TrustWellcome Trust n/a
6 · The paper itself

Abstract

key pointsFolate (folic acid) deficiency and mutations in folate-related genes in humans result in megaloblastic anaemia. Folate metabolism, which requires the enzyme methionine synthase reductase (MTRR), is necessary for DNA synthesis and the transmission of one-carbon methyl groups for cellular methylation. In this study, we show that the hypomorphic Mtrr ABSTRACT: The importance of the vitamin folate (also known as folic acid) in erythrocyte formation, maturation and/or longevity is apparent since folate deficiency in humans causes megaloblastic anaemia. Megaloblastic anaemia is a type of macrocytic anaemia whereby erythrocytes are enlarged and fewer in number. Folate metabolism is required for thymidine synthesis and one-carbon metabolism, though its specific role in erythropoiesis is not well understood. Methionine synthase reductase (MTRR) is a key enzyme necessary for the progression of folate metabolism since knocking down the Mtrr gene in mice results in hyperhomocysteinaemia and global DNA hypomethylation. We demonstrate here that abnormal folate metabolism in mice caused by Mtrr

Indexed as

HematopoiesisAge FactorsAnemia, MegaloblasticAnimalsCells, CulturedFemaleFerredoxin-NADP ReductaseFolic AcidFolic Acid DeficiencyHomozygoteMaleMiceMice, Inbred C57BLSex FactorsFerredoxin-NADP ReductaseFolic Acidmethionine synthase reductaseextramedullary haematopoiesislate-onsetmacrocytic anemiamiceMTRRparental effectsexual dimorphism

Identifiers

PMID30024025
PMCPMC6138292
OpenAlexW2889461006

What OpenQuestion holds

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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.