Evidence map›Paper›PMID 40996619›Full record

ArticleTransgenic research2025

Generation of a Ym1 deficient mouse utilising CRISPR-Cas9 in CB6 embryos.

J E Parkinson, G E Baldwin, P H Papotto, N E Humphreys, A J Day, A D Adamson, J E Allen, T E Sutherland

Abstract read
In one paragraph

Article in Transgenic research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

J E ParkinsonLydia Becker Institute of Immunology and Inflammation, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, M139PT, UK. james.parkinson@manchester.ac.uk.
G E BaldwinLydia Becker Institute of Immunology and Inflammation, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, M139PT, UK.
P H PapottoLydia Becker Institute of Immunology and Inflammation, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, M139PT, UK.
N E HumphreysGenome Editing Unit, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, Manchester, M139PT, UK.
A J DayLydia Becker Institute of Immunology and Inflammation, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, M139PT, UK.
A D Adamson *Genome Editing Unit, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, Manchester, M139PT, UK.
J E Allen *Lydia Becker Institute of Immunology and Inflammation, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, M139PT, UK.
T E Sutherland *Lydia Becker Institute of Immunology and Inflammation, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, M139PT, UK.

Funding

Asthma and Lung UK MRFAUK-2015-302Medical Research Council MR/K01207X/2Medical Research Council MRY0036831Wellcome TrustWellcome Trust 097820/Z/11/BWellcome Trust 203128/Z/16/Z
6 · The paper itself

Abstract

Chitinase-like proteins (CLPs) are of wide interest due to their significant roles during both homeostatic and pathological processes. Human CLPs such as YKL-40 have been proposed as biomarkers of disease severity in many conditions. Murine CLPs Brp39, Ym1, and Ym2 are similarly upregulated in multiple mouse models of pathology. Investigation of Ym1 and Ym2 is hampered by recent gene duplication events on the C57BL/6, but not BALB/c, background leading to complexity in the genomic locus. Here, we have generated a Ym1 deficient mouse using a novel CRISPR-Cas9 targeting approach involving CB6 (C57BL/6 X BALB/c) mixed background embryos. Validation using flow cytometry, ELISA, and immunofluorescence confirmed no expression of mature Ym1 protein. Additionally, expression of related genes including Chia, Chil1, and Chil4 were not altered in Ym1-deficent animals. This new transgenic mouse line will be key for future investigations of CLP functions and the utilised approach to genetic manipulation may provide a useful strategy for other genes which show differences in copy number between inbred mouse strains.

Indexed as

Chitinase-3-Like Protein 1CRISPR-Cas SystemsAnimalsEmbryo, MammalianFemaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, TransgenicChil1 protein, mouseChitinase-3-Like Protein 1CLPsCRISPRGene duplicationMixed backgroundMouse model

Identifiers

PMID40996619
PMCPMC12464116

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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.