Evidence map›Paper›PMID 26887046›Full record

ArticleOncotarget2016

Rapid generation of novel models of RAG1 deficiency by CRISPR/Cas9-induced mutagenesis in murine zygotes.

Lisa Ott de Bruin, Wei Yang, Kelly Capuder, Yu Nee Lee, Maddalena Antolini, Robin Meyers, Martin Gellert, Kiran Musunuru, John Manis, Luigi Notarangelo

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

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  11. HypomorphicBlood · 2018
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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

10 authors at 3 institutions in 2 countries.

Lisa Ott de BruinDivision of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Wei YangLaboratory of Molecular Biology, NIDDK, NIH, Bethesda, MD, USA.
Kelly CapuderDivision of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Yu Nee LeeDivision of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Maddalena AntoliniDivision of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Robin MeyersProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA, USA.
Martin GellertLaboratory of Molecular Biology, NIDDK, NIH, Bethesda, MD, USA.
Kiran MusunuruDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.
John ManisDivision of Transfusion Medicine, Department of Laboratory Medicine, Boston Children's hospital, Harvard Medical School, Boston, MA, USA.
Luigi NotarangeloDivision of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Boston Children's Hospital · USHarvard University · USUtrecht University · NL

Funding

MOLECULAR BASIS OF ALLERGIC AND IMMUNOLOGIC DISEASET32AI007512 · NIAID · CHILDREN'S HOSPITAL BOSTON · PI Janet Chou, Peter A Nigrovic · 1996 to 2026
$13.1M
Modeling and correcting human SCID using patient-derived iPS cellsR01AI100887 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI MANIS, JOHN P · 2012 to 2020
$4.5M
NIAID NIH HHS R01 AI100887NIAID NIH HHS T32 AI007512
6 · The paper itself

Abstract

Mutations in the Recombination Activating Gene 1 (RAG1) can cause a wide variety of clinical and immunological phenotypes in humans, ranging from absence of T and B lymphocytes to occurrence of autoimmune manifestations associated with expansion of oligoclonal T cells and production of autoantibodies. Although the mechanisms underlying this phenotypic heterogeneity remain poorly understood, some genotype-phenotype correlations can be made. Currently, mouse models of Rag deficiency are restricted to RAG1-/- mice and to knock-in models carrying severe missense mutations. The Clustered Regularly Interspaced Short Palindromic Repeat (CRISPR)/Cas9 system is a novel and powerful gene-editing strategy that permits targeted introduction of DNA double strand breaks with high efficiency through simultaneous delivery of the Cas9 endonuclease and a guide RNA (gRNA). Here, we report on CRISPR-based, single-step generation and characterization of mutant mouse models in which gene editing was attempted around residue 838 of RAG1, a region whose functional role had not been studied previously.

Indexed as

CRISPR-Cas SystemsAnimalsGene EditingHomeodomain ProteinsMiceMice, Mutant StrainsMutagenesis, Site-DirectedZygoteHomeodomain ProteinsRAG-1 proteinCRISPR/Cas9genome editingimmunodeficiencyRAG1recombination activation gene 1

Identifiers

PMID26887046
PMCPMC4914335
OpenAlexW2275704099

What OpenQuestion holds

Textmetadata
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.