Evidence map›Paper›PMID 34508276›Full record

ReviewSeminars in immunopathology2022

Functional interrogation of autoimmune disease genetics using CRISPR/Cas9 technologies and massively parallel reporter assays.

James Ding, Antonios Frantzeskos, Gisela Orozco

Open access · hybridAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
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

3 authors at 2 institutions in 1 country.

James DingCentre for Genetics and Genomics Versus Arthritis, Division of Musculoskeletal and Dermatological Sciences, School of Biological Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9LJ, UK. james.ding@manchester.ac.uk.ORCID 0000-0001-7273-9646
Antonios FrantzeskosCentre for Genetics and Genomics Versus Arthritis, Division of Musculoskeletal and Dermatological Sciences, School of Biological Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9LJ, UK.ORCID 0000-0002-2073-7750
Gisela OrozcoCentre for Genetics and Genomics Versus Arthritis, Division of Musculoskeletal and Dermatological Sciences, School of Biological Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9LJ, UK.ORCID 0000-0002-3479-0448
University of Manchester · GBManchester Academic Health Science Centre · GB

Funding

Department of HealthVersus Arthritis 21754Wellcome TrustWellcome Trust 207491/Z/17/Z
6 · The paper itself

Abstract

Genetic studies, including genome-wide association studies, have identified many common variants that are associated with autoimmune diseases. Strikingly, in addition to being frequently observed in healthy individuals, a number of these variants are shared across diseases with diverse clinical presentations. This highlights the potential for improved autoimmune disease understanding which could be achieved by characterising the mechanism by which variants lead to increased risk of disease. Of particular interest is the potential for identifying novel drug targets or of repositioning drugs currently used in other diseases. The majority of autoimmune disease variants do not alter coding regions and it is often difficult to generate a plausible hypothetical mechanism by which variants affect disease-relevant genes and pathways. Given the interest in this area, considerable effort has been invested in developing and applying appropriate methodologies. Two of the most important technologies in this space include both low- and high-throughput genomic perturbation using the CRISPR/Cas9 system and massively parallel reporter assays. In this review, we introduce the field of autoimmune disease functional genomics and use numerous examples to demonstrate the recent and potential future impact of these technologies.

Indexed as

Autoimmune DiseasesGenome-Wide Association StudyCRISPR-Cas SystemsGenomicsHumansAutoimmune diseaseCRISPR/Cas9Functional geneticsMPRA

Identifiers

PMID34508276
PMCPMC8837574
OpenAlexW3196527877

What Socratic 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 Socratic graph.