Evidence map›Paper›PMID 34155263›Full record

ArticleScientific reports2021

A genome-wide CRISPR/Cas9 screen to identify phagocytosis modulators in monocytic THP-1 cells.

Benjamin Lindner, Eva Martin, Monika Steininger, Aleksandra Bundalo, Martin Lenter, Johannes Zuber, Michael Schuler

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. 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
1.1field-weighted citation impact, top 23% 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, 21 citations in OpenAlex.

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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

7 authors at 2 institutions in 2 countries.

Benjamin LindnerDepartment of Drug Discovery Science, Boehringer Ingelheim Pharma GmbH & Co. KG, Birkendorferstr. 65, 88397, Biberach an der Riss, Germany. benjamin.lindner@boehringer-ingelheim.com.
Eva MartinDepartment of Drug Discovery Science, Boehringer Ingelheim Pharma GmbH & Co. KG, Birkendorferstr. 65, 88397, Biberach an der Riss, Germany.
Monika SteiningerResearch Institute of Molecular Pathology (IMP), Vienna BioCenter (VBC), 1030, Vienna, Austria.
Aleksandra BundaloResearch Institute of Molecular Pathology (IMP), Vienna BioCenter (VBC), 1030, Vienna, Austria.
Martin LenterDepartment of Drug Discovery Science, Boehringer Ingelheim Pharma GmbH & Co. KG, Birkendorferstr. 65, 88397, Biberach an der Riss, Germany.
Johannes ZuberResearch Institute of Molecular Pathology (IMP), Vienna BioCenter (VBC), 1030, Vienna, Austria.
Michael SchulerDepartment of Drug Discovery Science, Boehringer Ingelheim Pharma GmbH & Co. KG, Birkendorferstr. 65, 88397, Biberach an der Riss, Germany.
Boehringer Ingelheim (Germany) · DEResearch Institute of Molecular Pathology · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phagocytosis of microbial pathogens, dying or dead cells, and cell debris is essential to maintain tissue homeostasis. Impairment of these processes is associated with autoimmunity, developmental defects and toxic protein accumulation. However, the underlying molecular mechanisms of phagocytosis remain incompletely understood. Here, we performed a genome-wide CRISPR knockout screen to systematically identify regulators involved in phagocytosis of Staphylococcus (S.) aureus by human monocytic THP-1 cells. The screen identified 75 hits including known regulators of phagocytosis, e.g. members of the actin cytoskeleton regulation Arp2/3 and WAVE complexes, as well as genes previously not associated with phagocytosis. These novel genes are involved in translational control (EIF5A and DHPS) and the UDP glycosylation pathway (SLC35A2, SLC35A3, UGCG and UXS1) and were further validated by single gene knockout experiments. Whereas the knockout of EIF5A and DHPS impaired phagocytosis, knocking out SLC35A2, SLC35A3, UGCG and UXS1 resulted in increased phagocytosis. In addition to S. aureus phagocytosis, the above described genes also modulate phagocytosis of Escherichia coli and yeast-derived zymosan A. In summary, we identified both known and unknown genetic regulators of phagocytosis, the latter providing a valuable resource for future studies dissecting the underlying molecular and cellular mechanisms and their role in human disease.

Indexed as

CRISPR-Cas SystemsGenome-Wide Association StudyComputational BiologyGene Knockout TechniquesGene OntologyHumansMonocytesPhagocytosisReproducibility of ResultsRNA, Guide, CRISPR-Cas SystemsTHP-1 CellsWorkflowRNA, Guide, CRISPR-Cas Systems

Identifiers

PMID34155263
PMCPMC8217514
OpenAlexW3174219577

What OpenQuestion holds

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Registered trials

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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.