Evidence map›Paper›PMID 35970889›Full record

ArticleNature communications2022

Chimeric GPCRs mimic distinct signaling pathways and modulate microglia responses.

Rouven Schulz, Medina Korkut-Demirbaş, Alessandro Venturino, Gloria Colombo, Sandra Siegert

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

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  6. Do GPCRs constitute the target of 30% of newly approved drugs in Germany?Naunyn-Schmiedeberg's archives of pharmacology · 2026
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  7. A chemogenetic approach for temporal and cell-specific activation of endogenous GPCRs in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

5 authors at 1 institution in 1 country.

Rouven SchulzInstitute of Science and Technology Austria (ISTA), Am Campus 1, 3400, Klosterneuburg, Austria.ORCID 0000-0001-5297-733X
Medina Korkut-DemirbaşInstitute of Science and Technology Austria (ISTA), Am Campus 1, 3400, Klosterneuburg, Austria.ORCID 0000-0003-4309-2251
Alessandro VenturinoInstitute of Science and Technology Austria (ISTA), Am Campus 1, 3400, Klosterneuburg, Austria.ORCID 0000-0003-2356-9403
Gloria ColomboInstitute of Science and Technology Austria (ISTA), Am Campus 1, 3400, Klosterneuburg, Austria.ORCID 0000-0001-9434-8902
Sandra SiegertInstitute of Science and Technology Austria (ISTA), Am Campus 1, 3400, Klosterneuburg, Austria. ssiegert@ist.ac.at.ORCID 0000-0001-8635-0877
Institute of Science and Technology Austria · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G protein-coupled receptors (GPCRs) regulate processes ranging from immune responses to neuronal signaling. However, ligands for many GPCRs remain unknown, suffer from off-target effects or have poor bioavailability. Additionally, dissecting cell type-specific responses is challenging when the same GPCR is expressed on different cells within a tissue. Here, we overcome these limitations by engineering DREADD-based GPCR chimeras that bind clozapine-N-oxide and mimic a GPCR-of-interest. We show that chimeric DREADD-β2AR triggers responses comparable to β2AR on second messenger and kinase activity, post-translational modifications, and protein-protein interactions. Moreover, we successfully recapitulate β2AR-mediated filopodia formation in microglia, an immune cell capable of driving central nervous system inflammation. When dissecting microglial inflammation, we included two additional DREADD-based chimeras mimicking microglia-enriched GPR65 and GPR109A. DREADD-β2AR and DREADD-GPR65 modulate the inflammatory response with high similarity to endogenous β2AR, while DREADD-GPR109A shows no impact. Our DREADD-based approach allows investigation of cell type-dependent pathways without known endogenous ligands.

Indexed as

MicrogliaReceptors, G-Protein-CoupledChimeraHumansInflammationLigandsSignal TransductionLigandsReceptors, G-Protein-Coupled

Identifiers

PMID35970889
PMCPMC9378622
OpenAlexW4291551914

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.