Evidence map›Paper›PMID 18938246›Full record

ArticleInsect biochemistry and molecular biology2008

Functional characterization of kurtz, a Drosophila non-visual arrestin, reveals conservation of GPCR desensitization mechanisms.

Erik C Johnson, Frank W Tift, Anita McCauley, Lingzhi Liu, Gregg Roman

Open access · greenAbstract read
In one paragraph

Article in Insect biochemistry and molecular biology, 2008. 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
1.0field-weighted citation impact, top 26% 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, 24 citations in OpenAlex.

  1. The Functional Role of Gate Loop Residues in Arrestin Binding to GPCRs.International journal of molecular sciences · 2025
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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 2 institutions in 1 country.

Erik C JohnsonDepartment of Biology, Wake Forest University, 222 Winston Hall, Winston-Salem, NC 27109, USA. johnsoec@wfu.edu
Frank W Tift
Anita McCauley
Lingzhi Liu
Gregg Roman
University of Houston · USWake Forest University · US

Funding

The Function of Arrestin in Drosophila BehaviorR01NS042185 · NINDS · UNIVERSITY OF HOUSTON · PI ROMAN, GREGG W · 2002 to 2005
$1.1M
NINDS NIH HHS NS42185NINDS NIH HHS R01 NS042185
6 · The paper itself

Abstract

The arrestins are a family of molecules that terminate signaling from many different G protein-coupled receptors, by inhibiting the association between receptor and downstream effectors. We recently employed a human betaarrestin2-GFP fusion protein to explore the dynamics of different neuropeptide receptors in Drosophila and have previously used a betaarrestin translocation assay to identify ligands at orphan receptors. Here, we report that the Drosophila arrestin encoded by kurtz functions in a similar fashion and can be employed to investigate GPCR-arrestin associations. Specifically, a GFP-krz fusion protein, upon co-expression with various Drosophila peptide receptors, an amine receptor, and a mammalian peptide receptor translocates to the plasma membrane in specific response to ligand application. This molecular phenotype is exhibited in a mammalian cell line as well as in a Drosophila cell line. Notably, the details of receptor-arrestin associations in terms of endocytotic patterns are functionally conserved between the mammalian arrestins and kurtz. Furthermore, we report that kurtz mutants exhibit hypersensitivity to osmotic stress, implicating GPCR desensitization as an important feature of the endocrine events that shape this stress response.

Indexed as

AnimalsArrestinsCell LineCell MembraneCloning, MolecularDrosophilaDrosophila ProteinsGreen Fluorescent ProteinsHumansLigandsMutationOsmotic PressureReceptors, G-Protein-CoupledRecombinant Fusion ProteinsArrestinsDrosophila ProteinsGreen Fluorescent Proteinskrz protein, DrosophilaLigandsReceptors, G-Protein-CoupledRecombinant Fusion Proteins

Identifiers

PMID18938246
PMCPMC12120669
OpenAlexW2023765792

What OpenQuestion holds

Textmetadata
LicenceTDM
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.