Molecular basis underlying the specificity of an antagonist AA92593 for mammalian melanopsins.

Kohei Obayashi, Ruisi Zou, Tomoki Kawaguchi, Toshifumi Mori, Hisao Tsukamoto

Abstract read

In one paragraph

Article in The Journal of biological chemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing papers in PubMed

–field-weighted citation impact

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

1 citing paper in PubMed.

Coral anthozoan-specific opsins employ a novel chloride counterion for spectral tuning.eLife · 2025
Article

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.

Kohei ObayashiDepartment of Biology, Graduate School of Science, Kobe University, Kobe, Japan.

Ruisi ZouInterdisciplinary Graduate School of Engineering Sciences, Kyushu University, Fukuoka, Japan.

Tomoki KawaguchiDepartment of Biology, Graduate School of Science, Kobe University, Kobe, Japan.

Toshifumi MoriInterdisciplinary Graduate School of Engineering Sciences, Kyushu University, Fukuoka, Japan; Institute for Materials Chemistry and Engineering, Kyushu University, Fukuoka, Japan.

Hisao TsukamotoDepartment of Biology, Graduate School of Science, Kobe University, Kobe, Japan; Center of Optical Scattering Image Science, Kobe University, Kobe, Japan. Electronic address: tsukamoh@people.kobe-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melanopsin functions in intrinsically photosensitive retinal ganglion cells of mammals to regulate circadian clock and pupil constriction. The opsinamide AA92593 has been reported to specifically inhibit mouse and human melanopsin functions as a competitive antagonist against retinal; however, the molecular mechanisms underlying its specificity have not been resolved. In this study, we attempted to identify amino acid residues responsible for the susceptibility of mammalian melanopsins to AA92593. Our cell-based assays confirmed that AA92593 effectively inhibited the light-induced cellular responses of mammalian melanopsins, but not those of non-mammalian vertebrate and invertebrate melanopsins. These results suggest that amino acid residues specifically conserved among mammalian melanopsins are important for the antagonistic effect of AA92593, and we noticed Phe-94

Indexed as

Rod OpsinsAmino Acid SubstitutionAnimalsHEK293 CellsHumansMelanopsinMiceMolecular Docking SimulationMolecular Dynamics SimulationMelanopsinRod OpsinsantagonistGPCRmelanopsinmolecular dynamicsnon-visual photoreceptionopsin

Identifiers

PMID40154611

DOI10.1016/j.jbc.2025.108461

PMCPMC12051620

What Socratic holds

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LicenceCC BY

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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 Socratic graph.