ArticleJournal of cell science2026
Endosomal actin attenuation and fission are regulated by MICAL2.
Article in Journal of cell science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Endosome fission is essential for the generation of carrier vesicles and recycling of receptors to the plasma membrane. Early events in endosome fission depend on the generation of Arp2/3-mediated branched actin, which segregates cargo and constricts the endosomal membrane to form buds. It has been proposed that once membrane buds have been formed, branched actin attenuation is necessary for fission proteins, such as EHD1, to access the endosomal neck and complete the cleavage process. Whereas several proteins and complexes involved in actin growth at endosomes have been characterized, less is known about actin attenuation at endosomes. In our study, we identified MICAL2, a constitutively active actin-regulatory monooxygenase, as a key regulator of endosomal fission, likely through its regulation of branched actin. MICAL2 depletion, or inhibition of its monooxygenase activity, resulted in a substantial increase in branched actin associated with endosomes. Moreover, we demonstrate that MICAL2 is required for both endosome fission and the recycling of clathrin-dependent cargo. Overall, our study highlights a novel role for MICAL2 in regulating actin at endosomes, thereby facilitating fission and recycling.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.