ArticleCell communication and signaling : CCS2026
Nexilin promotes calcium-dependent endo-lysosomal fission required for retrograde transport.
Article in Cell communication and signaling : CCS, 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
No grant is acknowledged in the PubMed record.
Abstract
Late endosomes and lysosomes (LE/Lys) are dynamic organelles primarily involved in the degradation of macromolecules within cells. Beyond this role, they are crucial for nutrient sensing, calcium signalling, cell proliferation and migration. The cytoskeleton is essential for the proper trafficking and function of LE/Lys. However, while the role of microtubules is well-established, the function of the actin cytoskeleton at LE/Lys is less understood. In this work, we performed an siRNA screen to identify actin regulators that play a role at LE/Lys. The screen revealed that the F-actin-binding protein nexilin regulates LE/Lys size as its depletion leads to their enlargement. We show that this is a consequence of inhibited LE/Lys fission and affects the retrograde transport from late endosomes to Golgi. Moreover, our data demonstrate that nexilin interacts with the small GTPase Rab7b and the lysosomal calcium channel TRPML1, and that TRPML1 activation rescues the LE/Lys enlargement caused by nexilin depletion. Taken together, our results indicate that nexilin mediates the interaction between LE/Lys and the acto-myosin cytoskeleton required for the calcium-dependent fission of these organelles.
Indexed as
Identifiers
What Socratic 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 Socratic graph.