ArticleiScience2025
Coiled-coil interactions drive the ectopic condensation of overexpressed MAD1 to promote mitotic slippage in cancer cells.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Kinetic Control of Condensate Function: How the Formation Dynamics of APBs Influence ALT Cancer Telomere Length Heterogeneity.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
Corrections and comments
- Update of
Authors and funding
5 authors.
Funding
Abstract
The mitotic checkpoint protein MAD1 is overexpressed in cancers, weakening the mitotic checkpoint and promoting mitotic slippage. Overexpressed MAD1 forms ectopic foci in mitotic cells, but the biophysical nature of these foci and their roles in mitotic slippage remain unclear. Here, we report that MAD1 ectopic foci are phase-separated condensates that shorten mitosis by sequestering checkpoint proteins. We show that MAD1 ectopic foci display dynamic condensate behaviors, and Mad1 phase separation is driven by interactions between its coiled-coil and disordered domains at the N-terminus. By inducing MAD1 ectopic condensates in mitotic cells with low MAD1 levels, we decouple the effects of condensation from concentration and demonstrate the causal role of condensation in mitotic slippage. Mechanistically, MAD1 ectopic condensates trap the diffusive pool of MAD2, weakening the MAD2 conversion cycle needed for a robust checkpoint. Our work highlights a loss of function caused by ectopic condensates in cancer cells.
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.