ReviewMolecular biology of the cell2022
New signaling kid on the block: the role of the postmitotic midbody in polarity, stemness, and proliferation.
Review in Molecular biology of the cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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
12 citing papers in PubMed, 14 citations in OpenAlex.
- Condensates on the Move: Midbody Remnants as Large, Translation-Competent Extracellular Vesicles.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Somatic cells non-autonomously control germline incomplete cytokinesis through FGF signaling.bioRxiv : the preprint server for biology · 2026Article
- TPGS1 regulates central spindle microtubule glutamylation and remodeling during telophase and abscission.EMBO reports · 2026Article
- Clinical relevance of extracellular vesicles in cancer - therapeutic and diagnostic potential.Nature reviews. Clinical oncology · 2025Review
- The midbody and midbody remnant: from cellular debris to signaling organelle with diagnostic and therapeutic potential.Molecular biology of the cell · 2025Review
- Extracellular vesicles, including large translating vesicles called midbody remnants, are released during the cell cycle.Molecular biology of the cell · 2024Article
- Cytokinetic abscission requires actin-dependent microtubule severing.Nature communications · 2024Article
- The role of midbody-associated mRNAs in regulating abscission.The Journal of cell biology · 2023Article
- An oocyte meiotic midbody cap is required for developmental competence in mice.Nature communications · 2023Article
- An oocyte meiotic midbody cap is required for developmental competence in mice.Research square · 2023Article
- The biosynthetic-secretory pathway, supplemented by recycling routes, determines epithelial membrane polarity.Science advances · 2023Article
- Rab11 endosomes and Pericentrin coordinate centrosome movement during pre-abscission in vivo.Life science alliance · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
To complete cytokinesis, abscission of the proteinaceous and microtubule-rich intercellular bridge needs to occur. The midbody (MB), a structure that forms on the intercellular bridge, is a key regulator of cytokinesis and appears to play a role in downstream signaling after abscission. Initially, it was thought that after abscission was completed, the MB was degraded. However, a new body of evidence has emerged suggesting that one daughter cell or a surrounding non-daughter cell can inherit or internalize the MB, thus leading to changes in cell proliferation and differentiation. In this review, we highlight the role that the MB has after mitosis. We will focus on the rising evidence that the MB plays an important role in establishment of cell polarity, such as apical lumen formation, neurite extension, and ciliation. Additionally, we will discuss the evidence suggesting that MBs can also serve the role of signaling organelles (MBsomes) that lead to cell proliferation, differentiation, and even tumorigenicity.
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.