Evidence map›Paper›PMID 35469017›Full record

ArticleNature cell biology2022

CDK1-cyclin-B1-induced kindlin degradation drives focal adhesion disassembly at mitotic entry.

Nan-Peng Chen, Jonas Aretz, Reinhard Fässler

Abstract read
In one paragraph

Article in Nature cell biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed.

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  13. The Role of the Swollen State in Cell Proliferation.The Journal of membrane biology · 2025
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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

3 authors.

Nan-Peng ChenDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany. nchen@biochem.mpg.de.ORCID 0000-0001-8061-9732
Jonas AretzDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany.
Reinhard FässlerDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany. faessler@biochem.mpg.de.ORCID 0000-0002-0145-6937

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The disassembly of integrin-containing focal adhesions (FAs) at mitotic entry is essential for cell rounding, mitotic retraction fibre formation, bipolar spindle positioning and chromosome segregation. The mechanism that drives FA disassembly at mitotic entry is unknown. Here, we show that the CDK1-cyclin B1 complex phosphorylates the integrin activator kindlin, which results in the recruitment of the cullin 9-FBXL10 ubiquitin ligase complex that mediates kindlin ubiquitination and degradation. This molecular pathway is essential for FA disassembly and cell rounding, as phospho-inhibitory mutations of the CDK1 motif prevent kindlin degradation, FA disassembly and mitotic cell rounding. Conversely, phospho-mimetic mutations promote kindlin degradation in interphase, accelerate mitotic cell rounding and impair mitotic retraction fibre formation. Despite the opposing effects on kindlin stability, both types of mutations cause severe mitotic spindle defects, apoptosis and aneuploidy. Thus, the exquisite regulation of kindlin levels at mitotic entry is essential for cells to progress accurately through mitosis.

Indexed as

CDC2 Protein KinaseFocal AdhesionsCell Cycle ProteinsCyclin B1IntegrinsMitosisPhosphorylationSpindle ApparatusCDC2 Protein KinaseCell Cycle ProteinsCyclin B1Integrins

Identifiers

PMID35469017
PMCPMC9106588

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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 OpenQuestion graph.