Evidence map›Paper›PMID 27127172›Full record

ArticleOncotarget2016

Integrin signaling via FAK-Src controls cytokinetic abscission by decelerating PLK1 degradation and subsequent recruitment of CEP55 at the midbody.

Siamak A Kamranvar, Deepesh Kumar Gupta, Ying Huang, Rajesh Kumar Gupta, Staffan Johansson

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.0field-weighted citation impact, top 10% of its field
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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
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  7. Article
  8. Review
  9. Article
  10. [CEP55 may be a potential therapeutic target for non-obstructive azoospermia with maturation arrest].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019
    Article
  11. Article
  12. Connections between the cell cycle, cell adhesion and the cytoskeleton.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019
    Review
  13. Article
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  15. Article
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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

5 authors at 1 institution in 1 country.

Siamak A KamranvarDepartment of Medical Biochemistry and Microbiology, Biomedical Center, Uppsala University, Uppsala, Sweden.
Deepesh Kumar GuptaDepartment of Medical Biochemistry and Microbiology, Biomedical Center, Uppsala University, Uppsala, Sweden.
Ying HuangDepartment of Medical Biochemistry and Microbiology, Biomedical Center, Uppsala University, Uppsala, Sweden.
Rajesh Kumar GuptaDepartment of Immunology, Genetics and Pathology, The Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
Staffan JohanssonDepartment of Medical Biochemistry and Microbiology, Biomedical Center, Uppsala University, Uppsala, Sweden.
Uppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adhesion to extracellular matrix is required for cell cycle progression through the G1 phase and for the completion of cytokinesis in normal adherent cells. Cancer cells acquire the ability to proliferate anchorage-independently, a characteristic feature of malignantly transformed cells. However, the molecular mechanisms underlying this escape of the normal control mechanisms remain unclear. The current study aimed to identify adhesion-induced reactions regulating the cytokinesis of non-transformed human fibroblasts.The adhesion-dependent control of cytokinesis was found to occur at a late stage close to the abscission, during which the endosomal sorting complex required for transport (ESCRT) severs the thin intercellular bridge connecting two nascent daughter cells. CEP55, a key protein involved in the abscission process, was localized at the midbody in both adherent and non-adherent fibroblasts, but it was unable to efficiently recruit ALIX, TSG101, and consequently the ESCRT-III subunit CHMP4B was missing in the non-adherent cells. PLK1, a kinase that prevents premature recruitment of CEP55 to the midbody, disappeared from this site more rapidly in the non-adherent cells. A FAK-Src signaling pathway downstream of integrin-mediated cell adhesion was found to decelerate both PLK1 degradation and CEP55 accumulation at the midbody. These data identify the regulation of PLK1 and CEP55 as steps where integrins exert control over the cytokinetic abscission.

Indexed as

CytokinesisProteolysisCalcium-Binding ProteinsCell AdhesionCell Cycle ProteinsCell LineDNA-Binding ProteinsEndosomal Sorting Complexes Required for TransportExtracellular MatrixFibroblastsFluorescent Antibody TechniqueFocal Adhesion Protein-Tyrosine KinasesG1 Phase Cell Cycle CheckpointsHumansIntegrinsNuclear ProteinsCalcium-Binding ProteinsCell Cycle ProteinsCep55 protein, humanDNA-Binding ProteinsEndosomal Sorting Complexes Required for TransportFocal Adhesion Protein-Tyrosine KinasesIntegrinsNuclear ProteinsPDCD6IP protein, humanPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene Proteinssrc-Family KinasesTranscription FactorsTsg101 ProteinCEP55cytokinesisFAKintegrinPLK1

Identifiers

PMID27127172
PMCPMC5058720
OpenAlexW2343422984

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.