Plk1 negatively regulates Cep55 recruitment to the midbody to ensure orderly abscission is a research paper published in Journal of Cell Biology (2010). On theSindex it has a DataRank of 5.7. It has been cited 149 times, with 137 citing works in its 1-hop citation network.
Cytokinesis requires a membrane-remodeling and fission event termed abscission that occurs after chromosome segregation, cleavage furrow formation, and contraction have completed. In this study, we show how abscission factor recruitment is controlled by the Polo-like kinase 1 (Plk1). At the metaphase–anaphase transition, Plk1 initiates cleavage furrow formation and is then progressively degraded during mitotic exit. During this period, Plk1 phosphorylates the abscission factor Cep55 in trans and prevents its untimely recruitment to the anaphase spindle. A Plk1 phosphorylation site mutant of Cep55 is prematurely recruited to the anaphase spindle and fails to support abscission. Endogenous Cep55 behaves similarly after Plk1 inhibition by the drugs BI2536 or GW842862. Only once Plk1 is degraded can Cep55 target to the midbody and promote abscission. Blocking Plk1 degradation leads to elevated levels of Plk1 at the midbody and the failure of Cep55 recruitment. Thus, Plk1 activity negatively regulates Cep55 to ensure orderly abscission factor recruitment and ensures that this occurs only once cell contraction has completed.
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Base Score Contribution
0.752
From this paper's citation signal
Citation Network Contribution
4.9
From 120 citing papers with measurable signal
Ranked by citation count — the same ordering the engine uses when summing log1p(Cq) over citers.
DataRank blends this paper's own citation count with the influence of the papers that cite it. Here, roughly 13% comes from its base citations and 87% from the citation network (120 citing papers contributed measurable signal).
Citers are pulled from OpenAlex sorted by cited_by_count:descand capped per paper, so when the cap binds we keep the highest-signal references and the score is reproducible across reruns.
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