Cullin' PLK1 from kinetochores

McGourty, Colleen A.; Rapé, Michael

doi:10.1038/ncb2722

Cited by 6 publications

(6 citation statements)

References 15 publications

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“…For details see the main text. leads to accumulation of PLK1 at kinetochores, chromosome alignment defects, SAC potentiation and mitotic arrest resulting in apoptotic death [39,42,43]. It would be interesting to understand if kinetochore removal of K492-ubiquitylated PLK1 is helped by an action of a downstream ubiquitin receptor analogous to UBASH3B.…”

Section: Fig 2 Non-proteolytic Cul3 Pathways During Cell Divisionmentioning

confidence: 99%

Cullin 3, a cellular scripter of the non-proteolytic ubiquitin code

Jeřábková

Sumara

2019

Seminars in Cell & Developmental Biology

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Cullin-RING ubiquitin ligases (CRLs) represent the largest family of E3 ubiquitin ligases that control most if not all cellular processes. In CUL3-based CRLs, the substrate specificity is conferred by the interaction with one of around 183 existing BTB proteins, implying a broad spectrum of possible ubiquitylation signals and possible direct ubiquitylation substrates. Indeed, CUL3-based E3-ligases can catalyze various proteolytic and non-proteolytic ubiquitin signals regulating many physiological and pathophysiological states. Here, we discuss the recent studies focusing on the non-proteolytic CUL3-based signaling in mammalian cells, which emerge as important pathways during cell division, embryonic development as well as other biological processes. Mechanistically, non-proteolytic ubiquitin signals generated by CUL3 E3-ligases often regulate substrates' interactions with other downstream factors or their subcellular localization. Existing data also demonstrate an interplay with the proteolytic ubiquitylation catalyzed on the same substrates by different E3-ligases or by the same CUL3-BTB CRL3s on different substrates. In future, a deeper understanding of the upstream spatiotemporal regulatory mechanisms will help to dissect this fascinating CUL3 ubiquitin code.

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Section: Fig 2 Non-proteolytic Cul3 Pathways During Cell Divisionmentioning

confidence: 99%

Cullin 3, a cellular scripter of the non-proteolytic ubiquitin code

Jeřábková

Sumara

2019

Seminars in Cell & Developmental Biology

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“…It plays an important role in centriole maturation [11][12][13], Golgi disintegration [14], spindle assembling and function [15,16], kinetochore function [17,18], centromere assembling [19] and cytokinesis [20]. It also facilitates DNA replication [21], mitotic entry [22], separation of sister chromatid [23], chromosome condensation [24] and APC/C activity [25]. It has been reported that PLK1 is frequently over-expressed in numerous cancers (such as esophageal cancer, colon cancer, breast cancer, non-small cell lung cancer, endometrial cancer, etc.…”

Section: Introductionmentioning

confidence: 99%

Polo-like kinase 1 plays an oncogenic role in pan-cancer based on bioinformatics and biological assays

Luo

Zhang

Zhen

et al. 2022

Preprint

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Polo-like kinases (PLKs) are crucial regulatory factors of the cell cycle process and their dysregulations often cause various diseases including tumorigenesis. Although the PLKs, including PLK1, have been extensively studied and reported, few pan-cancer analyses are attainable. The potential oncogenic roles of PLK1 were thus explored among different cancers according to various online websites and datasets. PLK1 is always overexpressed in many cancers, and there is a significant relationship between its expression and the prognosis of cancer patients. In addition, the enrichment analysis suggested that PLK1 might related to “cell cycle”, “DNA replication”, “mismatch repair”, and “immune response” in pan-cancer, especially in glioma. Therefore, the analyses about genetic alterations and immune in pan-cancer were conducted. Furthermore, flow cytometry, CCK8 and EdU assays can further verify the above results of enrichment analysis. Moreover, DNA methylation and ceRNA network were analyzed to explore the potential mechanisms of aberrant expression of PLK1. In conclusion, our research about the oncogenic roles of PLK1 in pan-cancer further supplemented the oncogenic mechanisms of PLK1 and developed new potential therapeutic directions.

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“…[19,20] Experiments with antiPrc1 microinjection demonstrated that cell division is blocked, without any influence on the nuclear separation; this suggests that Prc1 would be essential for cytokinetic achievement. [21] Plk1, on the other hand, participates at several stages of the cell cycle, and is an essential protein in cytokinesis.…”

mentioning

confidence: 97%

“…To begin, Prc1 is inhibited during mitosis onset through Cdk1 phosphorylation in two action sites-T470 and T481and, indeed, mutation at such sites causes premature recruitment of Plk1 and Prc1, resulting in prometaphase arrest and blocking the progression of mitosis. [19,20] Experiments with anti-Prc1 microinjection demonstrated that cell division is blocked, without any influence on the nuclear separation; this suggests that Prc1 would be essential for cytokinetic achievement. [21] Plk1, on the other hand, participates at several stages of the cell cycle, and is an essential protein in cytokinesis.…”

mentioning

confidence: 99%

“…[21] Plk1, on the other hand, participates at several stages of the cell cycle, and is an essential protein in cytokinesis. [20] It is noteworthy that Plk1 is overexpressed in many types of tumours, is associated with a poor prognosis and has hence been examined as a therapeutic target. [22] Plk1 is responsible for mitotic entry, centrosome maturation, spindle assembly, recruitment of proteins to furrow assembly, anaphase-promoting complex (APC) regulation and cytokinesis.…”

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confidence: 99%

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Identification of Pyrroloformamide as a Cytokinesis Modulator

et al. 2014

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Discovered in the late 1940s, the pyrrolinonodithioles represent a family of potent disulfide-containing natural products. Although they are understood in a synthetic and biosynthetic context, the biological role of these materials remains unresolved. To date, their activity has been suggested to arise through regulating RNA metabolism, and more recently they have been suggested to function as backup thiols for detoxification. Using materials identified through a natural products program, we now identify the biological function of one member of this family, pyrroloformamide, as an antimitotic agent acting, in part, by disrupting cytokinesis.

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Cullin' PLK1 from kinetochores

Cited by 6 publications

References 15 publications

Cullin 3, a cellular scripter of the non-proteolytic ubiquitin code

Cullin 3, a cellular scripter of the non-proteolytic ubiquitin code

Polo-like kinase 1 plays an oncogenic role in pan-cancer based on bioinformatics and biological assays

Identification of Pyrroloformamide as a Cytokinesis Modulator

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