The Spindle Assembly Checkpoint

Lara-González, Pablo; Westhorpe, Frederick G.; Taylor, Stephen S.

doi:10.1016/j.cub.2012.10.006

Cited by 694 publications

(725 citation statements)

References 157 publications

(372 reference statements)

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“…Thereby the ubiquitylation of securin and cyclin is prevented. Securin binds and inhibits a protease called securase which cleaves cohesin, a protein that keeps the two sister chromatids together (Lara-Gonzalez et al, 2012;Musacchio and Salmon, 2007). In FAT10 overexpressing HCT116 cells as well as in TNF-␣-treated HCT116 cells, the localization of MAD2 at the kinetochores was much reduced in the prometaphase of the cell cycle, indicating that FAT10 interferes with the binding of MAD2 to kinetochores (Fig.…”

Section: Mad2 and Chromosomal Instabilitymentioning

confidence: 98%

The ubiquitin-like modifier FAT10 in cancer development

Aichem

Groettrup

2016

The International Journal of Biochemistry & Cell Biology

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a b s t r a c tDuring the last years it has emerged that the ubiquitin-like modifier FAT10 is directly involved in cancer development. FAT10 expression is highly up-regulated by pro-inflammatory cytokines IFN-␥ and TNF-␣ in all cell types and tissues and it was also found to be up-regulated in many cancer types such as glioma, colorectal, liver or gastric cancer. While pro-inflammatory cytokines within the tumor microenvironment probably contribute to FAT10 overexpression, an increasing body of evidence argues that pro-malignant capacities of FAT10 itself largely underlie its broad and intense overexpression in tumor tissues. FAT10 thereby regulates pathways involved in cancer development such as the NF-B-or Wnt-signaling. Moreover, FAT10 directly interacts with and influences downstream targets such as MAD2, p53 or ␤-catenin, leading to enhanced survival, proliferation, invasion and metastasis formation of cancer cells but also of non-malignant cells. In this review we will provide an overview of the regulation of FAT10 expression as well as its function in carcinogenesis.

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Section: Mad2 and Chromosomal Instabilitymentioning

confidence: 98%

The ubiquitin-like modifier FAT10 in cancer development

Aichem

Groettrup

2016

The International Journal of Biochemistry & Cell Biology

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“…63 To ensure all chromosomes are tightly bound to kinetochore microtubules before allowing chromatid separation, cyclin B degradation can be inhibited by a spindle assembly checkpoint (SAC) pathway that monitors kinetochore-microtubule attachment and tension. 64 This pathway must be disabled upon entry into anaphase, so as not to mistake loosely-secured kinetochores in metaphase chromosomes for those in actively-separating anaphase chromatids, in which tension has been released due to chromatid separation. 65 Desensitizing the cell to this surveillance mechanism is accomplished, at least in part, through complete removal of cyclin B by late anaphase.…”

Section: Centrosome Function Depends On the Proteasomementioning

confidence: 99%

The benefits of local depletion: The centrosome as a scaffold for ubiquitin-proteasome-mediated degradation

Vora

Phillips

2016

Cell Cycle

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The centrosome is the major microtubule-organizing center in animal cells but is dispensable for proper microtubule spindle formation in many biological contexts and is thus thought to fulfill additional functions. Recent observations suggest that the centrosome acts as a scaffold for proteasomal degradation in the cell to regulate a variety of biological processes including cell fate acquisition, cell cycle control, stress response, and cell morphogenesis. Here, we review the body of studies indicating a role for the centrosome in promoting proteasomal degradation of ubiquitin-proteasome substrates and explore the functional relevance of this system in different biological contexts. We discuss a potential role for the centrosome in coordinating local degradation of proteasomal substrates, allowing cells to achieve stringent spatiotemporal control over various signaling processes.

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“…Through this mechanism a cell ensures accurate chromosome segregation to maintain genomic stability, thus avoiding aneuploidy. [13][14][15][16][17] The key target of SAC is Cdc20, the activator of APC/C, and if Cdc20 is inhibited the APC/C will not be able to perform ubiquitin ligase activity thus cyclin B1 and securin remain stable, thereby delaying the anaphase onset and mitotic exit. 18,19 SAC proteins recruited onto kinetochores and other multiple components form a large complex between kinetochores and microtubules.…”

Section: Introductionmentioning

confidence: 99%

Cyclin B3 controls anaphase onset independent of spindle assembly checkpoint in meiotic oocytes

Zhang

Huang

et al. 2015

Cell Cycle

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Cyclin B3 is a relatively new member of the cyclin family whose functions are little known. We found that depletion of cyclin B3 inhibited metaphase-anaphase transition as indicated by a well-sustained MI spindle and cyclin B1 expression in meiotic oocytes after extended culture. This effect was independent of spindle assembly checkpoint activity, since both Bub3 and BubR1 signals were not observed at kinetochores in MI-arrested cells. The metaphase I arrest was not rescued by either Mad2 knockdown or cdc20 overexpression, but it was rescued by securin RNAi. We conclude that cyclin B3 controls the metaphase-anaphase transition by activating APC/C cdc20 in meiotic oocytes, a process that does not rely on SAC activity.

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The Spindle Assembly Checkpoint

Cited by 694 publications

References 157 publications

The ubiquitin-like modifier FAT10 in cancer development

The ubiquitin-like modifier FAT10 in cancer development

The benefits of local depletion: The centrosome as a scaffold for ubiquitin-proteasome-mediated degradation

Cyclin B3 controls anaphase onset independent of spindle assembly checkpoint in meiotic oocytes

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