Ube2s stabilizes β-Catenin through K11-linked polyubiquitination to promote mesendoderm specification and colorectal cancer development article
Cell Death and Disease, ISSN: 2041-4889, Vol: 9, Issue: 5, Page: 456
2018
- 54Citations
- 18Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations54
- Citation Indexes54
- 54
- CrossRef28
- Captures18
- Readers18
- 18
Article Description
The canonical Wnt/β-Catenin signaling pathway is widely involved in regulating diverse biological processes. Dysregulation of the pathway results in severe consequences, such as developmental defects and malignant cancers. Here, we identified Ube2s as a novel activator of the Wnt/β-Catenin signaling pathway. It modified β-Catenin at K19 via K11-linked polyubiquitin chain. This modification resulted in an antagonistic effect against the destruction complex/β-TrCP cascade-orchestrated β-Catenin degradation. As a result, the stability of β-Catenin was enhanced, thus promoting its cellular accumulation. Importantly, Ube2s-promoted β-Catenin accumulation partially released the dependence on exogenous molecules for the process of embryonic stem (ES) cell differentiation into mesoendoderm lineages. Moreover, we demonstrated that UBE2S plays a critical role in determining the malignancy properties of human colorectal cancer (CRC) cells in vitro and in vivo. The findings in this study extend our mechanistic understanding of the mesoendodermal cell fate commitment, and provide UBE2S as a putative target for human CRC therapy.
Bibliographic Details
Springer Science and Business Media LLC
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