ArticleEMBO reports2023
UBAP2L-dependent coupling of PLK1 localization and stability during mitosis.
Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Pharmacological inhibition of UBASH3B induces mitotic arrest and selectively reduces tumor growth.EMBO molecular medicine · 2026Article
- The CCHCR1-UBAP2L Interaction Promotes UBAP2L Release from P-Bodies for Stress Granule Assembly.International journal of molecular sciences · 2026Article
- HMMR mediates progression of nasopharyngeal carcinoma by inhibiting FAM83D ubiquitination and activating beta-catenin signaling pathway.Scientific reports · 2025Article
- The overexpression of HOXC6 in LUSC and pan-squamous cell carcinomas indicates the coexistence of nuclear division regulatory mechanisms.Cancer biomarkers : section A of Disease markers · 2025Article
- Metabolic plasticity drives specific mechanisms of chemotherapy and targeted therapy resistance in metastatic colorectal cancer.Exploration of targeted anti-tumor therapy · 2025Review
- UBAP2L ensures homeostasis of nuclear pore complexes at the intact nuclear envelope.The Journal of cell biology · 2024Article
- Whole-exome sequencing identified a novel heterozygous variant inFrontiers in genetics · 2024Article
- UBAP2L-dependent coupling of PLK1 localization and stability during mitosis.EMBO reports · 2023Article
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PLK1 is an important regulator of mitosis whose protein levels and activity fluctuate during the cell cycle. PLK1 dynamically localizes to various mitotic structures to regulate chromosome segregation. However, the signaling pathways linking localized PLK1 activity to its protein stability remain elusive. Here, we identify the Ubiquitin-Binding Protein 2-Like (UBAP2L) that controls both the localization and the protein stability of PLK1. We demonstrate that UBAP2L is a spindle-associated protein whose depletion leads to severe mitotic defects. UBAP2L-depleted cells are characterized by increased PLK1 protein levels and abnormal PLK1 accumulation in several mitotic structures such as kinetochores, centrosomes and mitotic spindle. UBAP2L-deficient cells exit mitosis and enter the next interphase in the presence of aberrant PLK1 kinase activity. The C-terminal domain of UBAP2L mediates its function on PLK1 independently of its role in stress response signaling. Importantly, the mitotic defects of UBAP2L-depleted cells are largely rescued by chemical inhibition of PLK1. Overall, our data suggest that UBAP2L is required to fine-tune the ubiquitin-mediated PLK1 turnover during mitosis as a means to maintain genome fidelity.
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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.