ArticleOncogene2011
Camptothecin-induced downregulation of MLL5 contributes to the activation of tumor suppressor p53.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- conMItion: an R package adjusting confounding factors for associations in multi-omics.Bioinformatics (Oxford, England) · 2026Article
- The Wheel of p53 Helps to Drive the Immune System.International journal of molecular sciences · 2023Review
- MLL5α activates AR/NDRG1 signaling to suppress prostate cancer progression.American journal of cancer research · 2020Article
- CRISPR/Cas9-mediated knockout of MLL5 enhances apoptotic effect of cisplatin in HeLa cellsEXCLI journal · 2020Article
- MLL5 (KMT2E): structure, function, and clinical relevance.Cellular and molecular life sciences : CMLS · 2017Review
- MLL5 maintains spindle bipolarity by preventing aberrant cytosolic aggregation of PLK1.The Journal of cell biology · 2016Article
- Transposon mutagenesis identifies genes driving hepatocellular carcinoma in a chronic hepatitis B mouse model.Nature genetics · 2014Article
- Functional p53 determines docetaxel sensitivity in prostate cancer cells.The Prostate · 2013Article
- Article
- MLL5 maintains genomic integrity by regulating the stability of the chromosomal passenger complex through a functional interaction with Borealin.Journal of cell science · 2012Article
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mixed lineage leukemia 5 (MLL5) has been implicated in multiple aspects of cell physiology, such as hematopoiesis, cell cycle control and chromatin regulatory network. In this study, we present evidence that MLL5 is involved in the camptothecin (CPT)-induced p53 activation. CPT promoted the degradation of MLL5 protein in a time- and dose-dependent manner in actively replicating cells. The downregulation of MLL5 led to phosphorylation of p53 at Ser392, which was abrogated by exogenous overexpression of MLL5. In MLL5-knockdown cells, p53 protein was stabilized and bound to DNA with higher affinity, leading to activation of downstream genes. Co-immunoprecipitation showed that MLL5 preferentially interacted with the tetramerized form of p53, and knockdown of MLL5 promoted chromatin accumulation of p53 tetramers, suggesting that the association of MLL5 with p53 may prevent the p53 tetramers from binding to the chromatin target sites. The role of MLL5 in CPT-induced p53 activation was conserved in developing zebrafish, where CPT downregulated zebrafish Mll5 protein, and the microinjection of zebrafish mll5 mRNA substantially blocked the CPT-induced apoptosis. In summary, our study proposed MLL5 as a novel component in the regulation of p53 homeostasis and a new cellular determinant of CPT.
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Registered trials
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.