ArticleGenes & cancer2012
Splicing up mdm2 for cancer proteome diversity.
Article in Genes & cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Oncogenic Functions of Alternatively SplicedInternational journal of molecular sciences · 2024Article
- The Interlinking Metabolic Association between Type 2 Diabetes Mellitus and Cancer: Molecular Mechanisms and Therapeutic Insights.Diagnostics (Basel, Switzerland) · 2024Review
- MDM2 Inhibitors for Cancer Therapy: The Past, Present, and Future.Pharmacological reviews · 2024Review
- MDM2- an indispensable player in tumorigenesis.Molecular biology reports · 2023Review
- Targeting p53-MDM2 interaction by small-molecule inhibitors: learning from MDM2 inhibitors in clinical trials.Journal of hematology & oncology · 2022Review
- Hereditary retinoblastoma iPSC model reveals aberrant spliceosome function driving bone malignancies.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Summit: Automated Analysis of Arrayed Single-Cell Gel Electrophoresis.SLAS technology · 2021Article
- The roles and regulation of MDM2 and MDMX: it is not just about p53.Genes & development · 2021Review
- Mdm2: Open questions.Cancer science · 2020Review
- MDM2-C Functions as an E3 Ubiquitin Ligase.Cancer management and research · 2020Article
- Lymphomas driven by Epstein-Barr virus nuclear antigen-1 (EBNA1) are dependant upon Mdm2.Oncogene · 2018Article
- Review
- Review
- Article
- Aberrant splicing of the DMP1-ARF-MDM2-p53 pathway in cancer.International journal of cancer · 2016Review
- The Roles of MDM2 and MDMX in Cancer.Annual review of pathology · 2016Review
- Global Profiling of the Cellular Alternative RNA Splicing Landscape during Virus-Host Interactions.PloS one · 2016Article
- Article
- MDM2's social network.Oncogene · 2014Review
- Doxorubicin and 5-fluorouracil induced accumulation and transcriptional activity of p53 are independent of the phosphorylation at serine 15 in MCF-7 breast cancer cells.Cancer biology & therapy · 2014Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Cancer cells often have high expression of Mdm2. However, in many cancers mdm2 is alternatively spliced, with more than 40 mRNA variants identified. Many of the alternative spliced mdm2 mRNAs have the potential to encode truncated Mdm2 isoforms. These putative Mdm2 isoforms can theoretically increase the diversity of the cancer proteome. The 3 best characterized are Mdm2-A, Mdm2-B, and Mdm2-C. As described in this review, the exogenous expression of these isoforms results in paradoxical phenotypes of transformation-associated growth as well as the inhibition of growth. Interestingly, these Mdm2 isoforms contribute tumor-promoting capacity in p53-null backgrounds. Herein we describe how alternative splicing of mdm2 may result in Mdm2 protein products that alter signal transduction to promote tumorigenesis. The tumor promoting capacity of Mdm2 isoforms is discussed in the context of functions that do not require the inhibition of p53. When N-terminal portions of Mdm2 are missing, the biochemical functions encoded by exon 12 are proposed to become more important. This may result in growth promoting functions when wild-type p53 is absent or compromised. The p53-independent tumor promoting activity of Mdm2 is proposed to result from C-terminal biochemical contributions of DNA binding, RNA binding, nucleolar localization, and nucleotide binding.
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What OpenQuestion holds
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.