ArticleOncotarget2016
Smyd2 is a Myc-regulated gene critical for MLL-AF9 induced leukemogenesis.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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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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
15 citing papers in PubMed, 22 citations in OpenAlex.
- Review
- Novel insights into SMYD2 and SMYD3 inhibitors: from potential anti-tumoural therapy to a variety of new applications.Molecular biology reports · 2021Review
- The SMYD family proteins in immunology: An update of their obvious and non-obvious relations with the immune system.Heliyon · 2021Review
- Epigenetics and beyond: targeting writers of protein lysine methylation to treat disease.Nature reviews. Drug discovery · 2021Review
- Characterizing the Role of SMYD2 in Mammalian Embryogenesis-Future Directions.Veterinary sciences · 2020Article
- The lysine methyltransferase SMYD2 is required for normal lymphocyte development and survival of hematopoietic leukemias.Genes and immunity · 2020Article
- Function of the MYND Domain and C-Terminal Region in Regulating the Subcellular Localization and Catalytic Activity of the SMYD Family Lysine Methyltransferase Set5.Molecular and cellular biology · 2020Article
- Collaboration of MYC and RUNX2 in lymphoma simulates T-cell receptor signaling and attenuates p53 pathway activity.Journal of cellular biochemistry · 2019Article
- Histone methyltransferase SMYD2: ubiquitous regulator of disease.Clinical epigenetics · 2019Review
- Smyd2 conformational changes in response to p53 binding: role of the C-terminal domain.Molecular oncology · 2019Article
- Is MYND Domain-Mediated Assembly of SMYD3 Complexes Involved in Calcium Dependent Signaling?Frontiers in molecular biosciences · 2019Article
- SMYD2 promotes cervical cancer growth by stimulating cell proliferation.Cell & bioscience · 2019Article
- Article
- SMYD2-Mediated Histone Methylation Contributes to HIV-1 Latency.Cell host & microbe · 2017Article
- SMYD2 lysine methyltransferase regulates leukemia cell growth and regeneration after genotoxic stress.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Smyd2 protein (Set- and Mynd domain containing protein 2) is a methyl-transferase that can modify both histones and cytoplasmic proteins. Smyd2 is over-expressed in several cancer types and was shown to be limiting for tumor development in the pancreas. However, genetic evidence for a role of Smyd2 in other cancers or in mouse development was missing to date. Using germ line-deleted mouse strains, we now show that Smyd2 and the related protein Smyd3 are dispensable for normal development. Ablation of Smyd2 did not affect hematopoiesis, but retarded the development of leukemia promoted by MLL-AF9, a fusion oncogene associated with acute myeloid leukemia (AML) in humans. Smyd2-deleted leukemic cells showed a competitive disadvantage relative to wild-type cells, either in vitro or in vivo. The Smyd2 gene was directly activated by the oncogenic transcription factor Myc in either MLL9-AF9-induced leukemias, Myc-induced lymphomas, or fibroblasts. However, unlike leukemias, the development of lymphomas was not dependent upon Smyd2. Our data indicate that Smyd2 has a critical role downstream of Myc in AML.
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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.