Редактирование: SMYD2

N-lysine methyltransferase SMYD2 (EC 2.1.1.-) (HSKM-B) (Histone methyltransferase SMYD2) (EC 2.1.1.354) (Lysine N-methyltransferase 3C) (SET and MYND domain-containing protein 2) [KMT3C]

==Publications==

{{medline-entry
|title=Collaboration of [[MYC]] and [[RUNX2]] in lymphoma simulates T-cell receptor signaling and attenuates p53 pathway activity.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31257681
|abstract=[[MYC]] and RUNX oncogenes each trigger p53-mediated failsafe responses when overexpressed in vitro and collaborate with p53 deficiency in vivo. However, together they drive rapid onset lymphoma without mutational loss of p53. This phenomenon was investigated further by transcriptomic analysis of premalignant thymus from [[RUNX2]]/[[MYC]] transgenic mice. The distinctive contributions of [[MYC]] and RUNX to transcriptional control were illustrated by differential enrichment of canonical binding sites and gene ontology analyses. Pathway analysis revealed signatures of [[MYC]], CD3, and [[CD28]] regulation indicative of activation and proliferation, but also strong inhibition of cell death pathways. In silico analysis of discordantly expressed genes revealed Tnfsrf8/CD30, Cish, and Il13 among relevant targets for sustained proliferation and survival. Although [[TP53]] mRNA and protein levels were upregulated, its downstream targets in growth suppression and apoptosis were largely unperturbed. Analysis of genes encoding p53 posttranslational modifiers showed significant upregulation of three genes, Smyd2, Set, and Prmt5. Overexpression of [[SMYD2]] was validated in vivo but the functional analysis was constrained by in vitro loss of p53 in [[RUNX2]]/[[MYC]] lymphoma cell lines. However, an early role is suggested by the ability of [[SMYD2]] to block senescence-like growth arrest induced by RUNX overexpression in primary fibroblasts.
|mesh-terms=* Animals
* Blotting, Western
* Cell Line, Tumor
* Cell Proliferation
* Cellular Senescence
* Computational Biology
* Core Binding Factor Alpha 1 Subunit
* Histone-Lysine N-Methyltransferase
* Lymphoma
* Mice
* Mice, Transgenic
* Principal Component Analysis
* Proto-Oncogene Proteins c-myc
* Receptors, Antigen, T-Cell
* Signal Transduction
* Thymus Gland
* Tumor Suppressor Protein p53
|keywords=* MYC
* RUNX
* SMYD2
* lymphoma
* p53
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6772115
}}