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SMYD2 specificly regulate BIX-01294 induced TP53 target genes revealed by RNA-Seq

ABSTRACT: We characterized expression profilings of SMYD2 knockdown and control cells treated by BIX-01294 and Rapamycin. We used siRNAs to knockdown SMYD2 in HCT116 cells, and NC as control. We treated those cell lines with BIX-01294 and Rapamycin, and the expression profilings were perfomed by Illumina high throughput sequencing.

ORGANISM(S): Homo sapiens

SUBMITTER: Min Wu

PROVIDER: E-GEOD-61255 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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SMYD2 specificly regulate BIX-01294 induced TP53 target genes revealed by RNA-Seq

Project description:We characterized expression profilings of SMYD2 knockdown and control cells treated by BIX-01294 and Rapamycin.

2015-01-01 | GSE61255 | GEO

The effects of SMYD2 overexpression on ectopic RB in SAOS cells

Project description:Expression analysis of wild-type SAOS cells and SAOS cells transiently transfected with RB, SMYD2, or RB and SMYD2.

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Genome-wide maps of chromatin state of Smyd2 binding in renal epithelial cells

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Quantitative profiling of the enzymatic activity of the protein lysine mono-methyltransferase SMYD2 using SILAC-based proteomics

Project description:The significance of non-histone lysine methylation in cell biology and human disease is an emerging area of research exploration, and small molecule inhibitors that selectively and potently target “writers” and “erasers” of methyl-lysine, such as the protein lysine mono-methyltransferase SMYD2, are active areas of drug discovery. It is therefore essential to clarify the substrates of these enzymes in cellular contexts in order to advance and to correctly understand the cellular mechanism(s) of action of these targets. Here, using stable isotopic labelling of amino acids in cell culture (SILAC) coupled with immunoaffinity enrichment of mono-methyl-lysine (Kme1) peptides and mass spectrometry, we report the most comprehensive and large-scale proteomic study of protein mono-methylation, comprising a total of 1032 Kme1 sites identified in esophageal squamous cell carcinoma (ESCC) cells and 1861 Kme1 sites in ESCC cells overexpressing SMYD2. Among these sites was a subset of 35 robust Kme1 sites that were potently down-regulated by both shRNA-mediated knockdown of SMYD2 and LLY-507, a small molecule inhibitor of SMYD2. In addition, we report specific protein sequence motifs that were enriched in Kme1 sites and that were also directly regulated by endogenous SMYD2 activity, indicating that the diversity of SMYD2 substrate specificity of SMYD2 exceeds previous expectations. Furthermore, we reveal that BTF3 and PDAP1 are novel and direct substrates of SMYD2, as well as AHNAK and AHNAK2, two large and highly-repetitive proteins directly and extensively mono-methylated by SMYD2 at several lysine residues. Collectively, our findings provide novel quantitative and insights into the cellular activity and substrate recognition of SMYD2 as well as the global landscape and regulation of protein mono-methylation in cells.

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Methylation of the epigenetic regulator KMT2D by SMYD2 contributes to therapeutic response in hormone-dependent breast cancer [KMT2D_KI_RNA]

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Methylation of the epigenetic regulator KMT2D by SMYD2 contributes to therapeutic response in hormone-dependent breast cancer [SMYD2_KD_RNA]

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Transcription profiling of human embryonic kidney cells overexpressing SMYD2 to identify which genes are regulated by SMYD2 through its histone lysine methylation activity

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