-
Study shows a significant association between the methylation status of CpGs in the SMYD2 promoter and SMYD2 gene decreased expression in abdominal aortic aneurysm.
-
We found that SMYD2 expression was significantly related to tumor size (P<0.001), lymph node metastasis (P<0.005), and TNM stage (P<0.005). However, no correlations were found between SMYD2 expression and patient age, sex, thyroid capsular invasion (TCI), or extrathyroidal extension (all P>0.05).
-
We show that tool compounds as well as CRISPR/Cas9 fail to reproduce many of the cell proliferation findings associated with SMYD2 and SMYD3 inhibition previously obtained with RNAi based approaches and with early stage chemical probes.
-
Lysine methylation represses p53 activity in teratocarcinoma cancer cells via up-regulation of SMYD2 and PR-Set7 and perpetuation of cancer cells proliferation.
-
SMYD2-H4K20me1-L3MBTL1 axis contributes to HIV-1 latency and can be targeted with small-molecule SMYD2 inhibitors.
-
identifie novel cellular substrates of the lysine methyltransferase SMYD2. Of the 14 novel putative SMYD2 substrates identified, six were confirmed in cells by immunoprecipitation: MAPT, CCAR2, EEF2, NCOA3, STUB1, and UTP14A. Treatment with the selective SMYD2 inhibitor BAY-598 abrogated the methylation signal, indicating that methylation of these novel substrates was dependent on the catalytic activity of SMYD2
-
The SMYD2 may promote BMP signaling by directly methylating BMPR2, which, in turn, stimulates BMPR2 kinase activity and activation of the BMP pathway.
-
Knockdown of SMYD2 as well as treatment with a SMYD2 inhibitor in two NSCLC cell lines with an EML4-ALK gene significantly attenuated the phosphorylation levels of the EML4-ALK protein.
-
SMYD2 knockdown confers relative resistance to human AML cells against multiple classes of DNA damaging agents.
-
Substrate crevices of Smyd2 and Smyd3 show distinct features in terms of spatial, hydration, and electrostatic properties that emphasize their characteristic modes of substrates interaction and entry pathways for inhibitor binding.
-
High expression of SMYD2 is associated with chronic lymphocytic leukemia.
-
Study reveals a collection of 10 enriched sequence motifs in Kme1 sites that were identified upon SMYD2 overexpression which were also downregulated in response to SMYD2 knockdown. These findings suggest that these motifs reflect the substrate specificity of SMYD2 in esophageal squamous cell carcinoma cell line.
-
Results show that high expression levels of SMYD2, SETD3, and NO66 in renal cell tumors. Their low expression levels were significantly associated with shorter disease-specific and disease-free survival.
-
Suggest that SMYD2 plays a role in tumor progression and might be a useful prognosticator in HPV-unrelated, nonmultiple head and neck squamous cell carcinomas.
-
SMYD2-mediated methylation negatively regulates PTEN tumor suppressor activity and results in activation of the phosphatidylinositol 3-kinase-AKT pathway.
-
Comprehensive motif-based searches and mutational analysis further established four additional substrates of SMYD2.
-
in addition to esophageal squamous cell carcinoma, SMYD2 is also amplified and/or overexpressed in breast and liver primary tumors
-
a novel mechanism of PARP1 in human cancer through its methylation by SMYD2
-
SMYD2 has a crucial role in tumor cell proliferation by its overexpression and highlight its usefulness as a prognostic factor and potential therapeutic target in gastric cancer.
-
Data indicate that irect estrogen receptor alpha (ERalpha) methylation by histone methyltransferase SMYD2 regulates estrogen signaling.
