SET Domain Containing (Lysine Methyltransferase) 8 Proteine (SETD8)

Human SET Domain Containing (Lysine Methyltransferase) 8 (SETD8) Interaktionspartner

1. Results suggest that SET domain-containing protein 8 (SET8) may be a key mediator in hyperglycemic memory.

2. that oncogenic SETD8 was regulated by miR-382 and involved glioma progression

3. Data found that KMT5A was overexpressed in papillary thyroid carcinoma (PTC) tumors. Its knockdown revealed that KMT5A participated in the proliferation, apoptosis, cell cycle, migration and invasion of PTC cells as well as attenuated fatty acid metabolism. These results provide mounting evidence of KMT5A as an oncogenic mediator in fatty acid metabolism of PTC.

4. Authors demonstrated that PR-Set7, an epigenetic regulator for H4K20me1 modification, was extensively expressed in the postnatal uteri, and its conditional deletion resulted in a complete lack of endometrial glands and infertility in mice.

5. MiR-502 medaited histone methyltransferase SET8 expression is associated with outcome of esophageal squamous cell carcinoma.

6. these date elucidated that NT21MP and miR335 mediated PR of breast cancer cells partly through regulation of Wnt/betacatenin signaling pathway. Activation of miR335 or inactivation of SETD8 could be a novel approach for the treatment of breast cancer.

7. High expression of SET8 is associated with cervical cancer.

8. This improves the binding of SAM, SAH, and sinefungin by up to 10,000-fold. A small collection of inhibitors structurally related to SAM were screened and 40 compounds were identified that only inhibit SETD8 when a nucleosome substrate is used

9. We demonstrated the expression levels of SET8 in TT genotype were higher than in CC genotypes, and high levels of SET8 were associated with poor survival in breast cancer

10. Lysine methylation represses p53 activity in teratocarcinoma cancer cells via up-regulation of SMYD2 and PR-Set7 and perpetuation of cancer cells proliferation.

11. The loss of SETD8 concurrently stimulated nucleolar function.

12. The PPARgamma-SETD8 axis constitutes an epigenetic, p53-independent checkpoint on p21-mediated cellular senescence.

13. rs16917496 polymorphism may be a risk for predisposition to prostate cancer in an Iranian population.

14. miR-502/SET8 regulatory circuit emerges as a key regulator of the pathobiology of breast cancer and a focal point for possible therapeutic intervention.

15. In non-small cell lung cancer cells, SETD8 expression suppression is involved in tumorigenesis and metastasis.

16. SET8 and ZEB1 are functionally interdependent in promoting the epithelial-mesenchymal transition and enhancing the invasive potential of prostate cancer cells in vitro.

17. SET8 expression is associated with overall survival in gastric cancer

18. analysis of a structural model for how Set8 uses multivalent interactions to bind and methylate the nucleosome based on crystallographic and solution studies of the Set8/nucleosome complex

19. This study showed SCF(beta-TRCP) earmarks Set8 for ubiquitination and degradation in a casein kinase I-dependent manner, which is activated by DNA-damaging agents.

20. Overall, the results revealed that miR-127-3p acts as a tumor suppressor and that its down-regulation in cancer may contribute to OS progression and metastasis.

Mouse (Murine) SET Domain Containing (Lysine Methyltransferase) 8 (SETD8) Interaktionspartner

1. KMT5a was identified as a target gene that was down-regulated in both mRNA and protein level when miR-127-3p mimics were introduced. miR-127-3p regulates the proliferation of myocytes through KMT5a.

2. Authors demonstrated that PR-Set7, an epigenetic regulator for H4K20me1 modification, was extensively expressed in the postnatal uteri, and its conditional deletion resulted in a complete lack of endometrial glands and infertility in mice.

3. PR-Set7 is a direct target of Cul4A for degradation and involved in the formation of lung tumors in the conditional Cul4A transgenic mouse model.

4. These results suggest that Setd8 is an important regulator of erythroid maturation that works in part through repression of Gata2 expression.

5. These results establish SetD8 as a determinant of erythroid cell maturation and provide a framework for understanding how a broadly expressed histone-modifying enzyme mediates cell-type-specific GATA factor function.

6. all of the H3K36-specific methyltransferases, including ASH1L, HYPB, NSD1, and NSD2 were inhibited by ubH2A, whereas the other histone methyltransferases, including PRC2, G9a, and Pr-Set7 were not affected by ubH2A.

7. Data indicate a vital link between GATA-1 and the histone H4 lysine 20 methyltransferase PR-Set7/SetD8 (SetD8).

8. Pr-set7 knockdown caused increased gammaH2AX foci on chromosomes indicating DNA damage on chromosomes.

9. Setd8 is a crucial inhibitor of apoptosis in skin and its activity is essential for epidermal stem cell survival, proliferation and differentiation

10. the SET8 and PCNA interaction couples H4-K20 methylation with DNA replication

11. PR-Set7 enzymatic activity is essential for mammalian cell cycle progression and for the maintenance of genomic stability, most likely by monomethylating histone H4K20.

12. Cell cycle analysis after synchronization indicated that defects at the S and G(2)/M phases were a consequence of decreased H4K20me1 due to the absence of PR-Set7.

13. Data show that the peroxisome proliferator-activated receptor gamma/retinoid X receptor alpha heterodimer targets the histone modification enzyme PR-Set7/Setd8 gene and regulates adipogenesis through a positive feedback loop.