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

Human SET Domain Containing (Lysine Methyltransferase) 8 (SETD8) interaction partners

1. Data found that KMT5A was overexpressed in papillary thyroid carcinoma (PTC (show F9 Proteins)) tumors. Its knockdown revealed that KMT5A participated in the proliferation, apoptosis, cell cycle, migration and invasion of PTC (show F9 Proteins) 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 (show F9 Proteins).

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. MiR (show MLXIP Proteins)-502 medaited histone methyltransferase SET8 expression is associated with outcome of esophageal squamous cell carcinoma.

4. these date elucidated that NT21MP and miR335 mediated PR of breast cancer cells partly through regulation of Wnt (show WNT2 Proteins)/betacatenin signaling pathway. Activation of miR335 or inactivation of SETD8 could be a novel approach for the treatment of breast cancer.

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

6. This improves the binding of SAM (show TTN Proteins), SAH (show ACSM3 Proteins), and sinefungin by up to 10,000-fold. A small collection of inhibitors structurally related to SAM (show TTN Proteins) were screened and 40 compounds were identified that only inhibit SETD8 when a nucleosome substrate is used

7. 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

8. Lysine methylation represses p53 (show TP53 Proteins) activity in teratocarcinoma cancer cells via up-regulation of SMYD2 (show SMYD2 Proteins) and PR-Set7 and perpetuation of cancer cells proliferation.

9. The loss of SETD8 concurrently stimulated nucleolar function.

10. The PPARgamma (show PPARG Proteins)-SETD8 axis constitutes an epigenetic, p53 (show TP53 Proteins)-independent checkpoint on p21 (show CDKN1A Proteins)-mediated cellular senescence.

Mouse (Murine) SET Domain Containing (Lysine Methyltransferase) 8 (SETD8) interaction partners

1. 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.

2. PR-Set7 is a direct target of Cul4A (show CUL4A Proteins) for degradation and involved in the formation of lung tumors in the conditional Cul4A (show CUL4A Proteins) transgenic mouse model.

3. These results suggest that Setd8 is an important regulator of erythroid maturation that works in part through repression of Gata2 (show GATA2 Proteins) expression.

4. 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.

5. all of the H3K36-specific methyltransferases, including ASH1L (show ASH1L Proteins), HYPB, NSD1, and NSD2 (show WHSC1 Proteins) were inhibited by ubH2A, whereas the other histone methyltransferases, including PRC2, G9a (show EHMT2 Proteins), and Pr-Set7 were not affected by ubH2A.

6. Data indicate a vital link between GATA-1 (show GATA1 Proteins) and the histone H4 lysine 20 methyltransferase PR-Set7/SetD8 (SetD8).

7. Pr-set7 knockdown caused increased gammaH2AX (show H2AFX Proteins) foci on chromosomes indicating DNA damage on chromosomes.

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

9. the SET8 and PCNA (show PCNA Proteins) interaction couples H4-K20 (show KRT20 Proteins) methylation with DNA replication

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