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

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

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

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

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

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

6. 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

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

8. The loss of SETD8 concurrently stimulated nucleolar function.

9. The PPARgamma (zeige PPARG Proteine)-SETD8 axis constitutes an epigenetic, p53 (zeige TP53 Proteine)-independent checkpoint on p21 (zeige CDKN1A Proteine)-mediated cellular senescence.

10. miR (zeige MLXIP Proteine)-502/SET8 regulatory circuit emerges as a key regulator of the pathobiology of breast cancer and a focal point for possible therapeutic intervention.

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

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 (zeige CUL4A Proteine) for degradation and involved in the formation of lung tumors in the conditional Cul4A (zeige CUL4A Proteine) transgenic mouse model.

3. These results suggest that Setd8 is an important regulator of erythroid maturation that works in part through repression of Gata2 (zeige GATA2 Proteine) 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 (zeige ASH1L Proteine), HYPB, NSD1, and NSD2 (zeige WHSC1 Proteine) were inhibited by ubH2A, whereas the other histone methyltransferases, including PRC2, G9a (zeige EHMT2 Proteine), and Pr-Set7 were not affected by ubH2A.

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

7. Pr-set7 knockdown caused increased gammaH2AX (zeige H2AFX Proteine) 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 (zeige PCNA Proteine) interaction couples H4-K20 (zeige KRT20 Proteine) 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.