anti-SET Domain Containing (Lysine Methyltransferase) 7 (SETD7) Antibodies

Human SET Domain Containing (Lysine Methyltransferase) 7 (SETD7) interaction partners

1. Setd7 knockdown decreases Nrf2 and Nrf2-target genes expression, and phenethyl isothiocyanate and ursolic acid induce Setd7 expression, which activates the Nrf2/antioxidant response element signaling pathway and protects DNA from oxidative damage.

2. Setd7 KD impacted a larger set of genes and caused a higher fold change compared to PEITC treatment. This study offers new insights into the mechanisms of action of the epigenetic modifier Setd7 and the effects of PEITC treatment in PCa cells and enhances our understanding of the potential cancer preventive/treatment effects of isothiocyanate compounds such as PEITC in PCa.

3. High SET7 expression is associated with hepatocellular carcinoma progression.

4. SET7/9 expression in nonadherent cells isolated from the effluent of peritoneal dialysis (PD) patients. SET7/9 expression was elevated in nonadherent cells isolated from the effluent of PD patients. SET7/9 expression was positively correlated with dialysate/plasma ratio of creatinine in PD patients.

5. Methylation at K436 and K595 respectively by Set7 increases the stability and DNA binding ability of Gli3, resulting in an enhancement of Shh signaling activation.

6. the methyltransferase Set9 potentiates TGF-beta signaling by targeting Smad7, an inhibitory downstream effector.

7. SET9 expression levels were significantly higher in samples from patients with pathological complete remission than in samples from patients with disease recurrence, which indicates that SET9 acts as a tumor suppressor in breast cancer and that its expression may serve as a prognostic marker for malignancy.

8. SETD7 plays a critical role in HCC, and its immunohistochemistry signature provides potential clinical significance for personalized prediction of HCC prognosis.

9. These findings underscore the role of KMT7 as an important monomethyltransferase regulating HIV transcription through Tat.

10. High SET7 expression is associated with breast cancer.

11. SET7 was required for GATA1-induced breast tumor angiogenesis and growth in nude mice. GATA1 and SET7 are independent poor prognostic factors in breast cancer.

12. SET7/SET9-mediated YY1 methylation was shown to be involved in YY1-regulated gene transcription and cell proliferation.

13. These results demonstrate that S...O chalcogen bonds contribute to AdoMet recognition and can enable methyltransferases to distinguish between substrate and product.

14. Reduced expression of SET7 is associated with gastric cancer progression.

15. study identified a novel locus associated with serum lycopene concentrations and results raise a number of possibilities regarding the nature of the relationship between SETD7 and lycopene, both independently associated with prostate cancer.

16. Lysine methylation by SETD7 is important for the fine-tuning of reactive oxygen species signaling through its regulation on pro-inflammatory responses.

17. Knock-down of SETD7 causes differentiation defects in human embryonic stem cell including delay in both the silencing of pluripotency-related genes and the induction of differentiation genes.

18. Unleashed expression of Mdm2 in cancer patients with diminished expression of Set7/9 is associated with poor survival outcome.

19. Based on our results miR-153 inhibits proliferation and suppresses EMT and the invasive potential of ovarian cancer cells through downregulation of SET7 and ZEB2, supporting the pursuit of miR-153 as a potential target for ovarian cancer intervention.

20. Findings indicate the regulation of Wnt/beta-catenin signaling and the role of SET domain-containing protein 7/9 (SET7/9) in cancer cells.

Mouse (Murine) SET Domain Containing (Lysine Methyltransferase) 7 (SETD7) interaction partners

1. Murine peritoneal fibrosis was induced by intraperitoneal injection of methylglyoxal (MGO). SET7/9 expression was elevated in MGO-injected mice.

2. spinal SET7/9 may contribute to the maintenance of CIBP

3. the methyltransferase Set9 potentiates TGF-beta signaling by targeting Smad7, an inhibitory downstream effector.

4. SETD7 plays an important role in intestinal epithelial cell (IEC) biology during infection.

5. We observe Set7-mediated modification of serum response factor (SRF) and mono-methylation of histone H4 lysine 4 (H3K4me1) regulate gene expression. We conclude the broad substrate specificity of Set7 serves to control key transcriptional networks in embryonic stem cells.

6. SETD7 is required for Wnt-driven intestinal tumorigenesis and regeneration. SETD7-dependent methylation of YAP facilitates Wnt-induced nuclear accumulation of beta-catenin.

7. SET7/9 regulates Nos2 expression through methylation of H3K4 in beta cells.

8. Data indicate that the ability of transcription factor Pdx1 to regulate genes in beta cells is partially dependent upon its methylation by methyltransferase Set7/9.

9. study found that Set7 is a modifier of the Hippo pathway. Mice that lack Set7 have a larger progenitor compartment in the intestine, coinciding with increased expression of Yes-associated protein target genes.

10. The response to hyperglycemia in vascular endothelial cells involves Set7 mediated changes in chromatin remodeling and gene expression.

11. Set7/9-mediated methylation of p53 does not represent a major regulatory event and does not appreciably control p53 activity in vivo.

12. Set7/9 is dispensable for p53 function in the mouse.

13. Define a biological function for Set7 in muscle differentiation and provide a molecular mechanism by which Set7 modulates myogenic transcription factors during muscle differentiation.

14. Pdx1-dependent Set7/9 expression may be crucial to enhancing chromatin accessibility and transcription of beta-cell genes.

15. Methylation of p53 by Set7 mediates p53 acetylation and activity in vivo.

16. a novel role for SET7/9 in inflammation and diabetes.

17. Data conclude that Set7/9 is required for normal beta-cell function, likely through the maintenance of euchromatin structure at genes necessary for glucose-stimulated insulin secretion.

18. ASCOM-MLL3 and ASCOM-MLL4 likely function as crucial but redundant H3K4MT complexes for PPARgamma-dependent adipogenesis