anti-Suppressor of Variegation 3-9 Homolog 2 (Drosophila) (SUV39H2) 抗体

Human Suppressor of Variegation 3-9 Homolog 2 (Drosophila) (SUV39H2) interaction partners

1. SUV39H2 elevation contributes to the progression of nasopharyngeal carcinoma via regulation of NRIP1

2. Results discovered that SUV39H2 is a potential oncogene in lung adenocarcinoma, whose expression was elevated in tumor tissues. SUV39H2 could potentiate the tumorigenesis and invasion of lung adenocarcinoma cells, probably by repressing OPTN and STOM.

3. Study revealed that high SUV39H2 expression positively predicted poor prognosis of CRC patients. Moreover, SUV39H2 promoted CRC proliferation in a SLIT1-dependent manner.

4. Knockdown of SUV39H2 expression by specific siRNAs in human osteosarcoma cell lines markedly suppressed cancer cell growth and caused an increase in the population of cells in G1 phase and induced apoptosis. Overexpression of SUV39H2 promoted cell proliferation, which indicated that SUV39H2 may possess oncogenic activity in human osteosarcoma.

5. Our finding unveils a novel autoregulatory mechanism of SUV39H2 through lysine automethylation

6. Our data show that the differential expression of SUV39H1 and SUV39H2 is associated with genomic instability and that the modulation of these HMTases can be an attractive approach to prevent CLL evolution

7. SUV39H2 functioned cooperatively with MAGE-A11 to increase androgen-dependent AR transcriptional activity.

8. histone H3 lysine 9 methylation reduction, which may be due to the downregulation of methyltransferase SUV39H2 and the upregulation of demethylase KDM4C, was found in CD4(+) T lymphocytes of Latent autoimmune diabetes in adults patients

9. data cannot finally exclude H2AX methylation of SUV39H2 in cells, additional experimental evidence is required to validate this claim.

10. Our results reveal the regulatory mechanism of LSD1 protein through its lysine methylation by SUV39H2 in human cancer cells

11. We also demonstrate that the N324K mutant in the SET domain of SUV39H2 that has been shown to cause an inherited nasal skin disease in Labrador Retrievers renders SUV39H2 inactive

12. Expression of JHDM2A was significantly increased but HDAC2, HDAC7, and SUV39H2 were significantly down-regulated in Systemic Sclerosis B cells relative to controls

13. genetic association studies in a Finnish population with type I diabetes: The minor T allele of exonic SNP rs17353856 in SUV39H2 is associated with diabetic retinopathy (in a larger meta-analysis); thus an genetic variation may be protective.

14. findings suggest that Suv39H1 and Suv39H2 are key hypoxia-induced methyltransferases; their decline in fetal lung during late gestation is critical for epigenetic changes resulting in the developmental induction of SP-A

15. a novel SUV39H2 polymorphism may have a role in lung cancer susceptibility for smokers

16. The SUV39H2 gene is found in tetrapods (e.g., human, mouse and frog) but not in zebrafish, suggesting that this gene is generated by a tetrapod lineage-specific gene duplication event.

Mouse (Murine) Suppressor of Variegation 3-9 Homolog 2 (Drosophila) (SUV39H2) interaction partners

1. The authors show here that the mouse Suv39h2 enzyme differs from Suv39h1 by containing an N-terminal basic domain that facilitates retention at mitotic chromatin and provides an additional affinity for major satellite repeat RNA.

2. Data indicate that histone methyltransferase Suv39h2 expression is up-regulated in the liver in liver steatosis.

3. Repeat-associated, Suv39h-dependent H3K9me3 displays a dynamic distribution that differs in the epigenome of pluripotent versus more committed cells.

4. ESET histone methyltransferase can form a large, multi-protein complex(es) with mSin3A/B co-repressors and HDAC1/2 that participates in multiple pathways of transcriptional repression.

5. Taken together, the results indicate epigenetic regulation of telomere length in mammals by Suv39h1 and Suv39h2.

Pig (Porcine) Suppressor of Variegation 3-9 Homolog 2 (Drosophila) (SUV39H2) interaction partners

1. Knockdown of SUV39H1 and SUV39H2 in embryonic stem-like cells and embryonic fibroblasts increases telomere length.