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化驗
≥98% (HPLC)
形狀
powder
顏色
white to beige
溶解度
DMSO: >5 mg/mL
儲存溫度
2-8°C
SMILES 字串
O=C(NC1=CC=CC2=C1C=CC=C2)OCC3=CC=C(CNCCCCN(O)C(/C=C/C(OC)=O)=O)C=C3
InChI
1S/C28H31N3O6/c1-36-27(33)16-15-26(32)31(35)18-5-4-17-29-19-21-11-13-22(14-12-21)20-37-28(34)30-25-10-6-8-23-7-2-3-9-24(23)25/h2-3,6-16,29,35H,4-5,17-20H2,1H3,(H,30,34)/b16-15+
InChI 密鑰
MUJOCHRZXRZONW-FOCLMDBBSA-N
生化／生理作用
Methylstat is an inhibitor of the Jumonji C domain-containing histone trimethyl demethylases (JHDMs).
Methylstat is an inhibitor of the Jumonji C domain-containing histone trimethyl demethylases (JHDMs). Methylstat inhibits the activity of JMJD2C (IC50 = 4.3 μM), with similar potency against JMJD2E and JMJD3. The compound has poor activity against dimethyl demethylases, and does not inhibit class I or II HDACs. Methylsat blocks proliferation of the esophageal carcinoma cell line KYSE150 with an IC50 value of 5.1 μM.
儲存類別代碼
11 - Combustible Solids
水污染物質分類（WGK）
WGK 3
閃點（°F）
Not applicable
閃點（°C）
Not applicable
Alexandre Fellous et al.
Genes, 10(9) (2019-09-13)
Histone methylation patterns are important epigenetic regulators of mammalian development, notably through stem cell identity maintenance by chromatin remodeling and transcriptional control of pluripotency genes. But, the implications of histone marks are poorly understood in distant groups outside vertebrates and
Qingsong Hu et al.
Nature immunology, 20(7), 835-851 (2019-06-05)
How tumor cells genetically lose antigenicity and evade immune checkpoints remains largely elusive. We report that tissue-specific expression of the human long noncoding RNA LINK-A in mouse mammary glands initiates metastatic mammary gland tumors, which phenotypically resemble human triple-negative breast
Qingsong Hu et al.
Cell research, 29(4), 286-304 (2019-01-12)
Despite the structural conservation of PTEN with dual-specificity phosphatases, there have been no reports regarding the regulatory mechanisms that underlie this potential dual-phosphatase activity. Here, we report that K27-linked polyubiquitination of PTEN at lysines 66 and 80 switches its phosphoinositide/protein
Wenyu Wang et al.
The Journal of experimental medicine, 215(11), 2833-2849 (2018-09-30)
PTEN deficiency in breast cancer leads to resistance to PI3K-AKT inhibitor treatment despite aberrant activation of this signaling pathway. Here, we report that genetic depletion or small molecule inhibition of KDM4B histone demethylase activates the unfolded protein response (UPR) pathway
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