推荐产品
product name
4-Hydroxytamoxifen Ready Made Solution, 5 mg/mL in ethanol: isopropanol (95:5)
生物源
synthetic
品質等級
形狀
solution
濃度
5 mg/mL in ethanol: isopropanol (95:5)
運輸包裝
dry ice
儲存溫度
−20°C
InChI
1S/C26H29NO2/c1-4-25(20-8-6-5-7-9-20)26(21-10-14-23(28)15-11-21)22-12-16-24(17-13-22)29-19-18-27(2)3/h5-17,28H,4,18-19H2,1-3H3/b26-25-
InChI 密鑰
TXUZVZSFRXZGTL-QPLCGJKRSA-N
生化／生理作用
4-羟基他莫昔芬是他莫昔芬的活性代谢产物。4-羟基他莫昔芬在人肝脏中由细胞色素 P450 2D6 形成，是一种强效选择性雌激素受体拮抗剂。4-羟基他莫昔芬用于刺激 LC3 脂化，并以超氧化物依赖的方式形成自噬囊泡。在原代培养的人肝细胞中，他莫昔芬和 4-羟基他莫昔芬显著诱导细胞色素 P450 3A4（一种主要的药物代谢酶）。4-羟基他莫昔芬经历反 (E-Z) 异构化—这一过程发生在所有常见的实验室溶剂中。
4-羟基他莫昔芬的反式 异构体具有抗雌激素活性，而 顺式 4-羟基他莫昔芬是雌激素受体的关键激动剂。4-羟基他莫昔芬通过激活 乳腺癌细胞中p38 通路促进凋亡。
準備報告
4-羟基他莫昔芬为 13 mM 溶液。推荐工作浓度为 10-100μM。因此，4-羟基他莫昔芬制备液应在细胞培养基中以 1:130-1:1,300 稀释。
訊號詞
Danger
危險分類
Aquatic Chronic 3 - Carc. 1B - Eye Irrit. 2 - Flam. Liq. 2 - Repr. 1B
儲存類別代碼
3 - Flammable liquids
水污染物質分類（WGK）
WGK 3
閃點（°F）
55.4 °F
閃點（°C）
13 °C
其他客户在看
Activation of the p38 mitogen-activated protein kinase pathway by estrogen or by 4-hydroxytamoxifen is coupled to estrogen receptor-induced apoptosis.
Zhang C C and Shapiro D J
The Journal of Biological Chemistry, 275(1), 479-486 (2000)
Characterization of tamoxifen and 4-hydroxytamoxifen glucuronidation by human UGT1A4 variants.
Sun D, et al.
Breast Cancer Research, 8(4), R50-R50 (2006)
Izumi Kaji et al.
JCI insight, 6(16) (2021-07-02)
Functional loss of myosin Vb (MYO5B) induces a variety of deficits in intestinal epithelial cell function and causes a congenital diarrheal disorder, microvillus inclusion disease (MVID). The impact of MYO5B loss on differentiated cell lineage choice has not been investigated.
Izumi Kaji et al.
Gastroenterology, 159(4), 1390-1405 (2020-06-15)
Myosin VB (MYO5B) is an essential trafficking protein for membrane recycling in gastrointestinal epithelial cells. The inactivating mutations of MYO5B cause the congenital diarrheal disease, microvillus inclusion disease (MVID). MYO5B deficiency in mice causes mislocalization of SGLT1 and NHE3, but
Jinming Zhao et al.
iScience, 24(12), 103425-103425 (2021-12-09)
We previously showed stabilization of NIK-induced activation of NF-κB non-canonical signaling suppresses MLL-AF9-induced AML. In the current study, we demonstrate that deletion of NF-κB non-canonical RelB prevents the inhibitory effect of NIK stabilization in MLL-AF9 AML. Mechanistically, RelB suppresses its
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