Hepcidin-1 (mouse) trifluoroacetate salt
CAS No. 1676104-75-8
Hepcidin-1 (mouse) trifluoroacetate salt ( ——— )
产品货号. M41734 CAS No. 1676104-75-8
Hepcidin-1 (mouse) 是一种参与铁稳态调节的内源性肽激素。Hepcidin-1 (mouse) 上调 TRAP、组织蛋白酶 K 和 MMP-9 的 mRNA 水平并增加 TRAP-5b 蛋白分泌。Hepcidin-1 (mouse) 下调 FPN1 蛋白水平并增加细胞内铁。Hepcidin-1 (mouse) 促进破骨细胞分化。
纯度: >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
| 规格 | 价格/人民币 | 库存 | 数量 |
| 25MG | 获取报价 | 有现货 |
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| 50MG | 获取报价 | 有现货 |
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| 100MG | 获取报价 | 有现货 |
|
生物学信息
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产品名称Hepcidin-1 (mouse) trifluoroacetate salt
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注意事项本公司产品仅用于科研实验,不得用于人体或动物的临床与诊断
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产品简述Hepcidin-1 (mouse) 是一种参与铁稳态调节的内源性肽激素。Hepcidin-1 (mouse) 上调 TRAP、组织蛋白酶 K 和 MMP-9 的 mRNA 水平并增加 TRAP-5b 蛋白分泌。Hepcidin-1 (mouse) 下调 FPN1 蛋白水平并增加细胞内铁。Hepcidin-1 (mouse) 促进破骨细胞分化。
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产品描述Hepcidin-1 (mouse) is an endogenous peptide hormone involved in the regulation of iron homeostasis. Hepcidin-1 (mouse) upregulates mRNA levels of TRAP, cathepsin K, and MMP-9 and increases TRAP-5b protein secretion. Hepcidin-1 (mouse) downregulates the level of FPN1 protein and increases intracellular iron. Hepcidin-1 (mouse) facilitates osteoclast differentiation.
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体外实验———
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体内实验Hepcidin-1 mouse (200-800 nM,4 天) 促进 RANKL (50 ng/mL) 诱导的 raw264.7 细胞分化。Hepcidin-1 mouse (0-800 nM,4 天) 上调 TRAP、CTK 和 MMP-9 mRNA 的表达。Hepcidin-1 mouse (0-800 nM,20 小时) 会增加 RAW264.7 细胞中 Trap-5b 蛋白的水平并降低铁转运蛋白 1 (FPN1) 蛋白。Western Blot Analysis Cell Line:RAW264.7 cells Concentration:0, 200, 400, or 800 nM Incubation Time:20 h Result:Decreased Ferroportin 1 (FPN1) protein.Real Time qPCR Cell Line:RAW264.7 cells Concentration:0, 200, 400, or 800 nM Incubation Time:4 days Result:Increased the gene expression of TRAP, CTK, and MMP-9 in a dose-dependent manner.
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同义词———
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通路Others
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靶点Other Targets
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受体MMP-9, cathepsin K
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研究领域———
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适应症———
化学信息
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CAS Number1676104-75-8
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分子量2754.28
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分子式C111H169N31O35S8
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纯度>98% (HPLC)
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溶解度———
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SMILES———
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化学全称———
运输与储存
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储存条件(-20℃)
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运输条件With Ice Pack
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稳定性≥ 2 years
参考文献
1. Zhao GY, et al. Effects of mouse hepcidin 1 treatment on osteoclast differentiation and intracellular iron concentration. Inflammation. 2015 Apr;38(2):718-27.?
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