HIF-1 alpha 556-574
CAS No. 1201633-99-9
HIF-1 alpha 556-574 ( —— )
产品货号. M30232 CAS No. 1201633-99-9
HIF-1 alpha (556-574) is a hypoxia-inducible factor-1 19-mer fragment. HIF-1 functions as master regulator of response to oxygen homeostasis. Hypoxia-induced gene expression is initiated when HIF-1subunit is stabilized in response to a lack of oxygen. This part of HIF-1 binds to the von Hippel-Lindau factor (VHL) an E3 ubiquitin ligase, and the proline 564 is absolutely vital to the binding process.
纯度: >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
规格 | 价格/人民币 | 库存 | 数量 |
100MG | 获取报价 | 有现货 |
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200MG | 获取报价 | 有现货 |
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500MG | 获取报价 | 有现货 |
|
100MG | 获取报价 | 有现货 |
|
200MG | 获取报价 | 有现货 |
|
500MG | 获取报价 | 有现货 |
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生物学信息
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产品名称HIF-1 alpha 556-574
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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HIF-1 alpha (556-574) is a hypoxia-inducible factor-1 19-mer fragment. HIF-1 functions as master regulator of response to oxygen homeostasis. Hypoxia-induced gene expression is initiated when HIF-1subunit is stabilized in response to a lack of oxygen. This part of HIF-1 binds to the von Hippel-Lindau factor (VHL) an E3 ubiquitin ligase, and the proline 564 is absolutely vital to the binding process.
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产品描述HIF-1 alpha (556-574) is a hypoxia-inducible factor-1 19-mer fragment. HIF-1 functions as master regulator of response to oxygen homeostasis. Hypoxia-induced gene expression is initiated when HIF-1subunit is stabilized in response to a lack of oxygen. This part of HIF-1 binds to the von Hippel-Lindau factor (VHL) an E3 ubiquitin ligase, and the proline 564 is absolutely vital to the binding process.
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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——
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研究领域——
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适应症——
化学信息
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CAS Number1201633-99-9
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分子量2254.6
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分子式C101H150D2N20O34S2
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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Sequence:{Asp}{Leu}{Asp}{Leu}{Glu}{Met}{Leu}{Ala}{Pro}{Tyr}{Ile}{Pro}{Met}{Asp}{Asp}{Asp}{Phe}{Gln}{Leu}
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
Ehrismann D, et al. Studies on the activity of the hypoxia-inducible-factor hydroxylases using an oxygen consumption assay. Biochem J. 2007 Jan 1;401(1):227-34.
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