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1)  Extracellular matrix metalloproteinase inducer
细胞外基质金属蛋白酶诱导因子
1.
Expression of extracellular matrix metalloproteinase inducer and matrix metalloproteinase-2 protein in human cervical squamous cell carcinoma tissue;
人宫颈鳞状细胞癌组织中细胞外基质金属蛋白酶诱导因子、基质金属蛋白酶-2蛋白的表达
2.
Relationship between extracellular matrix metalloproteinase inducer and clinical type of coronary heart disease
细胞外基质金属蛋白酶诱导因子与冠心病临床类型的关系
3.
Expressions and their significance of extracellular matrix metalloproteinase inducer mRNA and laminin receptor mRNA in human gliomas
细胞外基质金属蛋白酶诱导因子和层黏连蛋白受体在人脑胶质瘤中的表达及意义
2)  EMMPRIN
细胞外基质金属蛋白酶诱导因子
1.
Objective The study was aimed to investigate the extracellular matrixmetalloproteinase inducer expression(EMMPRIN) in lymphoma,as well as its clinical significance and relation to matrix metalloproteinases(MMPs) expression.
目的探讨恶性淋巴瘤中细胞外基质金属蛋白酶诱导因子(EMMPRIN)的表达及其与基质金属蛋白酶(MMPs)表达和疾病进展的关系。
2.
[Objective]EMMPRIN is a regular of MMPs , it has been poorly represented in literature about the expression pattern and regulation of EMMPRIN in end- ometriosis.
【目的】作为基质金属蛋白酶(MMPs)的上调因子,细胞外基质金属蛋白酶诱导因子(EMMPRIN)是否也参与了子宫内膜异位症(EMs)的发生报道尚少。
3)  Extracellular Matrix Metalloproteinase(EMMPRIN/CD147)
细胞外基质金属蛋白酶诱导因子(EMMPRIN/CD147)
4)  EMMPRIN
细胞外基质金属蛋白酶诱导物
1.
Resveratrol inhibits expression of EMMPRIN from macrophages;
白藜芦醇抑制巨噬细胞细胞外基质金属蛋白酶诱导物的表达
5)  extracellular matrix metalloproteinase
细胞外基质金属蛋白酶
1.
Objective To analyze the relationship of extracellular matrix metalloproteinase inducer (EMMPRIN) and the type of tumor pathology and the ways of metastasis.
目的探讨大肠癌组织中细胞外基质金属蛋白酶诱导因子 (extracellularmatrixmetalloproteinaseinduc er,EMMPRIN)的表达与肿瘤病理类型和转移方式的关系。
6)  extracellular matrix metalloproteinase inducer
基质金属蛋白酶诱导因子
1.
Objective To investigate the expression and clinical impact of membrane-type 1 matrix metalloproteinase(MT1-MMP) and extracellular matrix metalloproteinase inducer(EMMPRIN) in hepatocellular carcinoma(HCC).
目的研究基质金属蛋白酶诱导因子(EMMPRIN)和模型金属蛋白酶1(MT1-MMP)在肝细胞肝癌中的表达及其与肝癌临床病理生物学行为之间的关系。
补充资料:酶诱导
分子式:
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性质:对一种诱导物起反应而合成一种诱导酶的过程。当酶的诱导物存在时,诱导物与阻遏物结合,使阻遏物纯化失去活力,阻止了阻遏物对操纵基因的封闭。操纵基因控制酶的结构基因。有活性的未被封闭的操纵基因即可使该酶的结构基因得以转录,就可进一步合成酶。

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