首页> 美国卫生研究院文献>The Journal of Biological Chemistry >Withdrawal: Cooperative regulation of NOTCH1 protein-phosphatidylinositol 3-kinase (PI3K) signaling by NOD1 NOD2 and TLR2 receptors renders enhanced refractoriness to transforming growth factor-β (TGF-β)- or cytotoxic T-lymphocyte antigen 4 (CTLA-4)-mediated impairment of human dendritic cell maturation.

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Withdrawal: Cooperative regulation of NOTCH1 protein-phosphatidylinositol 3-kinase (PI3K) signaling by NOD1 NOD2 and TLR2 receptors renders enhanced refractoriness to transforming growth factor-β (TGF-β)- or cytotoxic T-lymphocyte antigen 4 (CTLA-4)-mediated impairment of human dendritic cell maturation.

机译：戒断：NOD1NOD2和TLR2受体对NOTCH1蛋白-磷脂酰肌醇3-激酶（PI3K）信号的协同调节可提高对转化生长因子-β（TGF-β）或细胞毒性T淋巴细胞抗原4（CTLA-4）的抵抗力介导的人类树突状细胞成熟受损。

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VOLUME 286 (2011) PAGES

机译：卷286（2011）页

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期刊名称 The Journal of Biological Chemistry
作者
Devram Sampat Ghorpade; Srini V. Kaveri; Jagadeesh Bayry; Kithiganahalli Narayanaswamy Balaji;
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作者单位

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年(卷),期 2019(294),50
年度 2019
页码 -1
总页数 1
原文格式 PDF
正文语种
中图分类分子生物学;
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1. Cooperative Regulation of NOTCH1 Protein-Phosphatidylinositol 3-Kinase (PI3K) Signaling by NOD1, NOD2, and TLR2 Receptors Renders Enhanced Refractoriness to Transforming Growth Factor-β (TGF-β)- or Cytotoxic T-lymphocyte Antigen 4 (CTLA-4)-mediated Impairment of Human Dendritic Cell Maturation [J] . Devram Sampat Ghorpade, Srini V. Kaveri, Jagadeesh Bayry, The Journal of biological chemistry . 2011,第36期

机译：NOD1，NOD2和TLR2受体的NOTCH1蛋白 - 磷脂酰肌醇3-激酶（PI3K）信号传导的协作调节使得增强的耐火性与转化生长因子-β（TGF-β） - 或细胞毒性T淋巴细胞抗原4（CTLA-4） - 人树突细胞成熟的介导的损伤
2. Hexachlorobenzene modulates the crosstalk between the aryl hydrocarbon receptor and transforming growth factor-β1 signaling, enhancing human breast cancer cell migration and invasion [J] . Noelia Miret, Carolina Pontillo, Clara Ventura, Toxicology: An International Journal Concerned with the Effects of Chemicals on Living Systems . 2016,第期

机译：六氯苯调制芳基烃受体与转化生长因子-β1信号传导之间的串扰，增强人乳腺癌细胞迁移和侵袭
3. Cooperative Regulation of NOTCH1 Protein-Phosphatidylinositol 3-Kinase (PI3K) Signaling by NOD1 NOD2 and TLR2 Receptors Renders Enhanced Refractoriness to Transforming Growth Factor-β (TGF-β)- or Cytotoxic T-lymphocyte Antigen 4 (CTLA-4)-mediated Impairment of Human Dendritic Cell Maturation [O] . Devram Sampat Ghorpade, Srini V. Kaveri, Jagadeesh Bayry, 2011

机译：通过NOD1NOD2和TLR2受体对NOTCH1蛋白-磷脂酰肌醇3-激酶（PI3K）信号的协同调节可增强对转化生长因子-β（TGF-β）或细胞毒性T淋巴细胞抗原4（CTLA-4）-的抵抗力。介导的人类树突状细胞成熟的损害
4. Cooperative Regulation of NOTCH1 Protein-Phosphatidylinositol 3-Kinase (PI3K) Signaling by NOD1, NOD2, and TLR2 Receptors Renders Enhanced Refractoriness to Transforming Growth Factor-β (TGF-β)- or Cytotoxic T-lymphocyte Antigen 4 (CTLA-4)-mediated Impairment of Human Dendritic Cell Maturation* [O] . Devram Sampat Ghorpade, Srini V. Kaveri, Jagadeesh Bayry, 2011

机译：NOD1，NOD2和TLR2受体的NOTCH1蛋白 - 磷脂酰肌醇3-激酶（PI3K）信号传导的协作调节使得增强的耐火性与转化生长因子-β（TGF-β） - 或细胞毒性T淋巴细胞抗原4（CTLA-4） - 介导人树突细胞成熟的损伤*

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