Low-dose BBR3610 toxicity in colon cancer cells is p53-independent and enhanced by inhibition of epidermal growth factor receptor (ERBB1)-phosphatidyl inositol 3 kinase signaling.

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第一作者： Clint,Mitchell

第一单位： Department of Biochemistry, Virginia Commonwealth University, Richmond, VA 23298-0035, USA.

作者： Clint,Mitchell ^[1] ; Peyman,Kabolizadeh ; John,Ryan ; John D,Roberts ; Adly,Yacoub ; David T,Curiel ; Paul B,Fisher ; Michael P,Hagan ; Nicholas P,Farrell ; Steven,Grant ; Paul,Dent

作者单位： Department of Biochemistry, Virginia Commonwealth University, Richmond, VA 23298-0035, USA. ^[1]

主题词抗肿瘤药(Antineoplastic Agents);细胞存活(Cell Survival);剂量效应关系, 药物(Dose-Response Relationship, Drug);HCT116细胞(HCT116 Cells);人类(Humans);分子结构(Molecular Structure);有机铂化合物(Organoplatinum Compounds);磷酸肌醇3-激酶类(Phosphatidylinositol 3-Kinases);信号传导(Signal Transduction);肿瘤抑制蛋白质p53(Tumor Suppressor Protein p53)

DOI 10.1124/mol.107.038406

PMID 17578896

发布时间 2025-02-13

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Molecular pharmacology

2007年72卷3期

704-14页

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Low-dose BBR3610 toxicity in colon cancer cells is p53-independent and enhanced by inhibition of epidermal growth factor receptor (ERBB1)-phosphatidyl inositol 3 kinase signaling.

Molecular pharmacology

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Molecular pharmacology

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Low-dose BBR3610 toxicity in colon cancer cells is p53-independent and enhanced by inhibition of epidermal growth factor receptor (ERBB1)-phosphatidyl inositol 3 kinase signaling.

Molecular pharmacology

相似文献

Molecular pharmacology

相关期刊

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