机译:通过通过PI3K / AKT / MTOR和MEK / ERK1 / 2信号通路通过横向激活通过自噬激活在H9C2细胞中低后葡萄糖下调CX43
Shanghai Jiao Tong Univ Affiliated Peoples Hosp 6 Dept Cardiol Shanghai Peoples R China;
Shanghai Jiao Tong Univ Affiliated Peoples Hosp 6 Dept Cardiol Shanghai Peoples R China;
Shanghai Jiao Tong Univ Affiliated Peoples Hosp 6 Dept Cardiol Shanghai Peoples R China;
Shanghai Jiao Tong Univ Affiliated Peoples Hosp 6 Dept Cardiol Shanghai Peoples R China;
Shanghai Jiao Tong Univ Affiliated Peoples Hosp 6 Dept Cardiol Shanghai Peoples R China;
Cx43; Low-after-high glucose; H9c2 cell; Autophagy; PI3K/Akt/mTOR; MEK/ERK1/2;
机译:通过通过PI3K / AKT / MTOR和MEK / ERK1 / 2信号通路通过横向激活通过自噬激活在H9C2细胞中低后葡萄糖下调CX43
机译:厚朴酚通过激活PI3K / Akt / mTOR和内质网状应力/ ERK1 / 2信号通路并抑制细胞迁移来诱导神经母细胞瘤细胞自噬
机译:MiR-129-5P通过靶向ATG14抑制通过PI3K / AKT / MTOR信号传导途径通过PI3K / AKT / MTOR信号传导途径诱导的H9C2细胞的自噬和凋亡
机译:阳离子聚苯乙烯纳米球通过抑制Akt / mTOR和激活巨噬细胞和上皮细胞中的AMPK信号通路来诱导自噬
机译:PI3k / AKT / mTOR信号通路的遗传分析。
机译:PI3K / AKT / mTOR途径的抑制激活前列腺癌中的自噬和补偿性Ras / Raf / MEK / ERK信号传导
机译:PI3K / AKT / mTOR途径的抑制激活前列腺癌中的自噬和补偿性Ras / Raf / MEK / ERK信号传导