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Updated: Jun 18, 2025

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在肺癌干细胞中,TIPRL通过CaMKK2-CaMK4-CREB反环激活来调节干细胞和存活率

In-Sung Song1, Yu-Jeong Jeong1, Jae Kwang Yun2

  • 1Department of Biochemistry and Molecular Biology, Brain Korea 21 Project, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 138-736, Republic of Korea.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)
|July 30, 2024
PubMed
概括

向TIPRL和CaMKK2信号可以克服耐药性,并通过抑制癌症干细胞存活和促进细胞死亡来减少肺癌转移.

关键词:
CaMKK2-CaMK4-CREB反循环激活方式在TIPRL上.癌症干细胞是一种癌症干细胞.药物耐药性 耐药性 药物耐药性肺癌是一种肺癌.转移 转移 转移 转移

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