条件基因敲除
mTORC1型
TSC2
基因剔除小鼠
体内
细胞生物学
生物
表型
遗传学
基因
信号转导
PI3K/AKT/mTOR通路
作者
Camila Lüdke Rossetti,Bruna Lourençoni Alves,Flavia Letícia Martins Peçanha,Aime T. Franco,Vânia Nosé,Everardo M. Carneiro,John I. Lew,Ernesto Bernal–Mizrachi,João Pedro Werneck‐de‐Castro
出处
期刊:Thyroid
[Mary Ann Liebert, Inc.]
日期:2024-04-25
卷期号:34 (8): 1047-1057
被引量:1
标识
DOI:10.1089/thy.2024.0053
摘要
The thyroid gland is susceptible to abnormal epithelial cell growth, often resulting in thyroid dysfunction. The serine-threonine protein kinase mechanistic target of rapamycin (mTOR) regulates cellular metabolism, proliferation, and growth through two different protein complexes, mTORC1 and mTORC2. The PI3K-Akt-mTORC1 pathway's overactivity is well associated with heightened aggressiveness in thyroid cancer, but recent studies indicate the involvement of mTORC2 as well.
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