Regulation of Beclin 1-Mediated Autophagy by Oncogenic Tyrosine Kinases

被引:37
|
作者
Vega-Rubin-de-Celis, Silvia [1 ]
Kinch, Lisa [2 ]
Pena-Llopis, Samuel [3 ,4 ]
机构
[1] Univ Hosp Essen, Inst Cell Biol Canc Res, D-45147 Essen, Germany
[2] Univ Texas Southwestern Med Ctr Dallas, Howard Hughes Med Inst, Dallas, TX 75390 USA
[3] Univ Hosp Essen, German Canc Consortium DKTK, Translat Genom Solid Tumors, D-45147 Essen, Germany
[4] Univ Hosp Essen, German Canc Res Ctr, D-45147 Essen, Germany
关键词
Beclin; 1; autophagy; tyrosine kinases; cancer; CHRONIC MYELOID-LEUKEMIA; BCR-ABL; RET PROTOONCOGENE; LUNG-CANCER; MEDIATED PHOSPHORYLATION; SELECTIVE INHIBITOR; CRYSTAL-STRUCTURE; COILED-COIL; RECEPTOR; TUMORIGENESIS;
D O I
10.3390/ijms21239210
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Beclin 1 is a major regulator of autophagy, and it is a core component of the class III PI3K complexes. Beclin 1 is a highly conserved protein and its function is regulated in a number of ways, including post-translational modifications. Several studies indicate that receptor and non-receptor tyrosine kinases regulate autophagy activity in cancer, and some suggest the importance of Beclin 1 tyrosine phosphorylation in this process. Here we summarize the current knowledge of the mechanism whereby some oncogenic tyrosine kinases regulate autophagy through Beclin 1.
引用
收藏
页码:1 / 15
页数:15
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