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

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2020年 / 21卷 / 23期

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

页码：1 / 15

页数：15

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