Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 529, Issue 4, Pages 1025-1032Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2020.05.223
Keywords
BAP1; LKB1; AMPK; mTOR; Deubiquitination
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Funding
- National Natural Science Foundation of China [31900804, 81525019, 31800700]
- Ministry of Science and Technology of the People's Republic of China [2019YFA0802103, 2018YFA0508200, 2018ZX10101004]
- Science and Technology Commission of Shanghai Municipality [19140903500, 2017SHZDZX01]
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Liver kinase B1 (LKB1), a tumour suppressor, participates in many cellular processes, including cell survival, growth, apoptosis, transformation, and metabolism. Upon performing yeast two-hybrid screening, co-immunoprecipitation, and GST pull-down, we identified that BRCA1-associated protein 1 (BAP1), a deubiquitinase, interacts with LKB1. Immunoblotting was performed to examine the effect of BAP1 on the activation of 50 AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR), downstream of LKB1. The relationship between BAP1 deficiency and cancer cell proliferation was examined using cell survival assay and soft agar assay. qRT-PCR and oil red O staining were performed to evaluate lipid synthesis. Our findings reveal that BAP1 deubiquitinates LKB1, inhibits its degradation, and stabilises it, thereby affecting AMPK activation and downstream mTOR activity. BAP1 deficiency may enhance cellular proliferation as well as lipid synthesis. (C) 2020 Elsevier Inc. All rights reserved.
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