Abstract：
:Mutations in BLM helicase predispose Bloom syndrome (BS) patients to a wide spectrum of cancers. We demonstrate that MIB1-ubiquitylated BLM in G1 phase functions as an adaptor protein by enhancing the binding of transcription factor c-Jun and its E3 ligase, Fbw7α. BLM enhances the K48/K63-linked ubiquitylation on c-Jun, thereby enhancing the rate of its subsequent degradation. Functionally defective Fbw7α mutants prevalent in multiple human cancers are reactivated by BLM. However, BS patient-derived BLM mutants cannot potentiate Fbw7α-dependent c-Jun degradation. The decrease in the levels of c-Jun in cells expressing BLM prevents effective c-Jun binding to 2,584 gene promoters. This causes decreases in the transcript and protein levels of c-Jun targets in BLM-expressing cells, resulting in attenuated c-Jun-dependent effects during neoplastic transformation. Thus, BLM carries out its function as a tumor suppressor by enhancing c-Jun turnover and thereby preventing its activity as a proto-oncogene.
journal_name
Cell Repjournal_title
Cell reportsauthors
Priyadarshini R,Hussain M,Attri P,Kaur E,Tripathi V,Priya S,Dhapola P,Saha D,Madhavan V,Chowdhury S,Sengupta Sdoi
10.1016/j.celrep.2018.06.101subject
Has Abstractpub_date
2018-07-24 00:00:00pages
947-961.e7issue
4issn
2211-1247pii
S2211-1247(18)31043-Xjournal_volume
24pub_type
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