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BLM Potentiates c-Jun Degradation and Alters Its Function as an Oncogenic Transcription Factor

BLM Potentiates c-Jun Degradation and Alters Its Function as an Oncogenic Transcription Factor

Raina Priyadarshini, Mansoor Hussain, Preeti Attri, Ekjot Kaur, Vivek Tripathi, Swati Priya, Parashar Dhapola, Dhurjhoti Saha, Vinoth Madhavan, Shantanu Chowdhury, Sagar Sengupta

Cell Rep. 2018 Jul 24;24(4):947-961.e7.

PMID: 30044990

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.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42414966	C-jun, proto oncogene human			Price

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