BET Bromodomain as a Target of Epigenetic Therapy
نویسندگان
چکیده
منابع مشابه
BET Bromodomain Inhibition as a Therapeutic Strategy to Target c-Myc
MYC contributes to the pathogenesis of a majority of human cancers, yet strategies to modulate the function of the c-Myc oncoprotein do not exist. Toward this objective, we have targeted MYC transcription by interfering with chromatin-dependent signal transduction to RNA polymerase, specifically by inhibiting the acetyl-lysine recognition domains (bromodomains) of putative coactivator proteins ...
متن کاملRegistered report: BET bromodomain inhibition as a therapeutic strategy to target c-Myc
The Reproducibility Project: Cancer Biology seeks to address growing concerns about reproducibility in scientific research by replicating selected results from a substantial number of high-profile papers in the field of cancer biology published between 2010 and 2012. This Registered report describes the proposed replication plan of key experiments from 'BET bromodomain inhibition as a therapeut...
متن کاملCancer Therapy: Preclinical BET Bromodomain Inhibition of MYC-Amplified Medulloblastoma
Purpose: MYC-amplified medulloblastomas are highly lethal tumors. Bromodomain and extraterminal (BET) bromodomain inhibition has recently been shown to suppress MYC-associated transcriptional activity in other cancers. The compound JQ1 inhibits BET bromodomain-containing proteins, including BRD4. Here, we investigate BET bromodomain targeting for the treatment of MYC-amplified
متن کاملSelective BET bromodomain inhibition as an antifungal therapeutic strategy
Invasive fungal infections cause significant morbidity and mortality among immunocompromised individuals, posing an urgent need for new antifungal therapeutic strategies. Here we investigate a chromatin-interacting module, the bromodomain (BD) from the BET family of proteins, as a potential antifungal target in Candida albicans, a major human fungal pathogen. We show that the BET protein Bdf1 i...
متن کاملBET bromodomain inhibition of MYC-amplified medulloblastoma.
PURPOSE MYC-amplified medulloblastomas are highly lethal tumors. Bromodomain and extraterminal (BET) bromodomain inhibition has recently been shown to suppress MYC-associated transcriptional activity in other cancers. The compound JQ1 inhibits BET bromodomain-containing proteins, including BRD4. Here, we investigate BET bromodomain targeting for the treatment of MYC-amplified medulloblastoma. ...
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ژورنال
عنوان ژورنال: CHEMICAL & PHARMACEUTICAL BULLETIN
سال: 2016
ISSN: 0009-2363,1347-5223
DOI: 10.1248/cpb.c16-00225