BET inhibition prevents aberrant RUNX1 and ERG transcription in STAG2 mutant leukaemia cells
作者机构：Department of PathologyDunedin School of MedicineUniversity of OtagoDunedin 9016New Zealand Maurice Wilkins Centre for Molecular BiodiscoveryThe University of AucklandPrivate Bag 92019AucklandNew Zealand Southern Community LaboratoriesDunedin 9016New Zealand Department of BiochemistryUniversity of OtagoDunedin 9054New Zealand
出 版 物：《Journal of Molecular Cell Biology》 (分子细胞生物学报（英文版）)
年 卷 期：2020年第12卷第5期
页 面：397-399页
核心收录：
学科分类：0710[理学-生物学] 07[理学] 09[农学] 071007[理学-遗传学] 0901[农学-作物学] 090102[农学-作物遗传育种]
基 金：supported by Health Research Council of NZ award a Cancer Research Trust of NZ award to J.A
摘 要：Cohesin is a multiprotein complex that not only is essential for cell division but also has key roles in genome organization that underpin its gene regulatory *** mutations of genes encoding cohesin subunits occur in myeloid malignancies at 10%–12%(Kon et al.,2013),and the frequency of cohesin mutation in Down syndrome-associated megakaryoblastic leukaemia is even higher(~50%)(Yoshida et al.,2013).Cohesin insufficiency reinforces stem cell programmes and impairs differentiation in haematopoietic stem cells(Mazumdar et al.,2015;Mullenders et al.,2015;Viny et al.,2015).The STAG2 subunit of cohesin is the most frequently mutated in myeloid malignancies(Kon et al.,2013).In contrast to other cohesin subunits,complete loss of STAG2 is tolerated due to partial compensation by ***2 and STAG1 have redundant roles in cell division(Benedetti et al.,2017;van der Lelij et al.,2017).However,cohesin-STAG1 and cohesin-STAG2 have non-redundant roles in facilitating 3D genome organization to delineate tissue-specific gene expression(Kojic et al.,2018).
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