منابع مشابه
Mcl-1 Ubiquitination and Destruction
Loss of the Fbw7 tumor suppressor is common in diverse human cancer types, including T-Cell Acute Lymphoblastic Leukemia (T-ALL), although the mechanistic basis of its anti-oncogenic activity remains largely unclear. We recently reported that SCFFbw7 regulates cellular apoptosis by controlling the ubiquitination and destruction of the pro-survival protein, Mcl-1, in a GSK3 phosphorylation-depen...
متن کاملThe MCL-1 BH3 Helix is an Exclusive MCL-1 inhibitor and Apoptosis Sensitizer
The development of selective inhibitors for discrete anti-apoptotic BCL-2 family proteins implicated in pathologic cell survival remains a formidable but pressing challenge. Such precisely tailored compounds would serve as molecular probes and targeted therapies to study and treat human diseases driven by specific anti-apoptotic blockades. In particular, MCL-1 has emerged as a major resistance ...
متن کاملMcl-1 degradation during hepatocyte lipoapoptosis.
The mechanisms of free fatty acid-induced lipoapoptosis are incompletely understood. Here we demonstrate that Mcl-1, an anti-apoptotic member of the Bcl-2 family, was rapidly degraded in hepatocytes in response to palmitate and stearate by a proteasome-dependent pathway. Overexpression of a ubiquitin-resistant Mcl-1 mutant in Huh-7 cells attenuated palmitate-mediated Mcl-1 loss and lipoapoptosi...
متن کاملTargeting Mcl-1 for multiple myeloma (MM) therapy: drug-induced generation of Mcl-1 fragment Mcl-1(128-350) triggers MM cell death via c-Jun upregulation.
Myeloid cell leukemia-1 (Mcl-1, HGNC: 6943), a pro-survival member of the Bcl-2 family, plays a crucial role in Multiple Myeloma (MM) pathogenesis and drug resistance, thus representing a promising therapeutic target in MM. A novel strategy to inhibit Mcl-1 activity is the induction of ubiquitin-independent Mcl-1 degradation. Our own and other previous studies have demonstrated caspase-dependen...
متن کاملMcl-1 and tumor cell persistence
Comment on: Jonchère B, et al. Irinotecan treatment and senescence failure promote the emergence of more transformed and invasive cells that depend on anti-apoptotic Mcl-1. Effective genotoxic cancer therapies induce not only classical apoptotic cell death, but also senescence, a persistent state of cell cycle arrest accompanied by distinct morphological and biochemical changes. A number of stu...
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ژورنال
عنوان ژورنال: Magyar kémiai folyóirat, Kémiai közlemények (Online)
سال: 2021
ISSN: ['1418-8600', '1418-9933']
DOI: https://doi.org/10.24100/mkf.2021.02.75