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• W2940889523 endingPage "562" @default.
• W2940889523 startingPage "549" @default.
• W2940889523 abstract "Recent advances in molecular oncology have led to the development of the BH3 mimetics – small-molecule drugs that neutralize antiapoptotic Bcl-2 family proteins and, thus, favor the mitochondrial pathway of apoptosis. Mcl-1-selective BH3 mimetics are at relatively early stages of drug development, so their adverse effects, including those relating to the nonapoptotic functions of Mcl-1, are poorly understood. Several BH3 mimetics preclude interactions between Mcl-1 and its proapoptotic partners while stabilizing Mcl-1. Understanding of the conformational changes that induce degradation of Mcl-1 would allow the rational design of alternative compounds that would cause a pronounced reduction of its cellular level. In the context of oncology, it is worth examining alternative strategies to target Mcl-1, such as an alternative splicing switch toward a proapoptotic Mcl-1S isoform and indirect antagonism of Mcl-1. Among cell death regulators, members of the Bcl-2 family are of interest because they are highly conserved across species and represent promising targets for anticancer therapy. This family and its associated proteins include more than 25 members, with either anti- or proapoptotic functions. Although the overall regulation of apoptosis by Bcl-2 family proteins is now well understood, targeted therapy requires careful consideration of individual members of the family and their crosstalk. One of the most studied representatives of the Bcl-2 family is antiapoptotic Mcl-1. After 25 years of investigations, a large amount of data regarding Mcl-1’s regulation and functions has been compiled. In this review, we summarize current knowledge about Mcl-1, focusing on molecular aspects relevant to Mcl-1-targeted therapies. Among cell death regulators, members of the Bcl-2 family are of interest because they are highly conserved across species and represent promising targets for anticancer therapy. This family and its associated proteins include more than 25 members, with either anti- or proapoptotic functions. Although the overall regulation of apoptosis by Bcl-2 family proteins is now well understood, targeted therapy requires careful consideration of individual members of the family and their crosstalk. One of the most studied representatives of the Bcl-2 family is antiapoptotic Mcl-1. After 25 years of investigations, a large amount of data regarding Mcl-1’s regulation and functions has been compiled. In this review, we summarize current knowledge about Mcl-1, focusing on molecular aspects relevant to Mcl-1-targeted therapies. short amino acid regions of sequence homology in Bcl-2 family proteins. a hydrophobic cleft on the surface of antiapoptotic Bcl-2-family members that is formed by the BH1, BH2, and BH3 domains and accommodates the BH3 helix of proapoptotic Bcl-2 family proteins. small molecules that mimic the BH3 domains of proapoptotic Bcl-2 family proteins and block the BH3-binding grooves of antiapoptotic members of the family, thus antagonizing their prosurvival activity. a family of cysteine-aspartic proteases that serve as initiators or effectors in the progression of PCD or inflammation. a critical ‘no-return’ point during apoptosis characterized by the formation of protein-permeable pores on the OMM by Bax and/or Bak oligomers and the ensuing release of various proapoptotic factors (e.g., cytochrome c, SMAC/Diablo) from the mitochondrial intermembrane space. an amino-terminal sequence characterized by a positive net charge and implicated in trafficking proteins through mitochondrial membranes. a lethal outcome due to the failure of a blastocyst to attach to and/or implant in the lining of the uterus. a protein region that is enriched in proline (P), glutamic acid (E), serine (S), and threonine (T), and typically associated with short-lived proteins. a method for studying protein or mRNA dynamics in cells after a short period of labeling, or ‘pulse’, and subsequent replacement of the label with an unlabeled precursor, or ‘chase’. Protein turnover rate is typically assessed by comparing the levels of target protein radioactivity after incubation of cells with [35S]Cys/Met and the residual radioactivity at certain time points after the release from labeling. a multiprotein machinery that transports proteins with a MTS from the cytosol into mitochondria." @default.
• W2940889523 created "2019-05-03" @default.
• W2940889523 creator A5052913973 @default.
• W2940889523 creator A5074294837 @default.
• W2940889523 creator A5080920861 @default.
• W2940889523 creator A5089390726 @default.
• W2940889523 date "2019-07-01" @default.
• W2940889523 modified "2023-10-14" @default.
• W2940889523 title "Molecular Comprehension of Mcl-1: From Gene Structure to Cancer Therapy" @default.
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