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Access through your institution Buy or subscribe Apoptosis is tuned by a fine balance between the activity of pro-apoptotic and pro-survival (anti-apoptotic) proteins of the BCL-2 family. Wu
_et al_. now show that the upregulation of pro-survival BCL-2 proteins — a hallmark of many cancers — can be driven by a feedforward loop, whereby pro-survival BCL-2 proteins promote the
activity of GLI transcription factors, thereby bolstering their own expression. GLI transcription factors are effectors of the Hedgehog signalling pathway, which has important roles in
development and can promote cancer when overactive. Screening for new positive regulators of Hedgehog signalling, the authors identified the pro-survival BCL-2 protein MCL1 as an activator
of GLI transcription. This is a preview of subscription content, access via your institution ACCESS OPTIONS Access through your institution Access Nature and 54 other Nature Portfolio
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during checkout ADDITIONAL ACCESS OPTIONS: * Log in * Learn about institutional subscriptions * Read our FAQs * Contact customer support REFERENCES * Wu, X. et al. Extra-mitochondrial
prosurvival BCL-2 proteins regulate gene transcription by inhibiting the SUFU tumour suppressor. _Nat. Cell Biol._ 19, 1226–1236 (2017) Article CAS Google Scholar Download references
Authors * Paulina Strzyz View author publications You can also search for this author inPubMed Google Scholar RELATED LINKS RELATED LINKS RELATED LINKS IN NATURE RESEARCH Czabotar, P. E. _et
al_. Control of apoptosis by the BCL-2 protein family: implications for physiology and therapy. _Nat. Rev. Mol. Cell Biol._ 15, 49–63 (2014) RIGHTS AND PERMISSIONS Reprints and permissions
ABOUT THIS ARTICLE CITE THIS ARTICLE Strzyz, P. BCL-2 proteins feed their own expression. _Nat Rev Mol Cell Biol_ 18, 652–653 (2017). https://doi.org/10.1038/nrm.2017.106 Download citation *
Published: 11 October 2017 * Issue Date: November 2017 * DOI: https://doi.org/10.1038/nrm.2017.106 SHARE THIS ARTICLE Anyone you share the following link with will be able to read this
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