USP11: A key regulator of cIAP2 stability and sensitivity to SMAC mimetics

Eun Woo Lee; Jaewhan Song

doi:10.1080/23723556.2015.1029829

USP11: A key regulator of cIAP2 stability and sensitivity to SMAC mimetics

Eun Woo Lee, Jaewhan Song

Research output: Contribution to journal › Article › peer-review

5 Citations (Scopus)

Abstract

The critical function of cellular inhibitor of apoptosis proteins (cIAPs) in the protection of cancer cells from numerous apoptotic stimuli prompted the development of second mitochondria-derived activator of caspases (SMAC) mimetics. We recently addressed a novel survival pathway in which cIAP2 is induced by tumor necrosis factor-α and is stabilized by its specific deubiquitylase, USP11, rendering cells resistant to SMAC mimetics.

Original language	English
Article number	e1029829
Journal	Molecular and Cellular Oncology
Volume	3
Issue number	3
DOIs	https://doi.org/10.1080/23723556.2015.1029829
Publication status	Published - 2016 May 3

Bibliographical note

Funding Information:
This research was supported by a grant from the National Research Foundation of Korea (NRF) funded by the Ministry of Education (2012R1A6A3A04040105) (E.W.L) and by the Ministry of Science, ICT and Future Planning (NRF- 2015R1A3A2066581) (to J.Song).

Publisher Copyright:
© 2016, © 2016 The Author(s). Published with license by Taylor & Francis Group, LLC. © 2016, © Eun-Woo Lee and Jaewhan Song.

All Science Journal Classification (ASJC) codes

Molecular Medicine
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1080/23723556.2015.1029829

Cite this

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title = "USP11: A key regulator of cIAP2 stability and sensitivity to SMAC mimetics",

abstract = "The critical function of cellular inhibitor of apoptosis proteins (cIAPs) in the protection of cancer cells from numerous apoptotic stimuli prompted the development of second mitochondria-derived activator of caspases (SMAC) mimetics. We recently addressed a novel survival pathway in which cIAP2 is induced by tumor necrosis factor-α and is stabilized by its specific deubiquitylase, USP11, rendering cells resistant to SMAC mimetics.",

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USP11: A key regulator of cIAP2 stability and sensitivity to SMAC mimetics

Abstract

Bibliographical note

All Science Journal Classification (ASJC) codes

UN SDGs

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