The expression of damage-regulated autophagy modulator 2 (DRAM2) contributes to autophagy induction

Jung Ho Yoon; Song Her; Moonhee Kim; Ik Soon Jang; Junsoo Park

doi:10.1007/s11033-011-0835-x

The expression of damage-regulated autophagy modulator 2 (DRAM2) contributes to autophagy induction

Jung Ho Yoon, Song Her, Moonhee Kim, Ik Soon Jang, Junsoo Park

Division of Bioscience and Biotechnology

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

44 Citations (Scopus)

Abstract

Autophagy is a membrane trafficking process involved in intracellular degradation and recycling in eukaryotic cells. DRAM2 (damage-regulated autophagy modulator 2) is a homologue of DRAM that regulates p53-mediated cell death. As its name implies, DRAM expression induces autophagy in a p53-dependent manner; however, the role of DRAM2 in autophagy is not clear. In this study, we report that DRAM2 expression contributes to autophagy induction. Overexpression of DRAM2 induces cytoplasmic GFP-LC3 punctuates, and increases the level of endogenous LC3-II. Moreover, the silencing of endogenous DRAM2 interferes with starvation-induced autophagy. Thus, we propose that DRAM2 as well as DRAM are involved in autophagy.

Original language	English
Pages (from-to)	1087-1093
Number of pages	7
Journal	Molecular Biology Reports
Volume	39
Issue number	2
DOIs	https://doi.org/10.1007/s11033-011-0835-x
Publication status	Published - 2012 Feb

Bibliographical note

Funding Information:
Acknowledgments We would particularly like to thank Kevin M. Ryan for providing the DRAM expression plasmid and T. Yoshimori for providing the GFP-LC3 plasmid. This study was supported by a National Research Foundation of Korea Grant funded by the Korean

All Science Journal Classification (ASJC) codes

Molecular Biology
Genetics

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10.1007/s11033-011-0835-x

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title = "The expression of damage-regulated autophagy modulator 2 (DRAM2) contributes to autophagy induction",

abstract = "Autophagy is a membrane trafficking process involved in intracellular degradation and recycling in eukaryotic cells. DRAM2 (damage-regulated autophagy modulator 2) is a homologue of DRAM that regulates p53-mediated cell death. As its name implies, DRAM expression induces autophagy in a p53-dependent manner; however, the role of DRAM2 in autophagy is not clear. In this study, we report that DRAM2 expression contributes to autophagy induction. Overexpression of DRAM2 induces cytoplasmic GFP-LC3 punctuates, and increases the level of endogenous LC3-II. Moreover, the silencing of endogenous DRAM2 interferes with starvation-induced autophagy. Thus, we propose that DRAM2 as well as DRAM are involved in autophagy.",

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note = "Funding Information: Acknowledgments We would particularly like to thank Kevin M. Ryan for providing the DRAM expression plasmid and T. Yoshimori for providing the GFP-LC3 plasmid. This study was supported by a National Research Foundation of Korea Grant funded by the Korean",

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AU - Her, Song

AU - Kim, Moonhee

AU - Jang, Ik Soon

AU - Park, Junsoo

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N2 - Autophagy is a membrane trafficking process involved in intracellular degradation and recycling in eukaryotic cells. DRAM2 (damage-regulated autophagy modulator 2) is a homologue of DRAM that regulates p53-mediated cell death. As its name implies, DRAM expression induces autophagy in a p53-dependent manner; however, the role of DRAM2 in autophagy is not clear. In this study, we report that DRAM2 expression contributes to autophagy induction. Overexpression of DRAM2 induces cytoplasmic GFP-LC3 punctuates, and increases the level of endogenous LC3-II. Moreover, the silencing of endogenous DRAM2 interferes with starvation-induced autophagy. Thus, we propose that DRAM2 as well as DRAM are involved in autophagy.

AB - Autophagy is a membrane trafficking process involved in intracellular degradation and recycling in eukaryotic cells. DRAM2 (damage-regulated autophagy modulator 2) is a homologue of DRAM that regulates p53-mediated cell death. As its name implies, DRAM expression induces autophagy in a p53-dependent manner; however, the role of DRAM2 in autophagy is not clear. In this study, we report that DRAM2 expression contributes to autophagy induction. Overexpression of DRAM2 induces cytoplasmic GFP-LC3 punctuates, and increases the level of endogenous LC3-II. Moreover, the silencing of endogenous DRAM2 interferes with starvation-induced autophagy. Thus, we propose that DRAM2 as well as DRAM are involved in autophagy.

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The expression of damage-regulated autophagy modulator 2 (DRAM2) contributes to autophagy induction

Abstract

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