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. 2012 Jul 6;1(3):284-312.
doi: 10.3390/cells1030284.

V体育安卓版 - Regulation of the autophagic bcl-2/beclin 1 interaction

Jean-Paul Decuypere  1 , Jan B Parys  2 , Geert Bultynck  3
Affiliations

Regulation of the autophagic bcl-2/beclin 1 interaction

Jean-Paul Decuypere et al. Cells. .

"V体育平台登录" Abstract

Autophagy is an intracellular degradation process responsible for the delivery of cellular material to the lysosomes. One of the key mechanisms for control of autophagy is the modulation of the interaction between the autophagic protein Beclin 1 and the members of the anti-apoptotic Bcl-2 family (e VSports手机版. g. , Bcl-2, Bcl-XL and Mcl-1). This binding is regulated by a variety of proteins and compounds that are able to enhance or inhibit the Bcl-2/Beclin 1 interaction in order to repress or activate autophagy, respectively. In this review we will focus on this interaction and discuss its characteristics, relevance and regulation. .

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Figures (VSports手机版)

Figure 1
Figure 1
Bcl-2 tethers Beclin 1 at the ER. Representation of mitochondria, ER and the proteins of interest in normal growth conditions. Since only ER-Bcl-2 regulates autophagy, it is able to recruit Beclin 1 at the ER. Bcl-2-binding mutants of Beclin 1 (indicated with a red cross), therefore are less able to interact with Vps34 at the ER and fail to induce autophagy or could induce autophagic cell death. Whether Bcl-2/Beclin 1 complexes are devoid of Vps34 is still unclear. Beclin 1 can also associate with mitochondria. Ambra-1 binds mitochondrial Bcl-2 and prevents it from binding to Beclin 1. See text for detailed information.
Figure 2
Figure 2
Regulation of the Bcl-2/Beclin 1 interaction at the ER. The Bcl-2/Beclin 1 interaction can be enhanced by RTN3, Naf-1, IP3R and ubiquitination of Bcl-2 by Parkin. Dissociation of Beclin 1 from Bcl-2 is promoted by BH3-only proteins binding to Bcl-2, phosphorylation of Bcl-2 by JNK1, phosphorylation of Beclin 1 by DAPK, viral Bcl-2 (v-Bcl-2) or HMGB1 binding to Beclin 1 or ubiquitination of Beclin 1 by TRAF6. The latter can be counteracted by deubiquitinating enzyme A20. See text for detailed information.
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