A TRIM16-Galactin3 Complex Mediates Autophagy of Damaged Endomembranes

Milana Fraiberg; Zvulun Elazar

doi:https://doi.org/10.1016/j.devcel.2016.09.025

A TRIM16-Galactin3 Complex Mediates Autophagy of Damaged Endomembranes

Milana Fraiberg, Zvulun Elazar

Department of Biomolecular Sciences

Weizmann Institute of Science

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

Abstract

Selective autophagy, an essential process for maintaining intracellular homeostasis, depends on precise target recognition and local activation. Reporting in Developmental Cell, Chauhan et al. (2016) elegantly demonstrate that interaction between TRIM16 and Galectin3 orchestrates the recruitment of core autophagic factors and activates selective autophagy at the site of damaged endomembranes.

Original language	English
Pages (from-to)	1-2
Number of pages	2
Journal	Developmental Cell
Volume	39
Issue number	1
DOIs	https://doi.org/10.1016/j.devcel.2016.09.025
State	Published - 10 Oct 2016

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title = "A TRIM16-Galactin3 Complex Mediates Autophagy of Damaged Endomembranes",

abstract = "Selective autophagy, an essential process for maintaining intracellular homeostasis, depends on precise target recognition and local activation. Reporting in Developmental Cell, Chauhan et al. (2016) elegantly demonstrate that interaction between TRIM16 and Galectin3 orchestrates the recruitment of core autophagic factors and activates selective autophagy at the site of damaged endomembranes.",

author = "Milana Fraiberg and Zvulun Elazar",

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year = "2016",

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AU - Elazar, Zvulun

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N2 - Selective autophagy, an essential process for maintaining intracellular homeostasis, depends on precise target recognition and local activation. Reporting in Developmental Cell, Chauhan et al. (2016) elegantly demonstrate that interaction between TRIM16 and Galectin3 orchestrates the recruitment of core autophagic factors and activates selective autophagy at the site of damaged endomembranes.

AB - Selective autophagy, an essential process for maintaining intracellular homeostasis, depends on precise target recognition and local activation. Reporting in Developmental Cell, Chauhan et al. (2016) elegantly demonstrate that interaction between TRIM16 and Galectin3 orchestrates the recruitment of core autophagic factors and activates selective autophagy at the site of damaged endomembranes.

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DO - https://doi.org/10.1016/j.devcel.2016.09.025

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JO - Developmental Cell

JF - Developmental Cell

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A TRIM16-Galactin3 Complex Mediates Autophagy of Damaged Endomembranes

Abstract

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