A TRIM16-Galactin3 Complex Mediates Autophagy of Damaged Endomembranes

Milana Fraiberg; Zvulun Elazar

doi:10.1016/j.devcel.2016.09.025

A TRIM16-Galactin3 Complex Mediates Autophagy of Damaged Endomembranes

Milana Fraiberg, Zvulun Elazar^*

^*Corresponding author for this work

Department of Biomolecular Sciences

Research output: Contribution to journal › Short survey › peer-review

11 Citations (Scopus)

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
Publication status	Published - 10 Oct 2016

All Science Journal Classification (ASJC) codes

Molecular Biology
General Biochemistry,Genetics and Molecular Biology
Developmental Biology
Cell Biology

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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.",

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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 - 10.1016/j.devcel.2016.09.025

M3 - Short survey

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JO - Developmental Cell

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IS - 1

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A TRIM16-Galactin3 Complex Mediates Autophagy of Damaged Endomembranes

Abstract

All Science Journal Classification (ASJC) codes

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