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Journal ArticleDOI

Autophagosome formation--the role of ULK1 and Beclin1-PI3KC3 complexes in setting the stage.

TLDR
How the mammalian ULK1 and Beclin1 complexes are controlled by post-translational modifications and protein-protein interactions is discussed and data linking these complexes together is highlighted.
About
This article is published in Seminars in Cancer Biology.The article was published on 2013-10-01. It has received 218 citations till now. The article focuses on the topics: Autophagy.

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Citations
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Journal ArticleDOI

The autophagosome: origins unknown, biogenesis complex

TL;DR: It is proposed that the isolation membrane forms from the mitochondria-associated endoplasmic reticulum (ER) membrane (MAM) and the role of ATG proteins and the vesicular trafficking machinery in autophagosome formation is proposed.
Journal Article

Global Analysis of Protein Phosphorylation in Yeast

TL;DR: The in vitro substrates recognized by most yeast protein kinases are described, with the use of proteome chip technology, and these results will provide insights into the mechanisms and roles of protein phosphorylation in many eukaryotes.
Journal ArticleDOI

WIPI2 Links LC3 Conjugation with PI3P, Autophagosome Formation, and Pathogen Clearance by Recruiting Atg12–5-16L1

TL;DR: Mutation experiments and ectopic localization of WIPI2b to plasma membrane show that WIPi2b is a PtdIns(3)P effector upstream of Atg16L1 and is required for LC3 conjugation and starvation-induced autophagy through recruitment of the Atg12–5- 16L1 complex.
Journal ArticleDOI

To Be or Not to Be? How Selective Autophagy and Cell Death Govern Cell Fate

TL;DR: The progress that has been made in the last few decades in determining the fates of damaged organelles and damaged cells through discrete, but genetically overlapping, pathways involving the selective autophagy and cell death machinery is considered.
Journal ArticleDOI

mTORC1 signaling and the metabolic control of cell growth.

TL;DR: As dysregulated mTORC1 underlies a variety of human diseases, including cancer, diabetes, autoimmune diseases, and neurological disorders, understanding the metabolic program downstream of m TORC1 provides insights into its role in these pathological states.
References
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Journal ArticleDOI

Crosstalk between apoptosis and autophagy within the Beclin 1 interactome

TL;DR: A novel protein, NAF-1 (nutrient-deprivation autophagy factor-1), is identified that binds Bcl-2 at the ER, providing mechanistic insights into how Autophagy- and apoptosis-regulatory molecules crosstalk at theER.
Journal ArticleDOI

A genome-wide siRNA screen reveals multiple mTORC1 independent signaling pathways regulating autophagy under normal nutritional conditions

TL;DR: This study suggests that the type III PI3 kinase integrates diverse signals to regulate cellular levels of autophagy, and that autophophagy and cell proliferation may represent two alternative cell fates that are regulated in a mutually exclusive manner.
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Mitochondrial BCL‐2 inhibits AMBRA1‐induced autophagy

TL;DR: A dynamic interaction exists between AMBRA1 and BCL‐2 at the mitochondria that could regulate both BECLIN 1‐dependent autophagy and apoptosis.
Journal ArticleDOI

Ulk1-mediated phosphorylation of AMPK constitutes a negative regulatory feedback loop

TL;DR: It is reported that Ulk1/2 in turn phosphorylates all three subunits of AMPK and thereby negatively regulates its activity and is proposed thatUlk1 is not only involved in the induction of autophagy, but also in terminating signaling events that trigger autophagic induction.
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