Cell Commun Signal May 2019 PMID 31060556

ATG5 and ATG7 induced autophagy interplays with UPR via PERK signaling.

Wei Zheng, Weiwei Xie, Danyang Yin, Rui Luo, Min Liu, Fengjin Guo

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Mentions

Peak: 3 in Aug 2022

across 3 sources since May 2019

Extended reach

63,148

potential audience

Total likes

2,588

Video views

62,576

Mentions per month

May 2019 – Aug 2022

Where it's discussed

X / Twitter2 posts
YouTube2 videos
News2 articles

AI synopsis

What people are saying

The discussions highlight the importance of autophagy, ER stress, and PERK signaling, with posts referencing the protective roles of ATG5 and ATG7, such as 'these proteins could be key targets' and 'the findings could revolutionize treatments.' The tone varies from optimistic to analytical, reflecting a genuine interest in both understanding and applying the research.

AgreementModerate agreement

Most discussions recognize the significance of the research, with some expressing strong support for its findings and implications.

InterestHigh interest

Participants show high curiosity about the mechanisms and potential therapies, indicating active interest in the topic.

EngagementModerate engagement

Comments include detailed reflections on the molecular pathways and potential future research directions, demonstrating moderate to high engagement.

ImpactModerate impact

People perceive the study as having meaningful implications for diseases related to cell stress and death, although some see it as preliminary.

Abstract in brief

The study investigates how proteins ATG5 and ATG7 promote autophagy and interact with ER stress in cells, specifically through the PERK pathway, which is a key part of the unfolded protein response (UPR).
It finds that inducing ER stress activates autophagy, and that ATG5 and ATG7 help reduce ER stress, enhance autophagy, and protect cell survival, especially in chondrocytes, by promoting cell cycle progression and inhibiting apoptosis.
The interactions between autophagy, ER stress, and cell survival are mainly mediated through PERK signaling, and manipulating this pathway can influence the protective effects of ATG5 and ATG7, highlighting potential targets for therapies related to cell stress and death.]

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