ArticleeLife2022
The E3 ligase Thin controls homeostatic plasticity through neurotransmitter release repression.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Ubiquitin ligase signalling networks shape presynaptic development, function and disease.The Journal of physiology · 2025Review
- A unifying mechanism for presynaptic homeostatic plasticity at mammalian peripheral and central synapses.Neuron · 2025Article
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- Article
- Nanoscaled RIM clustering at presynaptic active zones revealed by endogenous tagging.Life science alliance · 2023Article
- Molecular Logic of Synaptic Diversity BetweenbioRxiv : the preprint server for biology · 2023Article
- FMRP activity and control of Csw/SHP2 translation regulate MAPK-dependent synaptic transmission.PLoS biology · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Synaptic proteins and synaptic transmission are under homeostatic control, but the relationship between these two processes remains enigmatic. Here, we systematically investigated the role of E3 ubiquitin ligases, key regulators of protein degradation-mediated proteostasis, in presynaptic homeostatic plasticity (PHP). An electrophysiology-based genetic screen of 157 E3 ligase-encoding genes at the
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.