ArticlemicroPublication biology2024
Loss of the E3 ubiquitin ligase TRIM67 alters the post-synaptic density proteome.
Article in microPublication biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Chimeric degraders in neurodegenerative diseases: Challenges and future directions.Journal of translational internal medicine · 2025Article
- Coro1A and TRIM67 collaborate in netrin-dependent neuronal morphogenesis.The Journal of cell biology · 2025Article
- The E3 ubiquitin ligase TRIM9 regulates synaptic function and actin dynamics in response to netrin-1.Molecular biology of the cell · 2024Article
Corrections and comments
- Update of
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The E3 ubiquitin ligase TRIM67 is enriched in the central nervous system and is required for proper neuronal development. Previously we demonstrated TRIM67 coordinates with the closely related E3 ubiquitin ligase TRIM9 to regulate cytoskeletal dynamics downstream of the netrin-1 during axon guidance and axon branching in early neuronal morphogenesis. Interestingly, loss of
Identifiers
What OpenQuestion holds
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.