ReviewCurrent neuropharmacology2025
UFMylation: A Potential Modification for Neurological Diseases.
Review in Current neuropharmacology, 2025. 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.
- The UFM1 Conjugation System: A Master Regulator of Cellular Stress Surveillance in Human Disease.Biology · 2026Review
- Tubuloside B ameliorates blood-brain barrier disruption and cognitive deficits after cerebral ischemia by inhibiting TRIC protein ubiquitination and degradation.Journal of neuroinflammation · 2025Article
- Protein Lactylation Modulating Regulated Cell Death: A Novel Therapeutic Target in Neurological Diseases.Molecular neurobiology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Neurological disorders are the leading health threats worldwide, characterized by impairments in consciousness, cognition, movement, and sensation, and can even lead to death. UFMylation is a novel post-translational modification (PTM) that serves as an important regulatory factor, promoting the complexity of protein structures and enhancing the diversity and specificity of functions. In UFMylation, ubiquitin-fold modifier 1 (UFM1) is covalently transferred to the primary amine of a lysine residue on the target protein through the synergistic action of three enzymes: the activating enzyme E1 of UFM1, the coupling enzyme E2 of UFM1, and the ligase E3. UFMylation has been proven to be involved in various cellular processes, such as the maintenance of genome homeostasis, autophagy, signal transduction during antiviral responses, cell death, and differentiation. Additionally, a growing number of evidence suggests that polymorphisms in genes related to the UFMylation system are associated with the risk of epileptic encephalopathy, microcephaly, neurodegenerative diseases, and schizophrenia. Therefore, the concept, enzymatic cascade, and biological functions of UFMylation are carefully summarized, along with its potential role in neurological diseases.
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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.