ArticleThe Journal of biological chemistry2009
Control of rapsyn stability by the CUL-3-containing E3 ligase complex.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
14 citing papers in PubMed, 32 citations in OpenAlex.
- Rapsyn Homolog RPY-1 Modulates Locomotor Responses ofBiomedicines · 2026Article
- High-throughput behavioural phenotyping of 25 C. elegans disease models including patient-specific mutations.BMC biology · 2025Article
- Deciphering the alteration of MAP2 interactome caused by a schizophrenia-associated phosphorylation.Neurobiology of disease · 2024Article
- The role of Rapsyn in neuromuscular junction and congenital myasthenic syndrome.Biomolecules & biomedicine · 2023Review
- The roles of KLHL family members in human cancers.American journal of cancer research · 2022Review
- An Inside Job: Molecular Determinants for Postsynaptic Localization of Nicotinic Acetylcholine Receptors.Molecules (Basel, Switzerland) · 2021Review
- Cullin-3 dependent deregulation of ACTN1 represents a new pathogenic mechanism in nemaline myopathy.JCI insight · 2019Article
- Article
- Cullin-3-RING ubiquitin ligase activity is required for striated muscle function in mice.The Journal of biological chemistry · 2018Article
- Functional analysis of Cullin 3 E3 ligases in tumorigenesis.Biochimica et biophysica acta. Reviews on cancer · 2018Review
- Cullin E3 Ligase Activity Is Required for Myoblast Differentiation.Journal of molecular biology · 2017Article
- The emerging family of CULLIN3-RING ubiquitin ligases (CRL3s): cellular functions and disease implications.The EMBO journal · 2013Review
- The ubiquitin-fold modifier 1 (Ufm1) cascade of Caenorhabditis elegans.The Journal of biological chemistry · 2013Article
- Selective proteasomal degradation of the B'β subunit of protein phosphatase 2A by the E3 ubiquitin ligase adaptor Kelch-like 15.The Journal of biological chemistry · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rapsyn is a postsynaptic protein required for clustering of nicotinic acetylcholine receptors (nAChRs) at the neuromuscular junction. Here we report the mechanism for posttranslational control of rapsyn protein stability. We confirmed that C18H9.7-encoded RPY-1 is a rapsyn homolog in Caenorhabditis elegans by showing that human rapsyn rescued rpy-1 mutant phenotypes in nematodes, as determined by levamisole assays and micropost array behavioral assays. We found that RPY-1 was degraded in the absence of functional UNC-29, a non-alpha subunit of the receptor, in an allele-specific manner, but not in the absence of other receptor subunits. The cytoplasmic loop of UNC-29 was found to be critical for RPY-1 stability. Through RNA interference screening, we found that UBC-1, UBC-12, NEDD-8, and RBX-1 were required for degradation of RPY-1. We identified cullin (CUL)-3 as a component of E3 ligase and KEL-8 as the substrate adaptor of RPY-1. Mammalian rapsyn was ubiquitinated by the CUL3/KLHL8-containing E3 ligase in vitro, and the knockdown of KLHL-8, a mammalian KEL-8 homolog, inhibited rapsyn ubiquitination in vivo, implying evolutionary conservation of the rapsyn stability control machinery. kel-8 suppression and rpy-1 overexpression in C. elegans produced a phenotype similar to that of a loss-of-function mutation of rpy-1, suggesting that control of rapsyn abundance is important for proper function of the receptor. Our results suggest a link between the control of rapsyn abundance and congenital myasthenic syndromes.
Indexed as
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.