ArticlePloS one2015
KLHL12 Promotes Non-Lysine Ubiquitination of the Dopamine Receptors D4.2 and D4.4, but Not of the ADHD-Associated D4.7 Variant.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 14 citations in OpenAlex.
- Deciphering non-canonical ubiquitin signaling: biology and methodology.Frontiers in molecular biosciences · 2023Review
- Thioester and Oxyester Linkages in the Ubiquitin System.Methods in molecular biology (Clifton, N.J.) · 2023Review
- The roles of KLHL family members in human cancers.American journal of cancer research · 2022Review
- Post-Translational Modifications of G Protein-Coupled Receptors Control Cellular Signaling Dynamics in Space and Time.Pharmacological reviews · 2021Review
- Identification of a PGXPP degron motif in dishevelled and structural basis for its binding to the E3 ligase KLHL12.Open biology · 2020Article
- Targeted protein degradation: expanding the toolbox.Nature reviews. Drug discovery · 2019Article
- Isopeptide and ester bond ubiquitination both regulate degradation of the human dopamine receptor 4.The Journal of biological chemistry · 2017Article
- Regulation of G Protein-Coupled Receptors by Ubiquitination.International journal of molecular sciences · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DOPAMINE D4 RECEPTOR POLYMORPHISM: The dopamine D4 receptor has an important polymorphism in its third intracellular loop that is intensively studied and has been associated with several abnormal conditions, among others, attention deficit hyperactivity disorder. KLHL12 PROMOTES UBIQUITINATION OF THE DOPAMINE D4 RECEPTOR ON NON-LYSINE RESIDUES: In previous studies we have shown that KLHL12, a BTB-Kelch protein, specifically interacts with the polymorphic repeats of the dopamine D4 receptor and enhances its ubiquitination, which, however, has no influence on receptor degradation. In this study we provide evidence that KLHL12 promotes ubiquitination of the dopamine D4 receptor on non-lysine residues. By using lysine-deficient receptor mutants and chemical approaches we concluded that ubiquitination on cysteine, serine and/or threonine is possible. DIFFERENTIAL UBIQUITINATION OF THE DOPAMINE D4 RECEPTOR POLYMORPHIC VARIANTS: Additionally, we show that the dopamine D4.7 receptor variant, which is associated with a predisposition to develop attention deficient hyperactivity disorder, is differentially ubiquitinated compared to the other common receptor variants D4.2 and D4.4. Together, our study suggests that GPCR ubiquitination is a complex and variable process.
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.