ArticleThe EMBO journal2005
Phosducin-like protein acts as a molecular chaperone for G protein betagamma dimer assembly.
Article in The EMBO journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 104 citations in OpenAlex.
- G-protein regulatory network governs receptor internalization dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Disease-causing mutations in the G protein β5 β-propeller disrupt its chaperonin-mediated folding trajectory.bioRxiv : the preprint server for biology · 2025Article
- Comprehensive analysis of phosducin-like 3 as a diagnostic, prognostic and immunological marker in pan-cancer.Frontiers in immunology · 2025Article
- PDCL3 is a prognostic biomarker associated with immune infiltration in hepatocellular carcinoma.European journal of medical research · 2024Article
- A structural vista of phosducin-like PhLP2A-chaperonin TRiC cooperation during the ATP-driven folding cycle.Nature communications · 2024Article
- The evolutionarily conserved PhLP3 is essential for sperm development in Drosophila melanogaster.PloS one · 2024Article
- Visualizing the chaperone-mediated folding trajectory of the G protein β5 β-propeller.Molecular cell · 2023Article
- Structures of Ric-8B in complex with Gα protein folding clients reveal isoform specificity mechanisms.Structure (London, England : 1993) · 2023Article
- Phosducin-like proteinFrontiers in microbiology · 2023Article
- Review
- A genetic screen identifies a protective type III interferon response to Cryptosporidium that requires TLR3 dependent recognition.PLoS pathogens · 2022Article
- Prenatal diagnosis of 21 fetuses with balanced chromosomal abnormalities (BCAs) using whole-genome sequencing.Frontiers in genetics · 2022Article
- Novel Binding Partners for CCT and PhLP1 Suggest a Common Folding Mechanism for WD40 Proteins with a 7-Bladed Beta-Propeller Structure.Proteomes · 2021Article
- Fungal G-Protein-Coupled Receptors: A Promising Mediator of the Impact of Extracellular Signals on Biosynthesis of Ochratoxin A.Frontiers in microbiology · 2021Review
- Structures of Gα Proteins in Complex with Their Chaperone Reveal Quality Control Mechanisms.Cell reports · 2020Article
- Candidate Genes Associated With Neurological Findings in a Patient With Trisomy 4p16.3 and Monosomy 5p15.2.Frontiers in genetics · 2020Article
- Distinct RhoGEFs Activate Apical and Junctional Contractility under Control of G Proteins during Epithelial Morphogenesis.Current biology : CB · 2019Article
- Balancing the Photoreceptor Proteome: Proteostasis Network Therapeutics for Inherited Retinal Disease.Genes · 2019Review
- Structural and functional analysis of the role of the chaperonin CCT in mTOR complex assembly.Nature communications · 2019Article
- Archaeal Unfoldase Counteracts Protein Misfolding Retinopathy in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
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 at 2 institutions in 1 country.
Funding
Abstract
Phosducin-like protein (PhLP) is a widely expressed binding partner of the G protein betagamma subunit dimer (Gbetagamma). However, its physiological role is poorly understood. To investigate PhLP function, its cellular expression was blocked using RNA interference, resulting in inhibition of Gbetagamma expression and G protein signaling. This inhibition was caused by an inability of nascent Gbetagamma to form dimers. Phosphorylation of PhLP at serines 18-20 by protein kinase CK2 was required for Gbetagamma formation, while a high-affinity interaction of PhLP with the cytosolic chaperonin complex appeared unnecessary. PhLP bound nascent Gbeta in the absence of Ggamma, and S18-20 phosphorylation was required for Ggamma to associate with the PhLP-Gbeta complex. Once Ggamma bound, PhLP was released. These results suggest a mechanism for Gbetagamma assembly in which PhLP stabilizes the nascent Gbeta polypeptide until Ggamma can associate, resulting in membrane binding of Gbetagamma and release of PhLP to catalyze another round of assembly.
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.