ArticleMolecular and cellular biology2015
N-terminal α7 deletion of the proteasome 20S core particle substitutes for yeast PI31 function.
Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 16 citations in OpenAlex.
- Variants in the proteasome regulator PSMF1 cause a phenotypic spectrum from parkinsonism to perinatal lethality.Nature communications · 2026Article
- PI31 expression is neuroprotective in a mouse model of early-onset parkinsonism.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Rational design of proteasome inhibitors based on the structure of the endogenous inhibitor PI31/Fub1.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Yeast PI31 inhibits the proteasome by a direct multisite mechanism.Nature structural & molecular biology · 2022Article
- The proteasome regulator PI31 is required for protein homeostasis, synapse maintenance, and neuronal survival in mice.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- PI31 Is an Adaptor Protein for Proteasome Transport in Axons and Required for Synaptic Development.Developmental cell · 2019Article
- Dynamic Regulation of the 26S Proteasome: From Synthesis to Degradation.Frontiers in molecular biosciences · 2019Review
- Proteasome Structure and Assembly.Journal of molecular biology · 2017Review
- Evolution of proteasome regulators in eukaryotes.Genome biology and evolution · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proteasome core particle (CP) is a conserved protease complex that is formed by the stacking of two outer α-rings and two inner β-rings. The α-ring is a heteroheptameric ring of subunits α1 to α7 and acts as a gate that restricts entry of substrate proteins into the catalytic cavity formed by the two abutting β-rings. The 31-kDa proteasome inhibitor (PI31) was originally identified as a protein that binds to the CP and inhibits CP activity in vitro, but accumulating evidence indicates that PI31 is required for physiological proteasome activity. To clarify the in vivo role of PI31, we examined the Saccharomyces cerevisiae PI31 ortholog Fub1. Fub1 was essential in a situation where the CP assembly chaperone Pba4 was deleted. The lethality of Δfub1 Δpba4 was suppressed by deletion of the N terminus of α7 (α7ΔN), which led to the partial activation of the CP. However, deletion of the N terminus of α3, which activates the CP more efficiently than α7ΔN by gate opening, did not suppress Δfub1 Δpba4 lethality. These results suggest that the α7 N terminus has a role in CP activation different from that of the α3 N terminus and that the role of Fub1 antagonizes a specific function of the α7 N terminus.
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.