ArticleCell cycle (Georgetown, Tex.)2010
Int6 and Moe1 interact with Cdc48 to regulate ERAD and proper chromosome segregation.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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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.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Cdc48 influence on separase levels is independent of mitosis and suggests translational sensitivity of separase.Cell reports · 2022Article
- INT6/EIF3E Controls the RNF8-Dependent Ubiquitylation Pathway and Facilitates DNA Double-Strand Break Repair in Human Cells.Cancer research · 2016Article
- Assembly of eIF3 Mediated by Mutually Dependent Subunit Insertion.Structure (London, England : 1993) · 2016Article
- Knockdown of eIF3d inhibits cell proliferation through G2/M phase arrest in non-small cell lung cancer.Medical oncology (Northwood, London, England) · 2015Article
- Regulation of Ras localization and cell transformation by evolutionarily conserved palmitoyltransferases.Molecular and cellular biology · 2014Article
- Sequence, structure and functional diversity of PD-(D/E)XK phosphodiesterase superfamily.Nucleic acids research · 2012Article
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4 authors at 1 institution in 2 countries.
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Abstract
Int6/eIF3e is implicated in tumorigenesis, but its molecular functions remain unclear. We have studied its fission yeast homolog Yin6, reporting that it regulates proteolysis by controlling the assembly/localization of proteasomes, and binds directly to another conserved protein, Moe1. In the present study, we isolated Cdc48 as a Moe1-binding protein from a yeast two-hybrid screen, and confirmed biochemically that they form a stable complex in fission yeast. Overexpressing Moe1 or Yin6 partially rescued phenotypes of cdc48 mutants; conversely, overexpressing Cdc48 partially rescued phenotypes of moe1 or yin6 mutants. Mutants defective in both Cdc48 and the Yin6-Moe1 complex showed growth defects that were far more severe than either alone. These double mutants were severely deficient in endoplasmic reticulum associated degradation (ERAD), as they were hypersensitive to accumulation of misfolded proteins. In addition, their chromosomes showed frequent defects in spindle attachment and segregation--these mitotic defects correlated with Ase1 and Bir1/survivin mislocalization. These results suggest that Cdc48, Yin6 and Moe1 act in the same protein complex to concertedly control ERAD and chromosome segregation. Many of these properties are evolutionarily conserved in humans, since human Cdc48 rescued the lethality of the yeast cdc48Delta mutant, and Int6 and Moe1/eIF3d bind Cdc48 in human cells.
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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.