ArticleThe Journal of biological chemistry2011
A Cdc48p-associated factor modulates endoplasmic reticulum-associated degradation, cell stress, and ubiquitinated protein homeostasis.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- The vacuolar tauopathy-associated mutation D395G confers redox sensitivity to p97/VCP.bioRxiv : the preprint server for biology · 2026Article
- Genes controlling hydrolysate toxin tolerance identified by QTL analysis of the natural Saccharomyces cerevisiae BCC39850.Applied microbiology and biotechnology · 2024Article
- Bidirectional substrate shuttling between the 26S proteasome and the Cdc48 ATPase promotes protein degradation.Molecular cell · 2024Article
- The unfolded protein response of the endoplasmic reticulum supports mitochondrial biogenesis by buffering nonimported proteins.Molecular biology of the cell · 2023Article
- Aplysia Neurons as a Model of Alzheimer's Disease: Shared Genes and Differential Expression.Journal of molecular neuroscience : MN · 2022Article
- The Origin and Evolution of Release Factors: Implications for Translation Termination, Ribosome Rescue, and Quality Control Pathways.International journal of molecular sciences · 2019Review
- A Proteomic Variant Approach (ProVarA) for Personalized Medicine of Inherited and Somatic Disease.Journal of molecular biology · 2018Article
- Correcting the F508del-CFTR variant by modulating eukaryotic translation initiation factor 3-mediated translation initiation.The Journal of biological chemistry · 2018Article
- Cdc48/p97 segregase is modulated by cyclin-dependent kinase to determine cyclin fate during G1 progression.The EMBO journal · 2018Article
- A Futile Battle? Protein Quality Control and the Stress of Aging.Developmental cell · 2018Review
- Deviation of the typical AAA substrate-threading pore prevents fatal protein degradation in yeast Cdc48.Scientific reports · 2017Article
- Identification of Genes inG3 (Bethesda, Md.) · 2017Article
- Hallmarks of therapeutic management of the cystic fibrosis functional landscape.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2015Review
- Proteomics of yeast telomerase identified Cdc48-Npl4-Ufd1 and Ufd4 as regulators of Est1 and telomere length.Nature communications · 2015Article
- The requirement for Cdc48/p97 in nuclear protein quality control degradation depends on the substrate and correlates with substrate insolubility.Journal of cell science · 2014Article
- The Cdc48-Vms1 complex maintains 26S proteasome architecture.The Biochemical journal · 2014Article
- A conserved protein with AN1 zinc finger and ubiquitin-like domains modulates Cdc48 (p97) function in the ubiquitin-proteasome pathway.The Journal of biological chemistry · 2013Article
- Cdc48-associated complex bound to 60S particles is required for the clearance of aberrant translation products.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Statistical analysis reveals co-expression patterns of many pairs of genes in yeast are jointly regulated by interacting loci.PLoS genetics · 2013Article
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The hexameric AAA-ATPase, Cdc48p, catalyzes an array of cellular activities, including endoplasmic reticulum (ER)-associated degradation (ERAD), ER/Golgi membrane dynamics, and DNA replication. Accumulating data suggest that unique Cdc48p partners, such as Npl4p-Ufd1p and Ubx1p/Shp1p (p47 in vertebrates), target Cdc48p for these diverse functions. Other Cdc48p-associated proteins have been identified, but the interplay among these factors and their activities is largely cryptic. We now report on a previously uncharacterized Cdc48p-associated protein, Ydr049p, also known as Vms1p, which binds Cdc48p at both the ER membrane and in the cytosol under non-stressed conditions. Loss of YDR049 modestly slows the degradation of the cystic fibrosis transmembrane conductance regulator but does not impede substrate ubiquitination, suggesting that Ydr049p acts at a postubiquitination step in the ERAD pathway. Consistent with Ydr049p playing a role in Cdc48p substrate release, ydr049 mutant cells accumulate Cdc48p-bound ubiquitinated proteins at the ER membrane. Moreover, YDR049 interacts with genes encoding select UBX (ubiquitin regulatory X) and UFD (ubiquitin fusion degradation) proteins, which are Cdc48p partners. Exacerbated growth defects are apparent in some of the mutant combinations, and synergistic effects on the degradation of cystic fibrosis transmembrane conductance regulator and CPY*, which is a soluble ERAD substrate, are evident in specific ydr049-ufd and -ubx mutants. These data suggest that Ydr049p acts in parallel with Cdc48p partners to modulate ERAD and other cellular activities.
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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.