ArticleMolecular biology of the cell2025
The kinesin Kar3 is required for endoplasmic reticulum-associated degradation.
Article in Molecular biology of the cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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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Who cites it
3 citing papers in PubMed.
- From static definitions to dynamic landscapes: physiological states in yeast.Frontiers in microbiology · 2026Article
- Ubiquitin-elongating enzyme Ufd2 confers resistance to hygromycin B inmicroPublication biology · 2026Article
- Ubiquitin-conjugating enzyme membrane anchor Cue1 confers resistance to hygromycin B inmicroPublication biology · 2026Article
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Authors and funding
17 authors.
Funding
Abstract
Degradation of aberrant, excess, and regulatory proteins at the endoplasmic reticulum (ER) is a conserved feature of eukaryotic cells, disruption of which contributes to disease. While remarkable progress has been made in recent years, mechanisms and genetic requirements for ER-associated degradation (ERAD) remain incompletely understood. We recently conducted a screen for genes required for turnover of a model ER translocon-associated substrate of the Hrd1 ubiquitin ligase in
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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.