ArticleEMBO reports2022
UBXD8 mediates mitochondria-associated degradation to restrain apoptosis and mitophagy.
Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 49 citations in OpenAlex.
- FAF1 and FAF2 enhance unfolding by p97-UFD1-NPL4 complex enabling rational design of p97 activators.The EMBO journal · 2026Article
- Faf2 is required for neural differentiation in embryonic neural progenitor cells.bioRxiv : the preprint server for biology · 2026Article
- Gene Expression Analysis of Mitochondria-Associated Membrane (MAM)-Related Genes in ER Stress and Alzheimer's Disease.Cellular and molecular neurobiology · 2026Article
- Quality control of protein import into mammalian mitochondria.Protein science : a publication of the Protein Society · 2026Review
- The accessory adapters FAF1, FAF2, and UBXN7 accelerate proteasomal degradation by increasing prior p97-mediated substrate unfolding.Science advances · 2026Article
- The endoplasmic reticulum in mitochondrial protein targeting: A neuronal perspective on organelle crosstalk.Protein science : a publication of the Protein Society · 2026Review
- Intestine-specific Faf2 depletion ameliorates obesity and metabolic dysfunction-associated steatotic liver disease by impairing lipid absorption.International journal of biological sciences · 2026Article
- Mastering cardiomyocyte mitophagy: molecular governance, pathological derailment and therapeutics.PeerJ · 2026Review
- Faf2 is required for neural differentiation in embryonic neural progenitor cells.Frontiers in cell and developmental biology · 2026Article
- The many faces of p97/Cdc48 in mitochondrial homeostasis.Essays in biochemistry · 2025Review
- Lysosomal proteomics reveals mechanisms of neuronal APOE4-associated lysosomal dysfunction.Autophagy · 2025Article
- A UBH-UBX module amplifies p97/VCP's unfolding power to facilitate protein extraction and degradation.Nature communications · 2025Article
- Article
- The p97 ATPase and its adaptor UBXD8 maintain peroxisome pools by preventing pexophagy.The Journal of cell biology · 2025Article
- FAF2 is a bifunctional regulator of peroxisomal homeostasis and saturated lipid responses.Science advances · 2025Article
- Neurotoxicity of Realgar: Crosstalk Between UBXD8-DRP1-Regulated Mitochondrial Fission and PINK1-Parkin-Mediated Mitophagy.Molecular neurobiology · 2025Article
- Development of a prognostic model for osteosarcoma based on macrophage polarization-related genes using machine learning: implications for personalized therapy.Clinical and experimental medicine · 2025Article
- Lysosomal proteomics reveals mechanisms of neuronal apoE4-associated lysosomal dysfunction.bioRxiv : the preprint server for biology · 2025Article
- Mitochondrial protein import stress.Nature cell biology · 2025Review
- Targeting EGFR-binding protein SLC7A11 enhancing antitumor immunity of T cells via inducing MHC-I antigen presentation in nasopharyngeal carcinoma.Cell death & disease · 2025Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hexameric AAA-ATPase valosin-containing protein (VCP) is essential for mitochondrial protein quality control. How VCP is recruited to mammalian mitochondria remains obscure. Here we report that UBXD8, an ER- and lipid droplet-localized VCP adaptor, also localizes to mitochondria and locally recruits VCP. UBXD8 associates with mitochondrial and ER ubiquitin E3 ligases and targets their substrates for degradation. Remarkably, both mitochondria- and ER-localized UBXD8 can degrade mitochondrial and ER substrates in cis and in trans. UBXD8 also associates with the TOM complex but is dispensable for translocation-associated degradation. UBXD8 knockout impairs the degradation of the pro-survival protein Mcl1 but surprisingly sensitizes cells to apoptosis and mitochondrial stresses. UBXD8 knockout also hyperactivates mitophagy. We identify pro-apoptotic BH3-only proteins Noxa, Bik, and Bnip3 as novel UBXD8 substrates and determine that UBXD8 inhibits apoptosis via degrading Noxa and restrains mitophagy via degrading Bnip3. Collectively, our characterizations reveal UBXD8 as the major mitochondrial adaptor of VCP and unveil its role in apoptosis and mitophagy regulation.
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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.