Affinage

FAF2

FAS-associated factor 2 · UniProt Q96CS3

Length
445 aa
Mass
52.6 kDa
Annotated
2026-06-09
28 papers in source corpus 21 papers cited in narrative 22 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FAF2 (UBXD8/ETEA/UBXN3B) is a membrane-embedded UBA-UAS-UBX adaptor that recruits the p97/VCP AAA-ATPase to organelle membranes to drive ubiquitin-dependent substrate extraction and proteasomal degradation, coordinating lipid homeostasis, organelle quality control, and degradation-linked signaling (PMID:23297223, PMID:35979733, PMID:41790892). Mechanistically, a helix-UBX segment of FAF2 tethers the UT3 ubiquitin-binding module of the Ufd1 cofactor to the p97 N-domain, positioning Ufd1 for efficient substrate loading and thereby accelerating p97-Ufd1-Npl4-mediated substrate unfolding and degradation (PMID:41790892). FAF2 cycles dynamically between the ER and nascent lipid droplets in the plane of the membrane, with its ER↔LD partitioning set by the rhomboid pseudoprotease UBAC2 (PMID:23297223, PMID:19773358), and it controls triglyceride metabolism both by acting as a structural sensor for long-chain unsaturated fatty acids—its UAS domain polymerizing through positively charged surface residues to relieve inhibition of diacylglycerol-to-triglyceride conversion (PMID:21115839, PMID:23720822)—and by binding ATGL to displace its coactivator CGI-58 and limit lipolysis (PMID:23297223). As a degradation adaptor it is essential for sterol-stimulated dislocation of ubiquitylated HMGCR and for dislocation of lipidated ApoB-100 from the LD surface (PMID:22238364, PMID:28882874), and at mitochondria and ER-mitochondria contact sites it recruits p97 to degrade pro-apoptotic Noxa and Bnip3 and to regulate contact-site abundance and membrane lipid saturation via SREBP1-SCD1 (PMID:35979733, PMID:36746962). FAF2 also acts catalytically toward neurofibromin, ubiquitinating its GAP-related domain to suppress Ras activity (PMID:20160012), maintains peroxisome abundance by limiting ubiquitinated ABCD3/PMP70 to suppress pexophagy (PMID:39386596, PMID:39929145, PMID:40601736), and positively regulates STING-mediated antiviral interferon signaling by promoting STING ubiquitination and dimerization with TRIM56 (PMID:29899553).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 2009 High

    Establishing how an ER-resident protein reaches lipid droplets defined FAF2's bidirectional organelle trafficking, a prerequisite for understanding its lipid functions.

    Evidence Live-cell imaging with dominant-negative Sar1 and protein synthesis inhibition in mammalian cells

    PMID:19773358

    Open questions at the time
    • Molecular signal driving in-membrane ER→LD migration not defined
    • Did not address what FAF2 does once at the LD
  2. 2010 High

    Identifying FAF2 as a structural sensor of unsaturated fatty acids explained how it couples lipid composition to triglyceride synthesis.

    Evidence In vitro biochemistry on purified recombinant protein (thermal stability, limited proteolysis, oligomerization) plus cellular TG synthesis assay

    PMID:21115839

    Open questions at the time
    • Structural basis of FA-induced conformational change not resolved at this stage
    • Downstream effector linking FAF2 to DAG-to-TG conversion not identified
  3. 2010 High

    Demonstrating FAF2-dependent ubiquitination of neurofibromin assigned it a direct catalytic role in restraining Ras signaling.

    Evidence In vitro ubiquitination with purified proteins and UBX-deletion mutant, plus siRNA gain/loss-of-function with Ras activity readout

    PMID:20160012

    Open questions at the time
    • Whether FAF2 acts as the E3 itself or recruits an E3 not fully clarified
    • Physiological context of neurofibromin regulation not established
  4. 2012 High

    Linking FAF2 to p97 recruitment and ApoB dislocation established its role as a membrane extraction adaptor for lipoprotein quality control.

    Evidence siRNA knockdown, Co-IP with Derlin-1, and proteasome inhibitor assays in Huh7 cells

    PMID:22238364

    Open questions at the time
    • E3 ligase ubiquitinating ApoB at the LD not identified
    • Step ordering relative to Derlin-1 inferred from binding partitioning
  5. 2012 Medium

    Yeast Ubx2 complementation showed the LD/TAG-maintenance function of FAF2 is evolutionarily conserved.

    Evidence Yeast deletion genetics, TAG quantification, Lro1 localization, and complementation with mammalian UBXD8

    PMID:22454508

    Open questions at the time
    • Primary mechanistic data are from yeast
    • Lro1 has no direct mammalian counterpart tested here
  6. 2013 High

    Mapping UAS-domain polymerization to specific charged residues provided the molecular mechanism for FA sensing.

    Evidence In vitro polymerization of purified UAS domain with charge-reversal mutagenesis and cell-based TG assay

    PMID:23720822

    Open questions at the time
    • Atomic structure of the polymerized UAS filament not determined
    • How polymerization translates into altered TG synthesis enzymatically unresolved
  7. 2013 High

    Defining the ATGL-CGI-58 axis and UBAC2-controlled partitioning connected FAF2's localization to its control of lipolysis and droplet size.

    Evidence Reciprocal Co-IP, direct binding, knockdown/overexpression with LD-size and TG-hydrolysis readouts

    PMID:23297223

    Open questions at the time
    • Mechanism by which UBAC2 retains FAF2 in the ER not detailed
    • Whether p97 acts catalytically or structurally in CGI-58 displacement unclear
  8. 2013 High

    Showing the p97-FAF2 complex releases ubiquitinated HuR extended its extraction activity to mRNP remodeling and mRNA stability.

    Evidence Co-IP, RIP, ubiquitination assay, and mRNA stability measurements with knockdown

    PMID:23618873

    Open questions at the time
    • E3 generating K29 chains on HuR not identified
    • Subcellular site of mRNP remodeling not localized
  9. 2013 Medium

    An ALS-linked UBQLN2 mutation that disrupts FAF2 binding implicated FAF2 in cytosolic transport of ERAD substrates and neurodegenerative disease.

    Evidence Co-IP in vitro and in vivo with ERAD substrate accumulation assays

    PMID:24215460

    Open questions at the time
    • Single-lab study with mechanism partly inferred from prior FAF2 function
    • Direct demonstration of substrate hand-off to UBQLN2 lacking
  10. 2017 High

    An unbiased genetic screen identified FAF2 as essential for sterol-stimulated HMGCR dislocation, placing it centrally in cholesterol-synthesis feedback control.

    Evidence Haploid CRISPR fluorescent-reporter screen, ablation in multiple cell types, and HMGCR dislocation assay with UBX-domain analysis

    PMID:28882874

    Open questions at the time
    • Step at which FAF2 acts relative to known HMGCR E3s not resolved
    • Direct binding to HMGCR not demonstrated
  11. 2017 Low

    FAF2 was linked to DRP1-dependent mitochondrial fission under arsenic stress, hinting at a mitochondrial role.

    Evidence siRNA knockdown, Mdivi-1, DRP1 localization, and apoptosis assays in PC12 cells

    PMID:39570499

    Open questions at the time
    • Single-lab study in a specific toxicity context without reconstitution
    • Direct FAF2-DRP1 interaction not shown
    • Mechanism of DRP1 translocation control undefined
  12. 2018 High

    Identifying FAF2 as a positive regulator of STING ubiquitination and dimerization extended its adaptor role into antiviral innate immunity.

    Evidence Co-IP with STING and TRIM56, ubiquitination assay, inducible knockout mice, and in vivo viral challenge

    PMID:29899553

    Open questions at the time
    • Whether p97 recruitment is required for STING regulation not addressed
    • Structural basis of FAF2-STING-TRIM56 assembly unknown
  13. 2021 Medium

    FAF2 was shown to sustain BLNK stability and pre-BCR signaling, defining a role in B lymphopoiesis.

    Evidence Conditional and constitutive Ubxn3b knockout mice, bone marrow transfer, flow cytometry, and RNA sequencing (preprint)

    PMID:34462748

    Open questions at the time
    • Preprint, not peer-reviewed at this version
    • Direct mechanism of BLNK stabilization not biochemically defined
  14. 2022 High

    Localizing FAF2 to mitochondria and identifying Noxa and Bnip3 as substrates established it as a multi-organelle p97 adaptor restraining apoptosis and mitophagy.

    Evidence Subcellular fractionation, Co-IP with E3 ligases and TOM complex, and knockout with apoptosis/mitophagy phenotypes

    PMID:35979733

    Open questions at the time
    • In cis vs in trans substrate targeting rules not fully defined
    • How FAF2 selects among multiple membrane E3 partners unclear
  15. 2023 High

    Demonstrating p97-FAF2 control of ER-mitochondria contact sites and membrane lipid saturation tied its extraction activity to organelle architecture and lipid remodeling.

    Evidence Quantitative proteomics, lipidomics, proximity ligation assay, knockout, p97 inhibition, and SCD1/unsaturated FA rescue

    PMID:36746962

    Open questions at the time
    • Substrate whose degradation controls ERMCS abundance not identified
    • Link between contact-site regulation and SREBP1-SCD1 only partly mechanistic
  16. 2024 Medium

    FAF2 was found to suppress pexophagy by limiting ubiquitinated PMP70/ABCD3, defining a peroxisomal quality-control role.

    Evidence Peroxisomal-fraction proteomics, knockout, autophagy-protein and USP30 rescue, and PMP70 ubiquitination assay (preprint)

    PMID:39386596

    Open questions at the time
    • Preprint, not peer-reviewed
    • E3 ubiquitinating ABCD3 not identified
  17. 2025 Medium

    Peer-reviewed and genome-wide screen studies confirmed VCP-FAF2 control of peroxisome abundance and assigned UBX and UAS domains to this function and to saturated FA stress responses.

    Evidence Loss-of-function with ABCD3 ubiquitination, genome-wide CRISPR screen, and domain-deletion analysis with lipotoxicity readout

    PMID:39929145 PMID:40601736

    Open questions at the time
    • UAS domain mechanism in peroxisomal context inferred rather than reconstituted
    • Bifunctional coupling of lipid sensing and pexophagy not biochemically resolved
  18. 2025 Medium

    In vivo hepatic knockdown linked FAF2 to ATGL/CGI-58, Elmod2, and FOXO3-SIRT6-PCSK9/LDLR pathways in alcohol-induced steatosis, extending its lipid role to disease physiology.

    Evidence AAV-shRNA knockdown in mice, ethanol-binge model, ATGL activity and PCSK9/LDLR analyses

    PMID:39969435

    Open questions at the time
    • Direct vs transcriptional regulation of these pathways not separated
    • p97-dependence of the steatosis phenotype not tested
  19. 2025 High

    Engineering polyserine-targeted FAF2 to clear tau aggregates revealed a VCP-independent, ubiquitination- and membrane-dependent activity with therapeutic potential in neurodegeneration.

    Evidence Polyserine-fusion targeting, genetic VCP-independence dissection, domain mutants, and PS19 mouse and Drosophila tau models

    PMID:40902597

    Open questions at the time
    • Mechanism of VCP-independent tau clearance not biochemically defined
    • Endogenous relevance of this activity to native tau handling unclear
  20. 2026 High

    Reconstitution showed FAF2 accelerates degradation by tethering Ufd1 to the p97 N-domain, defining the molecular basis of its adaptor activity.

    Evidence Reconstituted in vitro p97-Ufd1-Npl4 unfolding coupled to proteasomal degradation with helix-UBX mutagenesis

    PMID:41790892

    Open questions at the time
    • How membrane substrate selection integrates with this core mechanism not addressed
    • Structure of the full FAF2-Ufd1-p97 assembly on a substrate not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How FAF2's distinct activities—FA sensing via UAS polymerization, catalytic ubiquitination, and p97-Ufd1 tethering—are integrated and selectively deployed across the ER, lipid droplets, mitochondria, and peroxisomes remains unresolved.
  • No unifying model linking membrane localization to substrate choice
  • E3 ligases for several substrates (ApoB, HMGCR, ABCD3, HuR) not all identified
  • No high-resolution structure of full-length membrane-embedded FAF2

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 5 GO:0008289 lipid binding 2 GO:0098772 molecular function regulator activity 2 GO:0140299 molecular sensor activity 2 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005811 lipid droplet 4 GO:0005777 peroxisome 3 GO:0005783 endoplasmic reticulum 3 GO:0005739 mitochondrion 2 GO:0005886 plasma membrane 1
Pathway
R-HSA-1430728 Metabolism 5 R-HSA-392499 Metabolism of proteins 4 R-HSA-9612973 Autophagy 4 R-HSA-168256 Immune System 1 R-HSA-5357801 Programmed Cell Death 1 R-HSA-8953854 Metabolism of RNA 1
Partners
ATGLDERL1STING1TRIM56UBAC2UBQLN2UFD1VCP
Complex memberships
p97/VCP-Ufd1-Npl4 complex

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2013 UBXD8 (FAF2) binds directly to ATGL (adipose triglyceride lipase) and promotes dissociation of its endogenous coactivator CGI-58, thereby inhibiting triacylglycerol hydrolysis and increasing lipid droplet size; this function requires recruitment of p97/VCP to lipid droplets. Co-immunoprecipitation, direct binding assay, knockdown/overexpression with functional lipid droplet size readout Proceedings of the National Academy of Sciences of the United States of America High 23297223
2013 Association of UBXD8 (FAF2) with the ER-resident rhomboid pseudoprotease UBAC2 restricts trafficking of UBXD8 to lipid droplets; relative expression of UBAC2 controls the steady-state partitioning of UBXD8 between the ER and lipid droplets. Co-immunoprecipitation, overexpression/knockdown with subcellular fractionation and imaging Proceedings of the National Academy of Sciences of the United States of America High 23297223
2009 UBXD8 (FAF2) migrates from its site of insertion in the ER membrane to forming lipid droplets in the plane of the membrane (not via the secretory pathway), and returns to the ER when lipid droplets regress, establishing a cyclic ER↔LD trafficking pathway. Live-cell imaging, dominant-negative Sar1 block of secretory pathway, protein synthesis inhibition, fluorescence microscopy Journal of cell science High 19773358
2012 UBXD8 (FAF2) is required for recruitment of p97 to lipid droplets and for the dislocation of lipidated ApoB-100 from the LD surface for proteasomal degradation; UBXD8 and Derlin-1 bind each other and both bind lipidated ApoB, acting at post-dislocation and pre-dislocation steps respectively. siRNA knockdown, Co-immunoprecipitation, immunofluorescence, proteasome inhibitor assays in Huh7 cells Molecular biology of the cell High 22238364
2010 Ubxd8 (FAF2) acts as a sensor for unsaturated fatty acids: unsaturated but not saturated long-chain FAs alter the structure of purified recombinant Ubxd8 (thermal stability, trypsin cleavage pattern, oligomerization), and this structural change relieves Ubxd8-mediated inhibition of diacylglycerol-to-triglyceride conversion. In vitro biochemical assay with purified recombinant protein (thermal stability, limited proteolysis, oligomerization), cell-based TG synthesis assay with FA supplementation Proceedings of the National Academy of Sciences of the United States of America High 21115839
2013 The UAS domain of Ubxd8 (FAF2) mediates polymerization in response to long-chain unsaturated fatty acids; positively charged surface residues in the UAS domain are required, and charge-reversal mutations (to glutamate) prevent FA-induced oligomerization and abolish unsaturated FA-dependent regulation in cells. In vitro polymerization assay with purified UAS domain, site-directed mutagenesis, cell-based TG synthesis assay Journal of lipid research High 23720822
2013 The p97-UBXD8 (FAF2) complex destabilizes mRNA by promoting release of ubiquitinated HuR from mRNP; K29-linked ubiquitin chain on HuR serves as the signal for its release from mRNA targets including p21, MKP-1, and SIRT1 mRNAs. Co-immunoprecipitation, mRNA stability assay, ubiquitination assay, RIP (RNA immunoprecipitation), knockdown Genes & development High 23618873
2013 Pathogenic ALS-linked mutation of UBQLN2 impairs its interaction with UBXD8 (FAF2) in vitro and in vivo, disrupting ERAD; UBQLN2 cooperates with UBXD8 to transport ubiquitinated ERAD substrates from the ER to the cytosol for degradation. Co-immunoprecipitation (in vitro and in vivo), ERAD substrate accumulation assay, knockdown/overexpression Journal of neurochemistry Medium 24215460
2010 ETEA (FAF2) directly interacts with neurofibromin and negatively regulates it; purified ETEA (but not a UBX-domain deletion mutant) ubiquitinates the neurofibromin GAP-related domain in vitro; ETEA overexpression downregulates neurofibromin and silencing increases neurofibromin levels and reduces Ras activity. Co-immunoprecipitation, in vitro ubiquitination assay with purified proteins, UBX-domain deletion mutant, siRNA knockdown with Ras activity assay Molecular and cellular biology High 20160012
2017 UBXD8 (FAF2) is an essential determinant of sterol-stimulated proteasomal degradation of HMGCR (HMG-CoA reductase); UBXD8 is required for sterol-stimulated dislocation of ubiquitylated HMGCR from the ER membrane en route to proteasomal degradation, and this function depends on its UBX domain. Haploid genetic screen (CRISPR/Cas9 fluorescent reporter), UBXD8 ablation in multiple cell types, UBX-domain functional analysis, HMGCR dislocation assay Arteriosclerosis, thrombosis, and vascular biology High 28882874
2018 UBXN3B (FAF2) interacts with both STING and its E3 ligase TRIM56, and facilitates STING ubiquitination, dimerization, trafficking, and consequent recruitment and phosphorylation of TBK1, thereby positively regulating STING-mediated antiviral interferon signaling. Co-immunoprecipitation, ubiquitination assay, tamoxifen-inducible Cre-LoxP knockout mice, in vivo viral challenge, primary cell immune assays Nature communications High 29899553
2022 UBXD8 (FAF2) localizes to mitochondria and locally recruits VCP/p97; it associates with mitochondrial and ER ubiquitin E3 ligases and targets their substrates for degradation in cis and in trans; UBXD8 degrades pro-apoptotic BH3-only proteins Noxa and Bnip3, thereby restraining apoptosis and mitophagy respectively. Subcellular fractionation, Co-immunoprecipitation with E3 ligases and TOM complex, UBXD8 knockout with substrate accumulation, apoptosis assays, mitophagy assays, identification of novel substrates EMBO reports High 35979733
2023 The p97-UBXD8 (FAF2) complex localizes to ER-mitochondria contact sites (ERMCS) and regulates their abundance; loss of UBXD8 increases ERMCS in a p97 catalytic activity-dependent manner, alters membrane lipid saturation via SREBP1-SCD1, and this aberrant phenotype can be rescued by unsaturated fatty acids or SCD1 overexpression. Quantitative proteomics, lipidomics, proximity ligation assay for ERMCS, UBXD8 knockout, p97 inhibition, SCD1/SREBP1 pathway analysis Nature communications High 36746962
2024 The p97-UBXD8 (FAF2) complex maintains peroxisome abundance by suppressing pexophagy; loss of UBXD8 increases ubiquitylation of the peroxisomal membrane protein PMP70/ABCD3 and triggers selective autophagic peroxisomal degradation that is rescued by depleting autophagy proteins or overexpressing deubiquitylase USP30. Quantitative proteomics of peroxisomal fraction, UBXD8 knockout, autophagy protein depletion rescue, USP30 overexpression rescue, PMP70 ubiquitination assay bioRxivpreprint Medium 39386596
2025 The VCP-FAF2 complex prevents excessive pexophagy by regulating the accumulation of ubiquitinated ABCD3 (peroxisomal membrane protein); FAF2 loss leads to ABCD3 ubiquitin accumulation and autophagic peroxisome degradation. UBXD8/FAF2 loss-of-function, ubiquitination assay for ABCD3, pexophagy measurement Autophagy Medium 39929145
2025 FAF2 (UBXD8) is a bifunctional regulator of peroxisomal homeostasis; its UBX and UAS thioredoxin-like domains are required for peroxisomal protein abundance and the cellular response to saturated fatty acid-induced stress. Genome-wide CRISPR knockout screen, domain deletion analysis, FAF2 knockout with peroxisomal protein abundance readout and lipotoxicity assay Science advances Medium 40601736
2026 FAF2 (and FAF1) are accessory adapters that accelerate proteasomal degradation by boosting p97-Ufd1-Npl4-mediated substrate unfolding; a helix-UBX segment in FAF2 tethers the UT3 ubiquitin-binding module of Ufd1 to the p97 N-domain, positioning Ufd1 for efficient substrate loading; mutations disrupting the helix-Ufd1 interaction reduce stimulation of degradation. Reconstituted in vitro p97-Ufd1-Npl4-mediated unfolding coupled to proteasomal degradation, mutagenesis of helix-UBX segment, functional degradation assay Science advances High 41790892
2025 Polyserine-targeted FAF2/UBXD8 suppresses tau aggregation independent of VCP but requires ubiquitination, membrane localization, and the UBX domain; delivery of targeted FAF2/UBXD8 reduces insoluble tau, seeding capacity, and gliosis in PS19 tau transgenic mice and rescues tau-induced neurodegeneration in Drosophila. Polyserine-fusion targeting, VCP-independent rescue (genetic dissection), domain deletion (UBX, ubiquitination-deficient mutants), Drosophila neurodegeneration model, PS19 mouse tau model with biochemical and behavioral readouts Neuron High 40902597
2012 Yeast Ubx2 (the ortholog of mammalian UBXD8/FAF2) is required for LD maintenance and TAG homeostasis; it redistributes from ER to LDs during LD formation and is required for proper localization of the TAG-synthesizing enzyme Lro1; mammalian UBXD8/FAF2 complements the ubx2Δ defect, indicating functional conservation. Yeast genetics (deletion mutant), TAG quantification, fluorescence microscopy of Lro1 localization, complementation with mammalian UBXD8 Journal of cell science Medium 22454508
2021 UBXN3B (FAF2) controls pre-B cell transition by maintaining BLNK protein stability and pre-BCR signaling; Ubxn3b deficiency leads to impaired pre-BI to pre-BII transition with cell cycle arrest and apoptosis, in a cell-intrinsic manner. Conditional and constitutive Ubxn3b knockout mice, bone marrow transfer, flow cytometry, immunoblotting for BLNK, single-cell and bulk RNA sequencing bioRxivpreprint Medium 34462748
2017 UBXD8 (FAF2) promotes mitochondrial fission by facilitating DRP1 translocation to mitochondria, where DRP1 undergoes phosphorylation; siRNA knockdown of UBXD8 reduces arsenic-induced DRP1 mitochondrial translocation and attenuates mitochondrial over-fission and apoptosis. siRNA knockdown, mitochondrial fission inhibitor (Mdivi-1), DRP1 localization by immunofluorescence/fractionation, apoptosis assay in PC12 cells Molecular neurobiology Low 39570499
2025 FAF2 knockdown in mouse liver enhances ATGL lipolytic activity by upregulating CGI-58 and downregulating Elmod2, and regulates PCSK9/LDLR via the FOXO3-SIRT6 pathway, contributing to alleviation of alcohol-induced steatosis. AAV-delivered shRNA knockdown in mice, ethanol-binge model, gene expression analysis, ATGL activity assay, PCSK9/LDLR quantification Hepatology communications Medium 39969435

Source papers

Stage 0 corpus · 28 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 Spatial regulation of UBXD8 and p97/VCP controls ATGL-mediated lipid droplet turnover. Proceedings of the National Academy of Sciences of the United States of America 195 23297223
2009 Targeting sequences of UBXD8 and AAM-B reveal that the ER has a direct role in the emergence and regression of lipid droplets. Journal of cell science 110 19773358
2012 Derlin-1 and UBXD8 are engaged in dislocation and degradation of lipidated ApoB-100 at lipid droplets. Molecular biology of the cell 95 22238364
2010 Identification of Ubxd8 protein as a sensor for unsaturated fatty acids and regulator of triglyceride synthesis. Proceedings of the National Academy of Sciences of the United States of America 87 21115839
2012 The ubiquitin-like (UBX)-domain-containing protein Ubx2/Ubxd8 regulates lipid droplet homeostasis. Journal of cell science 72 22454508
2018 UBXN3B positively regulates STING-mediated antiviral immune responses. Nature communications 66 29899553
2013 Pathogenic mutation of UBQLN2 impairs its interaction with UBXD8 and disrupts endoplasmic reticulum-associated protein degradation. Journal of neurochemistry 60 24215460
2013 The p97-UBXD8 complex destabilizes mRNA by promoting release of ubiquitinated HuR from mRNP. Genes & development 58 23618873
2022 UBXD8 mediates mitochondria-associated degradation to restrain apoptosis and mitophagy. EMBO reports 47 35979733
2010 The RasGAP proteins Ira2 and neurofibromin are negatively regulated by Gpb1 in yeast and ETEA in humans. Molecular and cellular biology 42 20160012
2023 The p97-UBXD8 complex regulates ER-Mitochondria contact sites by altering membrane lipid saturation and composition. Nature communications 38 36746962
2013 UAS domain of Ubxd8 and FAF1 polymerizes upon interaction with long-chain unsaturated fatty acids. Journal of lipid research 38 23720822
2017 Haploid Mammalian Genetic Screen Identifies UBXD8 as a Key Determinant of HMGCR Degradation and Cholesterol Biosynthesis. Arteriosclerosis, thrombosis, and vascular biology 29 28882874
2015 Hepatocyte-Specific Depletion of UBXD8 Induces Periportal Steatosis in Mice Fed a High-Fat Diet. PloS one 16 25970332
2002 Cloning and characterization of the highly expressed ETEA gene from blood cells of atopic dermatitis patients. Biochemical and biophysical research communications 15 12372427
2025 Silencing FAF2 mitigates alcohol-induced hepatic steatosis by modulating lipolysis and PCSK9 pathway. Hepatology communications 6 39969435
2024 Neurotoxicity of Realgar: Crosstalk Between UBXD8-DRP1-Regulated Mitochondrial Fission and PINK1-Parkin-Mediated Mitophagy. Molecular neurobiology 5 39570499
2025 FAF2 is a bifunctional regulator of peroxisomal homeostasis and saturated lipid responses. Science advances 4 40601736
2025 Polyserine-mediated targeting of FAF2/UBXD8 ameliorates tau aggregation. Neuron 4 40902597
2022 UBXN3B Controls Immunopathogenesis of Arthritogenic Alphaviruses by Maintaining Hematopoietic Homeostasis. mBio 2 36377866
2025 Quality control of ABCD3 by the VCP-FAF2 complex suppresses excessive pexophagy. Autophagy 1 39929145
2024 Sensing and regulation of long-chain polyunsaturated fatty acids pool in marine mollusks: Characterization of UBXD8 from the razor clam Sinonovacula constricta. Biochimica et biophysica acta. Molecular and cell biology of lipids 1 38181884
2024 UBXN3B is crucial for B lymphopoiesis. EBioMedicine 1 39018756
2024 The p97-UBXD8 complex maintains peroxisome abundance by suppressing pexophagy. bioRxiv : the preprint server for biology 1 39386596
2024 FAF2 is a bifunctional regulator of peroxisomal homeostasis and saturated lipid responses. bioRxiv : the preprint server for biology 1 39763943
2026 The accessory adapters FAF1, FAF2, and UBXN7 accelerate proteasomal degradation by increasing prior p97-mediated substrate unfolding. Science advances 0 41790892
2025 UBXD8 promotes lung cancer progression and activates the HIF-1α pathway. Biochemical pharmacology 0 40562127
2021 An Essential Role of UBXN3B in B Lymphopoiesis. bioRxiv : the preprint server for biology 0 34462748

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