Affinage

UBQLN1

Ubiquilin-1 · UniProt Q9UMX0

Length
589 aa
Mass
62.5 kDa
Annotated
2026-06-10
46 papers in source corpus 25 papers cited in narrative 25 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

UBQLN1 (PLIC-1, XDRP1, DA41) is a multidomain ubiquitin-like/ubiquitin-associated shuttle protein that controls the fate of diverse client proteins by coupling substrate recognition to the proteasome and to autophagy/lysosomal pathways (PMID:17082820, PMID:28075048). Its N-terminal UBL domain engages UIM-containing partners including ataxin-3, HSJ1a, and EPS15 and is required for transport of polyQ aggregates to perinuclear aggresomes, while its UBA domain binds polyubiquitinated cargo (PMID:17082820, PMID:17027914); the E6AP AZUL domain binds transiently to the UBA domain, allosterically reconfiguring an adjacent oligomerization element (PMID:36827983). Substrate destiny is set by which UBQLN1 domain contacts the client: STI-domain binding (to substrates such as BCLb, IGF1R, GPX4, and LCN2) plus UBA-mediated ubiquitin engagement stabilizes substrates, whereas UBL-mediated interactions route them toward turnover (PMID:28075048, PMID:41942632). Through these activities UBQLN1 governs proteostasis and protein quality control: the disease-associated E54D mutation impairs proteasomal degradation of ubiquitinated proteins and causes cytosolic aggregation with TDP-43 mislocalization (PMID:22766032), and a Sirt1/Foxc1 transcriptional axis upregulates UBQLN1 to protect neurons during ischemia/reperfusion (PMID:38452414). UBQLN1 also has substrate-specific regulatory roles in neurons, where it directly binds GABA(A) receptor subunits, stabilizes them in the ER, and increases their rate of surface insertion to enhance inhibitory synaptic transmission (PMID:11528422, PMID:18467327, PMID:26415648); in cell-cycle and growth control, where its UBL domain binds cyclin A and inhibits its degradation and its overexpression suppresses CDK2 activity (PMID:10487753, PMID:11050468); and in Gβγ-dependent G-protein signaling, which it inhibits by direct, UBL/UBA-independent association with Gβγ (PMID:14662753). More recent work places UBQLN1 in autophagy and metabolic disease, promoting proteasomal degradation of SNARE proteins (STX17, SNAP29, VAMP8) via a CD36 bridge to impair autophagosome–lysosome fusion (PMID:37014234), degrading PGC1β in a ubiquitination-independent manner to limit mitochondrial biogenesis (PMID:34001851), and being stabilized by OGT-dependent O-GlcNAcylation at T277 in a lipotoxic, MASH-relevant context (PMID:41795680). UBQLN1 additionally shuttles RPA1 off replication forks to support fork progression and telomere maintenance (PMID:37463174).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 1999 High

    Established the first functional handle on the protein by identifying it as a cyclin A-binding factor whose UBL domain selectively blocks cyclin A degradation and arrests cell division.

    Evidence Yeast two-hybrid, in vitro cyclin degradation in frog egg extract, and Xenopus microinjection

    PMID:10487753

    Open questions at the time
    • Did not connect cyclin A protection to a defined proteasome-targeting mechanism
    • Human ortholog function not yet demonstrated
  2. 2001 High

    Defined a neuronal substrate-stabilizing role, showing the protein binds GABA(A) receptor subunits and increases surface receptor availability without altering internalization.

    Evidence Co-IP, immunolocalization, and cell-surface/internalization assays in neurons

    PMID:11528422

    Open questions at the time
    • Mechanism of how binding promotes insertion not resolved at this stage
    • Domain requirement on UBQLN1 not mapped
  3. 2003 High

    Revealed a ubiquitin-independent signaling function: direct association with Gβγ inhibits chemokine-driven PLC activation, receptor internalization, and migration, separating signaling roles from the UBL/UBA domains.

    Evidence GST pulldown, Co-IP, chemotaxis and PLC assays

    PMID:14662753

    Open questions at the time
    • Structural basis of Gβγ binding unknown
    • Physiological context of this inhibition not defined in vivo
  4. 2006 High

    Connected the protein to protein quality control by demonstrating its UBL domain recruits UIM proteins (ataxin-3, HSJ1a, EPS15) to drive polyQ aggresome formation.

    Evidence Co-IP, RNAi, dominant-negative ΔUBL, and confocal microscopy in a polyQ model

    PMID:17082820

    Open questions at the time
    • Whether aggresome targeting reflects degradation or sequestration not resolved
    • Endogenous regulation of partner selection unclear
  5. 2008 High

    Mechanistically refined the GABA(A) receptor role, showing ER stabilization and increased poly-ubiquitinated subunit abundance accelerate membrane insertion.

    Evidence Pulse-chase, biotinylation, and ubiquitination assays in recombinant and neuronal systems

    PMID:18467327

    Open questions at the time
    • Identity of the ubiquitin ligase acting on receptor subunits not established
  6. 2011 Medium

    Extended quality-control function to innate immunity, showing the protein suppresses TLR3-TRIF IFN-β signaling by lowering TRIF abundance.

    Evidence Y2H, Co-IP, GST pulldown, luciferase reporter, shRNA knockdown, and LC3 colocalization

    PMID:21695056

    Open questions at the time
    • Whether TRIF loss is proteasomal or autophagic not fully resolved
    • Single lab
  7. 2012 Medium

    Linked the protein directly to neurodegenerative disease mechanism, showing the E54D mutation aggregates, mislocalizes TDP-43, and impairs proteasomal degradation of ubiquitinated substrates.

    Evidence In vitro UPS degradation assay and immunofluorescence of a single mutant

    PMID:22766032

    Open questions at the time
    • Single mutant in vitro only
    • Causality in a defined Mendelian disease not established here
  8. 2017 Medium

    Resolved the central logic of substrate fate, showing STI domains contact substrates (BCLb, IGF1R, ESYT2) and that UBA-ubiquitin binding stabilizes them while UBL interactions (PSMD4, BAG6) do not.

    Evidence Co-IP with domain deletion/mutation and ubiquitin/proteasome binding assays

    PMID:28075048

    Open questions at the time
    • Why some STI-bound substrates are stabilized and others degraded not fully delineated
    • Single lab
  9. 2023 High

    Broadened roles into autophagy, replication, and structural understanding: a CD36 bridge targets SNARE proteins for degradation impairing autophagosome-lysosome fusion; the protein shuttles RPA1 off forks for telomere maintenance; and NMR/AF2 mapped E6AP AZUL binding to the UBA domain.

    Evidence Co-IP/KO autophagic flux assays; RPA1 ChIP and telomere length; NMR NOE and AlphaFold2-Multimer with cellular Co-IP

    PMID:36827983 PMID:37014234 PMID:37463174

    Open questions at the time
    • Functional consequence of E6AP-UBA binding for substrate handling unknown
    • Whether CD36-SNARE and RPA1 roles intersect with canonical proteostasis unclear
  10. 2024 Medium

    Placed the protein in metabolic and disease networks, with substrate-specific control of GPX4, Pgm1, and SIKE, and an upstream Sirt1/Foxc1 transcriptional axis governing neuronal proteostasis.

    Evidence Co-IP, domain deletion, ubiquitination assays, ChIP/luciferase, and knockdown in disease models

    PMID:38452414 PMID:39159700 PMID:41287824 PMID:41814315

    Open questions at the time
    • Several substrate findings are abstract-level or single-study
    • Whether degradation routes are proteasomal vs lysosomal varies by substrate
  11. 2026 Medium

    Defined post-translational and competitive regulation of the protein itself: OGT-mediated O-GlcNAcylation at T277 stabilizes it in lipotoxic stress, and MYDGF competition at the STI1-4 domain blocks LCN2 degradation.

    Evidence Site-directed mutagenesis with PTM detection, LAMP1/lysosomal assays in MASH mice, and competitive domain-binding ferroptosis assays

    PMID:41795680 PMID:41942632

    Open questions at the time
    • Generality of T277 O-GlcNAc regulation beyond lipotoxic context unknown
    • Single lab per finding

Open questions

Synthesis pass · forward-looking unresolved questions
  • How UBQLN1 selects between stabilizing and degrading a given STI-bound substrate, and how its phase-separation behavior integrates with proteasomal versus autophagic routing, remains unresolved.
  • No unified rule distinguishing stabilized from degraded substrates
  • In vivo relevance of phase separation to substrate handling not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 4 GO:0098772 molecular function regulator activity 3 GO:0031386 protein tag activity 2 GO:0060090 molecular adaptor activity 2
Localization
GO:0005764 lysosome 2 GO:0005783 endoplasmic reticulum 2 GO:0005829 cytosol 2 GO:0005886 plasma membrane 2
Pathway
R-HSA-112316 Neuronal System 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-162582 Signal Transduction 2 R-HSA-1640170 Cell Cycle 2 R-HSA-9612973 Autophagy 2
Partners
CD36EPS15GABRA1GPX4PGC1BPSMD4RPA1TRIF

Evidence

Reading pass · 25 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 PLIC-1 (UBQLN1) directly interacts with GABA(A) receptor subunits, is enriched at inhibitory synapses and associated with subsynaptic membranes, facilitates GABA(A) receptor cell surface expression without affecting internalization rate, and enhances stability of intracellular GABA(A) receptor subunits to increase receptors available for plasma membrane insertion. Co-immunoprecipitation, immunolocalization (confocal microscopy/electron microscopy), cell surface expression assays, receptor internalization assays in neurons Nature neuroscience High 11528422
2008 Plic-1 (UBQLN1) increases the stability of GABA(A) receptor subunits within the endoplasmic reticulum, increases poly-ubiquitinated receptor subunit abundance, and elevates cell surface expression by selectively increasing rates of membrane insertion. Recombinant and neuronal preparations, pulse-chase and stability assays, cell surface biotinylation, poly-ubiquitination detection The Journal of biological chemistry High 18467327
1999 XDRP1 (Xenopus ortholog of UBQLN1) was identified as a cyclin A-binding protein via two-hybrid screen; it binds cyclin A1 and A2 (but not B-type cyclins) through its N-terminal UBL domain, requiring residues 130–160 of cyclin A1; bacterially expressed XDRP1 inhibits Ca2+-induced degradation of cyclin A but not cyclin B in frog egg extract; injection of XDRP1 into fertilized Xenopus eggs blocks embryonic cell division. Yeast two-hybrid, in vitro binding assays, cell-free degradation assay in frog egg extract, Xenopus microinjection The EMBO journal High 10487753
2006 Two isoforms of Xenopus XDRP1 (XDRP1L and XDRP1S) differ in their UBL domain; both bind polyubiquitinated proteins via their UBA domains, but only XDRP1L binds the proteasome via its UBL domain, whereas XDRP1S (with a truncated UBL) fails to bind the proteasome and instead binds monomeric cyclin A and prevents its degradation. In vitro binding assays, pulldown with polyubiquitinated proteins, proteasome binding assays, cyclin A degradation assay Biochemical and biophysical research communications Medium 17027914
2003 PLIC-1 (UBQLN1) inhibits Gβγ-dependent cell signaling (but not Gs-mediated adenylyl cyclase activation) by directly associating with Gβγ; this interaction does not require the UBL or UBA domains of PLIC-1; PLIC-1 co-localizes with G proteins in lamellae and pseudopods and inhibits SDF-1α-induced phospholipase C activation, CXCR4 internalization, and cell migration. GST pulldown, co-immunoprecipitation, confocal colocalization, chemotaxis assays, phospholipase C activation assay, adenylyl cyclase assay The Journal of cell biology High 14662753
2006 The UBL domain of PLIC-1 (UBQLN1) is required for aggresome formation; PLIC-1 binds UIM-containing proteins ataxin-3, HSJ1a, and EPS15 via its UBL domain; PLIC-1 and EPS15 localize to perinuclear aggresomes; polyQ expression enhances PLIC-1–EPS15 interaction; PLIC-1 knockdown reduces aggresome formation; a dominant-negative PLIC-1(ΔUBL) blocks polyQ transport to aggresomes and disrupts EPS15 association with aggregates; PLIC-1 is upregulated by arsenite-induced protein misfolding. Co-immunoprecipitation, RNAi knockdown, dominant-negative overexpression, immunofluorescence/confocal microscopy, polyQ disease model EMBO reports High 17082820
2011 PLIC-1 (UBQLN1) interacts with the TIR domain of TLR4 (via yeast two-hybrid) and with TRIF (confirmed by Co-IP and GST pulldown); PLIC-1 strongly suppresses TLR3-TRIF-dependent IFN-β promoter activation; PLIC-1 and TRIF co-localize with autophagosome marker LC3 in punctate structures; PLIC-1 overexpression decreases TRIF protein abundance in a nocodazole-sensitive manner; PLIC-1 knockdown by shRNA enhances TLR3 activation. Yeast two-hybrid, Co-IP, GST pulldown, luciferase reporter assay, shRNA knockdown, confocal microscopy, Western blot PloS one Medium 21695056
2010 UBQLN1 interacts with SPEM1 (identified by yeast two-hybrid) and both proteins co-localize to the manchette of elongating spermatids, implicating UBQLN1 in regulation of protein ubiquitination during spermiogenesis. Yeast two-hybrid, immunofluorescence co-localization Molecular and cellular endocrinology Low 20558241
1997 DA41 (UBQLN1) interacts with the EGF-like protein S(1-5) through amino acids 155–232 of DA41, identified by yeast two-hybrid. Yeast two-hybrid, domain mapping Biochemical and biophysical research communications Low 9268694
2017 The first two STI domains of UBQLN1 are critical for binding to the substrate BCLb (and similarly to IGF1R and ESYT2); interaction of UBQLN1 with BCLb is independent of BCLb ubiquitination, but interaction with ubiquitin via the UBA domain is required for substrate stabilization; UBL-mediated interactions (e.g., with PSMD4 and BAG6) do not result in substrate stabilization by UBQLN1. Thus, substrate fate (stabilization vs. degradation) is determined by the domain of UBQLN1 mediating substrate contact. Co-immunoprecipitation, domain deletion/mutation constructs, proteasome and ubiquitin-binding assays, Western blot Journal of cellular biochemistry Medium 28075048
2012 The missense mutation UBQLN1-E54D causes cytosolic aggregate formation and mislocalized TDP-43, and impairs degradation of ubiquitinated proteins through the proteasome in vitro, demonstrating that this mutation disrupts UPS function. In vitro functional studies, immunofluorescence, ubiquitinated protein degradation assay Neurobiology of disease Medium 22766032
2021 Upregulated UBQLN1 in sorafenib-resistant HCC cells induces degradation of PGC1β in a ubiquitination-independent manner, attenuating mitochondrial biogenesis and ROS production. Co-immunoprecipitation, Western blot, mitochondrial functional assays (oxygen consumption rate, mitochondrial DNA content), gain/loss-of-function experiments Signal transduction and targeted therapy Medium 34001851
2023 CD36 acts as a bridge molecule linking UBQLN1 to SNARE proteins (STX17, SNAP29, VAMP8) at the lysosome, promoting their proteasomal degradation in a UBQLN1-dependent manner, thereby impairing autophagosome-lysosome fusion. Co-immunoprecipitation, knockout and overexpression in mice and cells, autophagic flux assays, Western blot Autophagy Medium 37014234
2023 The E6AP AZUL domain binds transiently to the UBA domain of UBQLN1/2; NOE spectroscopy identified direct intermolecular contacts; an AlphaFold2-Multimer model of the AZUL:UBA complex was generated; an oligomerization domain (UBAA) adjacent to the UBA is α-helical and is allosterically reconfigured by AZUL binding; E6AP interacts with UBQLN1/2 in cellulo and E6AP AZUL is recruited to UBQLN2 condensates in vitro. NMR (NOE spectroscopy, transfer NOE), AlphaFold2-Multimer structure prediction, in vitro condensate assay, co-immunoprecipitation in cells Structure High 36827983
2023 UBQLN1 interacts with RPA1 and shuttles it off from the replication fork; UBQLN1 deficiency retains RPA1 at the replication fork, hinders replication, causes cell cycle arrest, genome instability, and rapid telomere shortening (particularly in telomere regions with G-rich sequences prone to replication stress). Co-immunoprecipitation, RPA1 ChIP at replication forks, UBQLN1 knockdown with telomere length measurement, cell cycle assays PLoS genetics Medium 37463174
2023 Full-length UBQLN1, UBQLN2, and UBQLN4 exhibit distinct phase separation behaviors in vitro; the short N-terminal disordered regions inhibit phase separation via electrostatic interactions; UBQLN1 does not phase separate with a temperature dependence (unlike UBQLN2, whose temperature-dependent behavior requires its unique proline-rich region absent in UBQLN1). In vitro phase separation assays with full-length proteins and charge variant/truncation constructs, biophysical characterization Biophysical journal Medium 38041404
2000 Overexpression of DA41 (UBQLN1) in v-Ha-ras-transformed 3Y1 cells suppresses cell growth and reduces CDK2 kinase activity without altering CDK2 protein levels, indicating a role in cell cycle regulation. Stable transfection/overexpression, growth assays, soft agar colony formation, CDK2 kinase activity assay, Western blot Japanese journal of cancer research Medium 11050468
2024 Foxc1 functions as a transcriptional activator of Ubqln1; Sirt1 promotes Foxc1 expression by deacetylating Ezh2 and inhibiting its repressive activity on Foxc1; the Sirt1/Foxc1/Ubqln1 axis regulates proteostasis (ubiquitinated protein aggregation) and neuronal survival during cerebral ischemia/reperfusion injury. Co-IP, ChIP, dual-luciferase reporter assay, siRNA knockdown, MCAO/R and OGD/R models International immunopharmacology Medium 38452414
2020 UBQLN1 knockdown reduces p53 protein levels through activation of autophagy (not proteasomal degradation); inhibition of autophagy restores p53 levels in UBQLN1-KD cells; UBQLN1 KD inhibits mTOR and its downstream S6K phosphorylation. siRNA knockdown, autophagy inhibitor treatment, proteasome activity assay, MTT, BrdU, TUNEL assays, Western blot Journal of thoracic disease Medium 33209421
2024 UBQLN1 interacts with SNARE proteins and promotes their ubiquitin-mediated proteasomal degradation; its STI domain mediates binding to substrate GPX4 and stabilizes it (demonstrated in HCC); separately, UBQLN1 was shown to stabilize substrates through STI-domain interaction independent of substrate ubiquitination. Co-immunoprecipitation, domain deletion experiments, Western blot, functional ferroptosis assays MedComm Low 41287824
2024 UBQLN1 mediates ubiquitin-dependent degradation of Pgm1; Sec13 competes with UBQLN1 for binding to Pgm1, thereby inhibiting UBQLN1-mediated Pgm1 ubiquitination and stabilizing Pgm1 to promote glycolysis. Co-immunoprecipitation demonstrating ternary complex (Sec13–Pgm1–Ubqln1), Ubqln1 overexpression/knockdown, Western blot for Pgm1 stability, ubiquitination assay Biochimica et biophysica acta. Molecular basis of disease Low 39159700
2026 Lipotoxic stress induces O-GlcNAcylation at T277 of UBQLN1 by OGT, which competitively inhibits phosphorylation at the same site and reduces ubiquitin-mediated degradation of UBQLN1, stabilizing it; UBQLN1 in hepatocytes regulates MVB–lysosome fusion via LAMP1, promoting sEV secretion; sEV-carried UBQLN1 degrades the V-ATPase subunit ATP6V1B2 through E54D-dependent ubiquitin ligase activity, inhibiting lysosomal acidification and mitophagy in hepatic stellate cells. Co-IP, site-directed mutagenesis (T277), O-GlcNAc and phosphorylation detection, LAMP1 interaction assays, lysosomal acidification assay, hepatocyte-specific Ubqln1/Ogt knockdown in MASH mice Autophagy Medium 41795680
2026 MYDGF competitively binds UBQLN1 at its STI1-4 domain, blocking UBQLN1-mediated ERAD recognition and degradation of LCN2, thereby stabilizing LCN2 and suppressing ferroptosis in gastric cancer under hypoxia. Co-immunoprecipitation, domain competition assay, LCN2 stability assay, ferroptosis assays in vitro and in vivo Oncogene Medium 41942632
2026 UBQLN1 promotes ubiquitin-mediated degradation of SIKE, activating the p38 MAPK pathway to drive lipid accumulation in hepatocytes during MASH; genetic knockdown of UBQLN1 reduces SIKE degradation and suppresses p38 MAPK signaling, hepatic steatosis, and fibrosis. LC-MS/MS proteomics, transcriptomics, Co-IP, UBQLN1 knockdown in MASH mouse models and hepatocytes, Western blot Journal of nanobiotechnology Low 41814315
2015 Disruption of PLIC-1 binding to GABA(A) receptors (by the PePα peptide) decreases miniature inhibitory postsynaptic currents (mIPSCs) in hippocampal pyramidal neurons, while lentiviral overexpression of Plic-1 increases mIPSCs; these effects are blocked by the GABA(A)R inhibitor picrotoxin, confirming that Plic-1 regulates inhibitory synaptic transmission specifically through GABA(A) receptors. Intrahippocampal peptide injection, lentiviral overexpression, whole-cell patch-clamp electrophysiology (mIPSC recording) in rat and mouse models Clinical science Medium 26415648

Source papers

Stage 0 corpus · 46 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 Family-based association between Alzheimer's disease and variants in UBQLN1. The New England journal of medicine 195 15745979
2001 GABA(A) receptor cell surface number and subunit stability are regulated by the ubiquitin-like protein Plic-1. Nature neuroscience 192 11528422
2014 MiR-200c inhibits autophagy and enhances radiosensitivity in breast cancer cells by targeting UBQLN1. International journal of cancer 116 25044403
2021 UBQLN1 mediates sorafenib resistance through regulating mitochondrial biogenesis and ROS homeostasis by targeting PGC1β in hepatocellular carcinoma. Signal transduction and targeted therapy 107 34001851
2006 The UBL domain of PLIC-1 regulates aggresome formation. EMBO reports 79 17082820
1999 Identification of XDRP1; a Xenopus protein related to yeast Dsk2p binds to the N-terminus of cyclin A and inhibits its degradation. The EMBO journal 54 10487753
2017 The STI and UBA Domains of UBQLN1 Are Critical Determinants of Substrate Interaction and Proteostasis. Journal of cellular biochemistry 48 28075048
2008 The ubiquitin-like protein Plic-1 enhances the membrane insertion of GABAA receptors by increasing their stability within the endoplasmic reticulum. The Journal of biological chemistry 45 18467327
2003 The ubiquitin-related protein PLIC-1 regulates heterotrimeric G protein function through association with Gbetagamma. The Journal of cell biology 43 14662753
2023 Hepatocyte CD36 modulates UBQLN1-mediated proteasomal degradation of autophagic SNARE proteins contributing to septic liver injury. Autophagy 40 37014234
2010 UBQLN1 interacts with SPEM1 and participates in spermiogenesis. Molecular and cellular endocrinology 39 20558241
2015 Epstein-Barr virus-encoded LMP1 increases miR-155 expression, which promotes radioresistance of nasopharyngeal carcinoma via suppressing UBQLN1. European review for medical and pharmacological sciences 35 26698246
2005 The UBQLN1 polymorphism, UBQ-8i, at 9q22 is not associated with Alzheimer's disease with onset before 70 years. Neuroscience letters 28 16214290
2006 Lack of association between UBQLN1 and Alzheimer disease. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 26 16526030
2017 The mir-675-5p regulates the progression and development of pancreatic cancer via the UBQLN1-ZEB1-mir200 axis. Oncotarget 20 28212565
2023 E6AP AZUL interaction with UBQLN1/2 in cells, condensates, and an AlphaFold-NMR integrated structure. Structure (London, England : 1993) 19 36827983
2023 Breast cancer cell-derived exosome-delivered microRNA-155 targets UBQLN1 in adipocytes and facilitates cancer cachexia-related fat loss. Human molecular genetics 19 37017334
2015 Plic-1, a new target in repressing epileptic seizure by regulation of GABAAR function in patients and a rat model of epilepsy. Clinical science (London, England : 1979) 19 26415648
2012 Association of UBQLN1 mutation with Brown-Vialetto-Van Laere syndrome but not typical ALS. Neurobiology of disease 19 22766032
2024 Fisetin alleviates cerebral ischemia/reperfusion injury by regulating Sirt1/Foxc1/Ubqln1 pathway-mediated proteostasis. International immunopharmacology 18 38452414
2011 The ubiquitin-like protein PLIC-1 or ubiquilin 1 inhibits TLR3-Trif signaling. PloS one 17 21695056
2023 Short disordered termini and proline-rich domain are major regulators of UBQLN1/2/4 phase separation. Biophysical journal 15 38041404
2020 Overexpression of UBQLN1 reduces neuropathology in the P497S UBQLN2 mouse model of ALS/FTD. Acta neuropathologica communications 14 33028421
2020 The impacts of ubiquilin 1 (UBQLN1) knockdown on cells viability, proliferation, and apoptosis are mediated by p53 in A549 lung cancer cells. Journal of thoracic disease 10 33209421
2021 miR-337-5p promotes the development of cardiac hypertrophy by targeting Ubiquilin-1 (UBQLN1). Bioengineered 9 34515612
2008 Analysis of UBQLN1 variants in a Polish Alzheimer's disease patient: control series. Dementia and geriatric cognitive disorders 9 18340109
1997 Interaction of DA41, a DAN-binding protein, with the epidermal growth factor-like protein, S(1-5). Biochemical and biophysical research communications 9 9268694
2023 Knockdown of UBQLN1 Functions as a Strategy to Inhibit CRC Progression through the ERK-c-Myc Pathway. Cancers 6 37370699
2022 Towards a molecular understanding of the overlapping and distinct roles of UBQLN1 and UBQLN2 in lung cancer progression and metastasis. Neoplasia (New York, N.Y.) 5 35063704
2022 GABAA Receptor-Stabilizing Protein Ubqln1 Affects Hyperexcitability and Epileptogenesis after Traumatic Brain Injury and in a Model of In Vitro Epilepsy in Mice. International journal of molecular sciences 5 35409261
2024 Downregulation of Lnc-ABCA12-3 modulates UBQLN1 expression and protein homeostasis pathways in amyotrophic lateral sclerosis. Scientific reports 4 39271939
2023 UBQLN1 deficiency mediates telomere shortening and IPF through interacting with RPA1. PLoS genetics 4 37463174
2010 Extremely rare incidence of the UBQLN1 polymorphism (UBQ-8i) in Taiwan Chinese with Alzheimer's disease. Neuroscience letters 4 20350585
2024 Humoral immune response to tumor-associated antigen Ubiquilin 1 (UBQLN1) and its tumor-promoting potential in lung cancer. BMC cancer 3 38431566
2024 UBQLN1 links proteostasis and mitochondria function to telomere maintenance in human embryonic stem cells. Stem cell research & therapy 3 38902824
2006 Identification of two isoforms of Dsk2-related protein XDRP1 in Xenopus eggs. Biochemical and biophysical research communications 3 17027914
2000 Molecular cloning and expression analysis of the human DA41 gene and its mapping to chromosome 9q21.2-q21.3. Journal of human genetics 3 10807547
2025 Induction of UBQLN1-mediated PGC1α stability by isoliensinine overcame hypoxia-induced resistance in liver cancer cells. BioFactors (Oxford, England) 2 40135717
2024 Sec13 promotes glycolysis by inhibiting Ubqln1 mediated Pgm1 ubiquitination in ALI. Biochimica et biophysica acta. Molecular basis of disease 1 39159700
2023 Short N-terminal disordered regions and the proline-rich domain are major regulators of phase transitions for full-length UBQLN1, UBQLN2 and UBQLN4. bioRxiv : the preprint server for biology 1 37808720
2026 Lipotoxic hepatocyte-derived UBQLN1-enriched small extracellular vesicles activate hepatic stellate cells to promote hepatic fibrosis. Autophagy 0 41795680
2026 UBQLN1 Inhibition reduces MASH progression through downregulating SIKE/p38 MAPK pathway in hepatocyte. Journal of nanobiotechnology 0 41814315
2026 Hypoxia-induced XBP1s-MYDGF axis suppresses ferroptosis through UBQLN1-mediated stabilization of LCN2 in gastric cancer. Oncogene 0 41942632
2025 circRNA-SORE/UBQLN1/GPX4 Mediates the Acquisition of Sorafenib Resistance in Hepatocellular Carcinoma Through Inhibition of Ferroptosis. MedComm 0 41287824
2023 1H, 15N, 13C backbone and Cβ resonance assignments for UBQLN1 UBA and UBAA domains. Biomolecular NMR assignments 0 37022617
2000 Overexpression of DA41 in v-Ha-ras-3Y1 cells causes growth suppression. Japanese journal of cancer research : Gann 0 11050468

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