Affinage

FBXL19

F-box/LRR-repeat protein 19 · UniProt Q6PCT2

Length
694 aa
Mass
75.7 kDa
Annotated
2026-06-09
39 papers in source corpus 16 papers cited in narrative 16 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FBXL19 is the substrate-recognition F-box subunit of an SCF-type E3 ubiquitin ligase that controls inflammatory, cytoskeletal, and proliferative signaling by targeting diverse substrates for site-specific ubiquitination and proteasomal degradation, frequently gated by prior substrate phosphorylation (PMID:22660580, PMID:23512198, PMID:23871831). It degrades the IL-33 receptor ST2L following GSK3β phosphorylation at Ser442, thereby damping IL-33 pro-inflammatory signaling and lessening lung injury (PMID:22660580), and similarly degrades the FOXM1 transcription factor to limit lung inflammation (PMID:36964598). A coherent theme is its control of Rho-family GTPase signaling: it ubiquitinates Rac1 (at Lys166, requiring AKT phosphorylation of Ser71), RhoA (at Lys135, requiring Erk2 phosphorylation), Rac3 (at Lys166), and Cdc42, suppressing cell migration, lamellipodia formation, and stress-fiber assembly (PMID:23512198, PMID:23871831, PMID:24684802, PMID:29522376). Additional substrates include TTF1 in thyroid carcinoma cells (PMID:31238008) and STK11 in airway epithelium during cigarette-smoke stress (PMID:38712759). Beyond canonical ubiquitination, FBXL19 acts as an ISG15 E3 ligase that ISGylates NF-κBp65 to restrain endothelial inflammation (PMID:36994728), and catalyzes K27-linked ubiquitination of STING1 (at Lys338/347/370) to route it for SQSTM1-mediated autophagic degradation and downregulate antiviral type I interferon signaling (PMID:40413753). In the nucleus, FBXL19 binds unmethylated CpG islands via its CxxC domain and recruits the CDK-Mediator complex and the Rnf20 E3 ligase, priming silent developmental gene promoters—partly through long-range chromatin contacts—and promoting H2B Lys120 mono-ubiquitination during embryonic stem cell differentiation (PMID:29809150, PMID:28453857, PMID:31996894). FBXL19 abundance is itself regulated: CBP-mediated acetylation stabilizes it and enhances its ligase activity, while SCFFBXW17 ubiquitinates it at Lys114 for degradation (PMID:29522376, PMID:33053230).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 2012 High

    Established FBXL19 as a functional SCF E3 ligase substrate receptor by showing it degrades the IL-33 receptor ST2L in a phosphorylation-gated manner, linking it to control of inflammatory signaling.

    Evidence Reciprocal Co-IP, in vitro ubiquitination, Ser442 mutagenesis, and mouse pneumonia models in lung epithelial cells

    PMID:22660580

    Open questions at the time
    • Did not define the full SCF complex composition or other Skp/Cullin partners
    • Generality of phospho-gating beyond ST2L unknown at the time
  2. 2013 High

    Extended FBXL19 substrate scope to Rho-family GTPases, showing it degrades Rac1 and RhoA at defined lysines following AKT- or Erk2-mediated phosphorylation, establishing a role in cytoskeletal and migratory control.

    Evidence F-box library screening, in vitro ubiquitination, Co-IP, phospho- and ubiquitin-site mutagenesis, and migration/cytoskeleton assays in MLE12/lung epithelial cells

    PMID:23512198 PMID:23871831

    Open questions at the time
    • Kinase-to-FBXL19 coupling mechanism not resolved
    • Whether different GTPases compete for the same FBXL19 pool unknown
  3. 2014 Medium

    Showed substrate specificity is encoded in FBXL19 domain architecture by mapping Rac3 recognition to the C-terminus, with N-terminal truncation enhancing degradation.

    Evidence Co-IP, K166R mutagenesis, FBXL19 truncation variants, and TGFβ1/E-cadherin readouts in esophageal cancer cells

    PMID:24684802

    Open questions at the time
    • Single lab; reciprocal validation limited
    • Structural basis of C-terminal Rac3 binding not defined
  4. 2017 High

    Revealed a non-degradative nuclear function: FBXL19 binds CpG islands via its CxxC domain and partners with Rnf20 to promote H2Bub1 at target promoters during ES cell differentiation.

    Evidence ChIP-seq, Fbxl19-Rnf20 Co-IP, gain/loss-of-function with global H2Bub1 quantification, and differentiation assays in mouse ES cells

    PMID:28453857

    Open questions at the time
    • How the same protein partitions between E3 ligase and chromatin roles unknown
    • Whether SCF activity contributes to H2Bub1 unresolved
  5. 2018 Medium

    Defined regulation of FBXL19 stability and additional GTPase substrate Cdc42, showing CBP acetylation extends FBXL19 half-life and boosts its ligase activity.

    Evidence Co-IP, cycloheximide chase, MG132, acetylation-mimic mutagenesis, CBP perturbation, and in vitro Cdc42 ubiquitination

    PMID:29522376

    Open questions at the time
    • Acetylated residues not fully mapped
    • Deacetylase responsible not identified
  6. 2018 High

    Demonstrated CpG-island recognition by FBXL19 recruits CDK-Mediator to prime developmental gene promoters and is essential for mouse development.

    Evidence ChIP-seq, Co-IP for CDK-Mediator, and FBXL19 knockout with developmental/differentiation phenotypes in mouse ES cells

    PMID:29809150

    Open questions at the time
    • Mechanism linking Mediator recruitment to delayed activation unclear
    • Relationship between Mediator recruitment and Rnf20/H2Bub1 not integrated
  7. 2019 Medium

    Showed FBXL19 substrate selection can be cell-type specific (TTF1 in thyroid carcinoma) and that FBXL19 itself is a miR-26 target controlling adipocyte progenitor differentiation.

    Evidence Co-IP, K151R mutagenesis, cell-type-specific overexpression (FBXL19/HECW1); miR-26 locus deletion, transgenic overexpression, and adipogenesis assays

    PMID:31238008 PMID:31488578

    Open questions at the time
    • Determinant of cell-type-specific E3 choice unknown
    • Molecular mechanism of FBXL19 in adipogenesis not resolved
  8. 2020 Medium

    Identified FBXL19's destabilizer (SCFFBXW17) and showed FBXL19-CDK-Mediator supports long-range promoter–distal-element contacts via an atypical enhancer mechanism.

    Evidence Co-IP, K114R mutagenesis, FBXW17 perturbation, migration assays; chromatin conformation capture and targeted genomic deletions in ESCs

    PMID:31996894 PMID:33053230

    Open questions at the time
    • How distal elements act without H3K27ac unclear
    • Single-lab chromatin findings
  9. 2023 High

    Expanded FBXL19's modifier repertoire to ISG15, showing it ISGylates NF-κBp65 to restrain endothelial inflammation, and confirmed FOXM1 as a degradative substrate in lung infection.

    Evidence In vitro ISGylation assay, p65-WIP1 Co-IP, EC-specific transgenic mice in lung injury; FBXL19-FOXM1 Co-IP, ubiquitination, and rescue in mouse infection model

    PMID:36964598 PMID:36994728

    Open questions at the time
    • Structural basis for dual Ub/ISG15 ligase activity unknown
    • How stimulation switches between modifications unresolved
  10. 2024 High

    Demonstrated linkage-specific and degradation-route diversification: FBXL19 degrades STK11 in smoke-stressed airway epithelium and catalyzes K27-linked ubiquitination routing STING1 to autophagy, dampening antiviral interferon signaling.

    Evidence FBXL panel screening, chase, ubiquitination assays for STK11; K27-specific in vitro ubiquitination, triple-site STING1 mutagenesis, Co-IP, EXOC4 KO mice with HSV-1 challenge, and MST

    PMID:38712759 PMID:40413753

    Open questions at the time
    • Determinants of ubiquitin linkage choice (K48 vs K27) unknown
    • How EXOC4 antagonism is regulated unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How FBXL19 integrates its cytoplasmic degradative E3/ISG15 ligase activities with its nuclear CpG-island/chromatin-priming role, and what governs substrate and ubiquitin-linkage selection, remains unresolved.
  • No structural model of substrate or CpG recognition
  • Spatial partitioning between nucleus and cytoplasm uncharacterized
  • Rules for K48 vs K27 vs ISGylation outputs undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 8 GO:0016874 ligase activity 4 GO:0140110 transcription regulator activity 3 GO:0003677 DNA binding 2
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 3
Pathway
R-HSA-392499 Metabolism of proteins 4 R-HSA-168256 Immune System 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-4839726 Chromatin organization 2 R-HSA-9612973 Autophagy 1
Partners
CBPEXOC4FOXM1RAC1RHOARNF20ST2LSTING1
Complex memberships
CDK-MediatorSCF (SKP1-Cullin-F-box) E3 ubiquitin ligase

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 FBXL19, as the F-box subunit of an SCF E3 ubiquitin ligase complex, binds ST2L (the IL-33 receptor) and mediates its polyubiquitination and proteasomal degradation. GSK3β-catalyzed phosphorylation of ST2L at Ser442 is required for FBXL19-mediated ST2L degradation. FBXL19 overexpression abrogated IL-33/ST2L pro-inflammatory and pro-apoptotic signaling and lessened lung injury severity in mouse pneumonia models. Co-immunoprecipitation, in vitro ubiquitination assay, site-directed mutagenesis (Ser442), proteasome inhibitor treatment, overexpression/knockdown in lung epithelial cells, mouse pneumonia models Nature immunology High 22660580
2013 SCF(FBXL19) E3 ubiquitin ligase targets Rac1 for polyubiquitination and proteasomal degradation. AKT-mediated phosphorylation of Rac1 at Ser71 is required for FBXL19-mediated ubiquitination. Lys166 within Rac1 is the ubiquitination acceptor site. FBXL19 overexpression reduced cell migration and diminished lamellipodia formation; Rac1(S71A) and Rac1(K166R) mutants were resistant to FBXL19-mediated degradation. F-box protein library screening, in vitro ubiquitination assay, Co-IP, site-directed mutagenesis (Rac1 S71A, K166R), cell migration assay, FBXL19 overexpression/knockdown in MLE12 cells FASEB journal High 23512198
2013 SCF(FBXL19) E3 ubiquitin ligase targets RhoA for ubiquitination at Lys135 and proteasomal degradation in lung epithelial cells. Erk2-mediated phosphorylation of RhoA is both necessary and sufficient for SCF(FBXL19)-mediated RhoA ubiquitination and degradation. RhoA(K135R) mutant was resistant to FBXL19-mediated degradation. FBXL19 expression reduced p27 phosphorylation, cell proliferation, LPA-induced MLC phosphorylation, and stress fiber formation. Co-IP, in vitro ubiquitination assay, site-directed mutagenesis (RhoA K135R), cycloheximide chase, FBXL19 overexpression/knockdown, cell proliferation and cytoskeleton assays Biochimica et biophysica acta High 23871831
2014 SCF(FBXL19) interacts with and polyubiquitinates Rac3 at Lys166, targeting it for proteasomal degradation. The C-terminus of FBXL19 is required for Rac3 interaction and ubiquitination, while N-terminal truncation increases Rac3 degradation. FBXL19 overexpression attenuated TGFβ1-induced E-cadherin downregulation and esophageal cancer cell elongation, linking Rac3 degradation to TGFβ1 signaling. Co-immunoprecipitation, immunoblotting, site-directed mutagenesis (Rac3 K166R), FBXL19 truncation variants, overexpression/knockdown in esophageal cancer cells (OE19, OE33), immunostaining Molecular cancer Medium 24684802
2018 FBXL19 is an unstable protein (half-life ~3 h) degraded by the ubiquitin-proteasome system. The acetyltransferase CBP acetylates FBXL19, reducing its ubiquitination and extending its half-life. Acetylation-mimicking FBXL19 mutants exhibit longer half-lives. CBP-mediated stabilization of FBXL19 enhances SCF(FBXL19) E3 ligase activity, promoting Cdc42 ubiquitination and degradation; CBP inhibition reverses these effects. Co-IP, cycloheximide chase, proteasome inhibitor (MG132) treatment, acetyltransferase/deacetylase inhibitor assays, acetylation-mimic mutagenesis, CBP overexpression/knockdown, in vitro ubiquitination of Cdc42 FASEB journal Medium 29522376
2018 FBXL19 is a CpG island-binding protein in mouse embryonic stem (ES) cells that associates with the CDK-Mediator complex. FBXL19 recruits CDK-Mediator to CpG island-associated promoters of non-transcribed developmental genes, priming them for activation during cell lineage commitment. Recognition of CpG islands by FBXL19 is essential for mouse development. Genome-wide chromatin immunoprecipitation (ChIP-seq), Co-IP/protein interaction studies identifying CDK-Mediator association, genetic knockout of FBXL19 in mouse ES cells with developmental phenotype readout, differentiation assays eLife High 29809150
2017 Fbxl19, via its CxxC domain, binds CpG island-containing promoters and physically interacts with Rnf20 E3 ligase. Fbxl19 promotes H2B Lys120 mono-ubiquitination (H2Bub1) at CpG island-containing gene promoters; upregulation of Fbxl19 increases global H2Bub1 in mouse ES cells while downregulation reduces it. Chromosomal binding of Fbxl19 is required for H2Bub1 at its target loci, and Fbxl19 is required for proper ES cell differentiation in collaboration with Rnf20. ChIP-seq (genome-wide occupancy mapping), Co-IP (Fbxl19-Rnf20 interaction), Fbxl19 overexpression/knockdown in mouse ES cells, quantification of global H2Bub1 by immunoblot, ES cell differentiation assays Nucleic acids research High 28453857
2019 FBXL19 mediates ubiquitination and degradation of TTF1 (thyroid transcription factor 1) in follicular thyroid carcinoma (FTC133) cells but not in normal thyroid epithelial cells (Htori3). Lys151 of TTF1 is the ubiquitin acceptor site in both cell types, but cell-type-specific E3 ligases (FBXL19 in FTC133 vs. HECW1 in Htori3) govern its degradation. Co-IP, ubiquitination assay, site-directed mutagenesis (TTF1 K151R), FBXL19 and HECW1 overexpression in FTC133 and Htori3 cells, immunoblotting FASEB journal Medium 31238008
2019 miR-26 family members suppress adipocyte progenitor cell differentiation by repressing expression of Fbxl19, a conserved miR-26 target. Fbxl19 plays a cell-autonomous role in adipocyte progenitor differentiation; its repression by miR-26 blocks adipogenesis in vivo. Genetic deletion of all miR-26-encoding loci in mice, transgenic overexpression of miR-26a, identification of Fbxl19 as miR-26 target by bioinformatics and reporter assays, cell-autonomous adipogenesis assays Genes & development Medium 31488578
2020 SCFFBXW17 E3 ubiquitin ligase ubiquitinates FBXL19 and induces its proteasomal degradation; Lys114 of FBXL19 is identified as the ubiquitin acceptor site. Acetylation of FBXL19 attenuates SCFFBXW17-mediated FBXL19 degradation. FBXW17 overexpression reduces FBXL19 levels, attenuating SCF(FBXL19)-mediated Rac1 degradation and cell migration suppression; FBXW17 knockdown attenuates LPA-induced lamellipodia formation. Co-IP, ubiquitination assay, site-directed mutagenesis (FBXL19 K114R), FBXW17 overexpression/knockdown, cycloheximide chase, cell migration and lamellipodia assays Journal of cellular biochemistry Medium 33053230
2020 FBXL19 and CDK-Mediator support long-range chromatin interactions between silent developmental gene promoters and atypical distal regulatory elements in mouse ESCs. These distal elements are required for appropriate gene induction during differentiation, as shown by targeted deletions. During gene activation, most distal elements do not acquire H3K27ac and lose interaction with their target promoters, indicating an atypical enhancer mechanism. Chromatin conformation capture / 3D genome interaction assays (Hi-C or similar), targeted genomic deletions, gene expression analysis during ESC differentiation, FBXL19 and CDK-Mediator ChIP Nucleic acids research Medium 31996894
2023 SCF(FBXL19) functions as an ISG15 E3 ligase that catalyzes ISGylation of NF-κBp65 in resting endothelial cells. TNFα and endotoxin stimulation reduce p65 ISGylation by FBXL19, promoting p65 serine phosphorylation through reduced association with the phosphatase WIP1. FBXL19 depletion increases p65 phosphorylation and endothelial cell inflammation; EC-specific FBXL19 transgenic mice show reduced lung inflammation and acute lung injury severity. In vitro ISGylation assay, Co-IP (p65-WIP1 interaction), FBXL19 knockdown in endothelial cells, EC-specific transgenic FBXL19 overexpressing mice in acute lung injury model, immunoblotting for p65 phosphorylation Arteriosclerosis, thrombosis, and vascular biology High 36994728
2023 FBXL19 binds FOXM1 and mediates its ubiquitination and proteasomal degradation in lung epithelial cells. In Streptococcus pneumoniae lung infection in immature mice, FBXL19 is downregulated while FOXM1 is upregulated; FBXL19 overexpression reduced lung injury and inflammation, and overexpression of FOXM1 reversed these protective effects. Co-IP (FBXL19-FOXM1 binding), MG132 proteasome inhibitor treatment, ubiquitination assay, FBXL19 overexpression in mouse model, rescue experiments with FOXM1 overexpression, immunoblotting Journal of cardiothoracic surgery Medium 36964598
2024 FBXL19 (as an SCF E3 ligase subunit) mediates ubiquitination and proteasomal degradation of STK11 in airway epithelial cells; cigarette smoke extract accelerates this process. FBXL19 overexpression led to dose-dependent acceleration of STK11 ubiquitination and degradation. STK11 depletion augments while STK11 overexpression attenuates cigarette smoke-induced cytotoxicity. FBXL19 screening assay (panel of FBXL E3 ligase subunit transfections), cycloheximide chase for half-life determination, MG132/leupeptin treatment, STK11 overexpression/siRNA knockdown, ubiquitination assay, immunoblotting COPD Medium 38712759
2025 FBXL19 E3 ligase catalyzes K27-linked ubiquitination of STING1 at Lys338, Lys347, and Lys370, marking it for recognition by SQSTM1 and autophagic degradation. EXOC4/SEC8 suppresses this FBXL19-mediated ubiquitination of STING1, thereby stabilizing STING1 and enhancing antiviral type I interferon signaling. In vitro ubiquitination assay (K27-linkage specificity), site-directed mutagenesis of STING1 ubiquitination sites (K338R, K347R, K370R), Co-IP (FBXL19-STING1 and SQSTM1-STING1 interactions), EXOC4 KO mice challenged with HSV-1, microscale thermophoresis (MST) for binding Autophagy High 40413753
2004 Bioinformatic identification and characterization of FBXL19 as a novel CXXC-domain family member (CXXC11) encoding a 674-amino-acid protein. Domain architecture established: CXXC domain resides within a novel FBXHA domain (aa 11-128), and F-box domain resides within an FBXHB domain (aa 404-674). FBXL19 lacks the JmjC domain present in the paralogs FBXL10/FBXL11. Bioinformatics/in silico analysis, cDNA assembly from genome sequence, sequence alignment International journal of molecular medicine Low 15547684

Source papers

Stage 0 corpus · 39 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 F-box protein FBXL19-mediated ubiquitination and degradation of the receptor for IL-33 limits pulmonary inflammation. Nature immunology 126 22660580
2013 A new mechanism of RhoA ubiquitination and degradation: roles of SCF(FBXL19) E3 ligase and Erk2. Biochimica et biophysica acta 77 23871831
2013 SCF E3 ligase F-box protein complex SCF(FBXL19) regulates cell migration by mediating Rac1 ubiquitination and degradation. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 68 23512198
2019 miR-26 suppresses adipocyte progenitor differentiation and fat production by targeting Fbxl19. Genes & development 59 31488578
2014 F-box protein complex FBXL19 regulates TGFβ1-induced E-cadherin down-regulation by mediating Rac3 ubiquitination and degradation. Molecular cancer 56 24684802
2017 Long non-coding RNA FBXL19-AS1 plays oncogenic role in colorectal cancer by sponging miR-203. Biochemical and biophysical research communications 39 28479250
2019 FBXL19-AS1 exerts oncogenic function by sponging miR-431-5p to regulate RAF1 expression in lung cancer. Bioscience reports 38 30610161
2018 lncRNA FBXL19-AS1 regulates osteosarcoma cell proliferation, migration and invasion by sponging miR-346. OncoTargets and therapy 36 30555237
2018 FBXL19 recruits CDK-Mediator to CpG islands of developmental genes priming them for activation during lineage commitment. eLife 26 29809150
2020 IGF2BP2 stabilized FBXL19-AS1 regulates the blood-tumour barrier permeability by negatively regulating ZNF765 by STAU1-mediated mRNA decay. RNA biology 25 32713259
2020 ETS1-activated SNHG10 exerts oncogenic functions in glioma via targeting miR-532-3p/FBXL19 axis. Cancer cell international 23 33298070
2019 FBXL19-AS1 promotes cell proliferation and inhibits cell apoptosis via miR-876-5p/FOXM1 axis in breast cancer. Acta biochimica et biophysica Sinica 22 31696201
2019 LncRNA FBXL19-AS1 promotes breast cancer cells proliferation and invasion via acting as a molecular sponge to miR-718. Bioscience reports 21 30886065
2019 LIN28A-stabilized FBXL19-AS1 promotes breast cancer migration, invasion and EMT by regulating WDR66. In vitro cellular & developmental biology. Animal 21 31140103
2019 Long noncoding RNA FBXL19-AS1 induces tumor growth and metastasis by sponging miR-203a-3p in lung adenocarcinoma. Journal of cellular physiology 20 31566718
2018 Histone acetyltransferase CBP promotes function of SCF FBXL19 ubiquitin E3 ligase by acetylation and stabilization of its F-box protein subunit. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 19 29522376
2021 LncRNA FBXL19-AS1 promotes proliferation and metastasis of cervical cancer through upregulating COL1A1 as a sponge of miR-193a-5p. Journal of biological research (Thessalonike, Greece) 17 34399848
2022 FLVCR1-AS1 and FBXL19-AS1: Two Putative lncRNA Candidates in Multiple Human Cancers. Non-coding RNA 15 36649030
2019 LncRNA FBXL19-AS1 promotes proliferation and metastasis via regulating epithelial-mesenchymal transition in non-small cell lung cancer. European review for medical and pharmacological sciences 15 31210311
2019 Two distinct E3 ligases, SCFFBXL19 and HECW1, degrade thyroid transcription factor 1 in normal thyroid epithelial and follicular thyroid carcinoma cells, respectively. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 15 31238008
2020 Long Noncoding RNA FBXL19-AS1 Expedites Cell Growth, Migration and Invasion in Cervical Cancer by miR-193a-5p/PIN1 Signaling. Cancer management and research 13 33116834
2021 lncRNA FBXL19-AS1 is a diagnosis biomarker for paediatric patients with acute myeloid leukemia. The journal of gene medicine 11 33474753
2020 CDK-Mediator and FBXL19 prime developmental genes for activation by promoting atypical regulatory interactions. Nucleic acids research 11 31996894
2017 Fbxl19 recruitment to CpG islands is required for Rnf20-mediated H2B mono-ubiquitination. Nucleic acids research 10 28453857
2004 Identification and characterization of FBXL19 gene in silico. International journal of molecular medicine 10 15547684
2020 SCF FBXW17 E3 ubiquitin ligase regulates FBXL19 stability and cell migration. Journal of cellular biochemistry 9 33053230
2022 Long Noncoding RNA FBXL19-AS1-Mediated Ulcerative Colitis-Associated Intestinal Epithelial Barrier Defect. Tissue engineering and regenerative medicine 8 36048401
2021 FBXL19-AS1 aggravates the progression of hepatocellular cancer by downregulating KLF2. Journal of B.U.ON. : official journal of the Balkan Union of Oncology 7 34564989
2023 ISGylation of NF-κBp65 by SCFFBXL19 E3 Ligase Diminishes Endothelial Inflammation. Arteriosclerosis, thrombosis, and vascular biology 6 36994728
2024 FBXL19 Targeted STK11 Degradation Enhances Cigarette Smoke-Induced Airway Epithelial Cell Cytotoxicity. COPD 5 38712759
2023 Protective role of FBXL19 in Streptococcus pneumoniae-induced lung injury in pneumonia immature mice. Journal of cardiothoracic surgery 5 36964598
2025 Unveiling EXOC4/SEC8: a key player in enhancing antiviral immunity by inhibiting the FBXL19-STING1-SQSTM1 signaling axis. Autophagy 4 40413753
2020 [Mechanism of flavonoids of Sophorae Fructus in inhibiting proliferation, migration and invasion of hepatocellular carcinoma cells by regulating LncRNA FBXL19-AS1/miR-342-3p pathway]. Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica 4 33164374
2020 Identify and Validate the Transcriptomic, Functional Network, and Predictive Validity of FBXL19-AS1 in Hepatocellular Carcinoma. Frontiers in oncology 4 33344260
2024 Exploring the regulatory role of FBXL19-AS1 in triple-negative breast cancer through the miR-378a-3p/OTUB2 axis. Cell biochemistry and function 3 38702967
2024 Significant Correlation Between Cutaneous Abundance of Streptococcus and Psoriasis Severity in Patients with FBXL19 Gene Variants. Acta dermato-venereologica 3 38898675
2024 FBXL19 in endothelial cells protects the heart from influenza A infection by enhancing antiviral immunity and reducing cellular senescence programs. American journal of physiology. Heart and circulatory physiology 2 39150394
2021 FBXL19‑AS1 promotes the progression of nasopharyngeal carcinoma by acting as a competing endogenous RNA to sponge miR‑431 and upregulate PBOV1. Molecular medicine reports 2 34278444
2023 CIZ1 aggravates gastric cancer progression via mediating FBXL19-AS1 and miR-339-3p. Heliyon 0 37954363

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