Affinage

LOXL4

Lysyl oxidase homolog 4 · UniProt Q96JB6

Length
756 aa
Mass
84.5 kDa
Annotated
2026-06-10
34 papers in source corpus 17 papers cited in narrative 17 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

LOXL4 is a secreted, copper-dependent lysyl oxidase family member that catalyzes extracellular matrix collagen cross-linking and, beyond this canonical role, exerts context-dependent control over tumor cell signaling, immune evasion, and angiogenesis (PMID:11691588, PMID:37235663). Structurally it is defined by a conserved C-terminal copper-binding catalytic domain plus four N-terminal SRCR domains, including one bearing a unique 13-amino-acid insertion that distinguishes it from LOXL2 and LOXL3 (PMID:11691588). In the lung, genetic ablation studies establish LOXL4 as the dominant LOX family activity driving pathological collagen cross-linking in fibrosis, with LOXL4 loss reducing fibrosis more strongly than LOXL2 loss and even lowering expression of other LOX members (PMID:37235663). Its expression is transcriptionally induced by TGF-β1 through cooperative Smad and JunB/Fra2 (AP-1) signaling at the LOXL4 promoter and by the Zn2+-activated transcription factor ZEB1, which couples LOXL4 to EMT and invasion (PMID:23572561, PMID:36910659), while at the protein level TGF-β1 can conversely drive its proteasomal degradation through MEK/ERK (PMID:39862152), and multiple microRNAs (including miR-193a-3p, miR-29b, and miR-30d) repress it (PMID:25311867, PMID:32754259). Functionally, intracellular LOXL4 promotes migration and invasion via amine-oxidase-dependent, hydrogen-peroxide-mediated activation of the FAK/Src pathway, and is packaged into exosomes/extracellular vesicles for transfer to recipient cells to drive angiogenesis and, in macrophages, STAT1-dependent PD-L1 induction that suppresses CD8+ T cell killing (PMID:25216702, PMID:30704479, PMID:38047403). LOXL4 also engages discrete protein partners: it binds and reactivates wild-type p53 to trigger liver cancer cell death (PMID:30728460), and promotes ubiquitination and degradation of SOCS3 to sustain JAK2/STAT3 signaling and radiotherapy resistance in glioma (PMID:42134289). In bladder cancer LOXL4 instead behaves as a tumor suppressor by antagonizing Ras-driven ERK activation (PMID:17456585).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2001 High

    Established LOXL4 as a distinct lysyl oxidase family member, defining the catalytic copper-binding domain and SRCR architecture that distinguish it from its paralogs.

    Evidence cDNA cloning, sequence and genomic structure analysis

    PMID:11691588

    Open questions at the time
    • No enzymatic activity measured directly on substrates
    • No tissue expression or functional role defined
  2. 2007 Medium

    Defined an early functional role by showing LOXL4 can act as a tumor suppressor through antagonism of the Ras/ERK pathway, framing LOXL4 function as context-dependent.

    Evidence Gene reintroduction, colony formation and ERK western blot in bladder cancer cells

    PMID:17456585

    Open questions at the time
    • Mechanism of Ras antagonism not resolved
    • Whether amine oxidase activity is required is untested
  3. 2008 Medium

    Connected LOXL4 dysregulation in HNSCC to specific promoter elements and identified its perinuclear/cell-surface localization, hinting at adhesion/ECM functions rather than nuclear roles.

    Evidence Promoter deletion/reporter assays, EMSA, and immunocytochemistry in HNSCC cells

    PMID:18499440 PMID:18949373

    Open questions at the time
    • TATA/SP1 binding inferred from EMSA, not validated by ChIP
    • Functional consequence of cell-surface localization not tested
  4. 2013 High

    Resolved how LOXL4 is induced by TGF-β1, demonstrating combinatorial Smad/AP-1 (JunB/Fra2) promoter control and confirming LOXL4 secretion and contribution to ECM assembly.

    Evidence Promoter mutagenesis, ChIP, reporter assays, and secretion assays in aortic endothelial cells

    PMID:23572561

    Open questions at the time
    • Direct enzymatic cross-linking activity not measured
    • In vivo relevance of this transcriptional circuit untested
  5. 2014 Medium

    Linked LOXL4 to pro-tumorigenic signaling by showing it activates FAK/Src to enhance cell-ECM adhesion, migration and invasion, including via recombinant extracellular protein.

    Evidence Overexpression/RNAi, recombinant protein treatment, FAK/Src western blot, migration/invasion assays in gastric cancer

    PMID:25216702

    Open questions at the time
    • Whether activity is intracellular or extracellular not disentangled here
    • Catalytic dependence not directly tested
  6. 2014 Medium

    Identified LOXL4 as a direct miR-193a-3p target whose suppression drives multidrug resistance via oxidative stress, establishing microRNA-mediated control of LOXL4.

    Evidence miRNA gain/loss, luciferase reporter, xenograft model in bladder cancer

    PMID:25311867

    Open questions at the time
    • Molecular basis of oxidative-stress-mediated resistance not detailed
    • Direct LOXL4 enzymatic contribution not isolated
  7. 2017 Medium

    Revealed a suppressive ECM role in breast cancer, where LOXL4 loss increased collagen deposition, bundle thickening, and tumor growth, contrasting with its pro-invasive roles elsewhere.

    Evidence shRNA knockdown, mouse xenografts, second harmonic generation imaging, collagen-protein western blot

    PMID:28060764

    Open questions at the time
    • Mechanism reconciling collagen suppression with cross-linking activity unclear
    • No biochemical cross-linking assay
  8. 2019 High

    Distinguished intracellular from extracellular LOXL4 function and showed amine-oxidase-dependent, H2O2-mediated FAK/Src activation drives migration, while exosomal transfer drives paracrine angiogenesis.

    Evidence Exosome transfer, domain-deletion mutants, shRNA, FAK/Src western blot, in vivo metastasis models in HCC

    PMID:30704479

    Open questions at the time
    • Direct H2O2 measurement linking activity to FAK/Src not fully detailed
    • Mechanism of exosomal packaging unknown
  9. 2019 High

    Uncovered a non-catalytic protein-interaction function: LOXL4 binds the p53 basic domain to reactivate compromised wild-type p53 and induce liver cancer cell death.

    Evidence Genome-wide screen, Co-IP with domain mapping, xenograft, viability assays

    PMID:30728460

    Open questions at the time
    • Whether amine oxidase activity contributes to p53 reactivation untested
    • Reciprocal structural validation of the interface absent
  10. 2020 High

    Placed LOXL4 within an epigenetic regulatory circuit, identifying it as a direct miR-29b/miR-30d target whose EZH2-mediated derepression promotes breast cancer progression.

    Evidence Dual-luciferase, ChIP, qRT-PCR, western blot, xenografts

    PMID:32754259

    Open questions at the time
    • Downstream effector pathway from elevated LOXL4 not defined here
    • Catalytic requirement untested
  11. 2021 Medium

    Tested a vascular requirement and found LOXL4 dispensable for angiotensin II-induced aortic aneurysm, bounding its physiological role in vascular pathology.

    Evidence LOXL4 knockout mice with angiotensin II infusion and aneurysm assessment

    PMID:33807332

    Open questions at the time
    • Negative result limited to one aneurysm model
    • Possible compensation by other LOX members not assessed
  12. 2023 High

    Established LOXL4 as the primary LOX activity driving pathological collagen cross-linking in lung fibrosis, with epistasis over LOXL2.

    Evidence Single and double Loxl2/Loxl4 knockout mice, pulmonary fibrosis model, collagen cross-linking and expression analysis

    PMID:37235663

    Open questions at the time
    • Cell-type source of fibrotic LOXL4 not pinpointed
    • Reason LOXL4 loss reduces other LOX members unknown
  13. 2023 Medium

    Defined an immune-evasion mechanism in which EV-delivered LOXL4 activates STAT1/PD-L1 in macrophages to suppress CD8+ T cell killing in HCC.

    Evidence EV delivery, macrophage/T cell co-culture, orthotopic xenograft, STAT1/PD-L1 western blot

    PMID:38047403

    Open questions at the time
    • How LOXL4 engages STAT1 mechanistically unclear
    • Catalytic dependence of STAT1 activation untested
  14. 2023 Medium

    Identified ZEB1, in its Zn2+-bound active form, as a transcriptional driver of LOXL4 coupling its expression to EMT and invasion.

    Evidence MutZEB1 (ΔZn) stable expression, invasion assays, RNA-Seq in MDA-MB-231 cells

    PMID:36910659

    Open questions at the time
    • Direct ZEB1 occupancy at LOXL4 promoter not shown by ChIP
    • Functional contribution of induced LOXL4 to invasion not isolated
  15. 2025 Medium

    Showed post-translational control of LOXL4 by TGF-β1, which reduces LOXL4 protein via MEK/ERK-driven proteasomal degradation and N-glycosylation-linked secretion defects, revealing regulation opposing its transcriptional induction.

    Evidence Proteasome and MEK/ERK inhibition, ROS measurement, protein vs mRNA western blot, N-glycosylation analysis in MDA-MB-231 cells

    PMID:39862152

    Open questions at the time
    • E3 ligase mediating degradation not identified
    • Reconciliation with TGF-β1 transcriptional induction in other contexts unresolved
  16. 2026 Medium

    Defined a LOXL4-SOCS3-STAT3 axis in which LOXL4 promotes SOCS3 ubiquitination/degradation to sustain JAK2/STAT3 signaling and radiotherapy resistance in glioma.

    Evidence Co-IP, mass spectrometry, RT-resistant cell models, DNA repair/apoptosis assays, orthotopic glioma model

    PMID:42134289

    Open questions at the time
    • Whether LOXL4 acts as or recruits a ubiquitin ligase unknown
    • Catalytic requirement for SOCS3 degradation untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How LOXL4's single catalytic amine-oxidase activity is reconciled with its divergent context-dependent outputs—tumor suppression versus promotion, ECM cross-linking versus protein-partner signaling—remains unresolved.
  • No unified model linking catalytic activity to non-catalytic interactions
  • Structural basis of partner binding (p53, SOCS3) undetermined
  • In vivo determinants of tumor-suppressive vs oncogenic behavior unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016491 oxidoreductase activity 3 GO:0140096 catalytic activity, acting on a protein 2
Localization
GO:0005576 extracellular region 2 GO:0031410 cytoplasmic vesicle 2 GO:0005886 plasma membrane 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1474244 Extracellular matrix organization 2 R-HSA-168256 Immune System 1
Partners
SOCS3TP53

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 LOXL4 was identified as a novel lysyl oxidase family member with a conserved C-terminal copper-binding site, lysyl and tyrosyl residues, and a cytokine receptor-like domain. It contains four N-terminal SRCR domains, one of which has a unique 13 amino acid insertion encoded by a short exon not present in LOXL2 or LOXL3. The gene is located on chromosome 10q24 and spans 14 exons. cDNA cloning, sequence analysis, genomic structure determination Matrix biology High 11691588
2007 Reintroduction of LOXL4 into human bladder cancer cells decreased colony formation ability and antagonized Ras in activating the ERK signaling pathway, establishing LOXL4 as a functional tumor suppressor acting through inhibition of the Ras/ERK pathway. Gene reintroduction (overexpression), colony formation assay, ERK signaling western blot, promoter methylation analysis Cancer research Medium 17456585
2008 LOXL4 gene overexpression in HNSCC cells is driven by de novo transcription, with TATA (-25) and SP1 (-181) binding sites showing increased nuclear extract binding activity in HNSCC cells compared to normal epithelial cells, indicating these transcription factors regulate LOXL4 upregulation. Promoter deletion analysis, reporter gene assays, DNA-binding (EMSA) experiments with nuclear extracts International journal of oncology Medium 18949373
2008 LOXL4 protein in cultured primary hypopharyngeal HTB-43 carcinoma cells localizes perinuclearly and at the cell surface, but not in the nucleus, suggesting cell surface-associated functions in tumor cell adhesion and extracellular matrix interactions. Immunocytochemistry in cultured HNSCC cells with LOXL4-specific antibody European journal of cancer Medium 18499440
2013 TGF-β1 induces LOXL4 expression in aortic endothelial cells via a mechanism requiring both a distal AP-1 site and a Smad binding element in the LOXL4 promoter. Functional cooperation between Smad proteins and the AP-1 complex composed of JunB/Fra2 mediates TGF-β1 induction, involving ERK-dependent phosphorylation of Fra2. LOXL4 is extracellularly secreted and contributes to ECM deposition and assembly. Promoter deletion mapping, mutagenesis analysis, reporter gene assays, western blotting for ERK phosphorylation, chromatin immunoprecipitation, secretion assays Molecular and cellular biology High 23572561
2014 LOXL4 promotes gastric cancer cell proliferation, migration and invasion, and activates the FAK/Src pathway to enhance cell-extracellular matrix adhesion. Recombinant human LOXL4 protein also promoted GC cell proliferation and migration, indicating extracellular LOXL4 activity. Overexpression, RNA interference, recombinant protein treatment, western blot for FAK/Src pathway, migration/invasion assays Journal of cancer research and clinical oncology Medium 25216702
2014 LOXL4 is a direct target of miR-193a-3p; miR-193a-3p promotes multi-drug resistance in bladder cancer cells through suppression of LOXL4, and this resistance is mediated downstream via the Oxidative Stress pathway. miRNA overexpression/inhibition, luciferase reporter assay, xenograft tumor model, oxidative stress pathway analysis Molecular cancer Medium 25311867
2017 LOXL4 knockdown in triple-negative breast cancer cells increased primary tumor growth and lung colonization in mouse xenograft models, accompanied by increased collagen I and IV, lysine hydroxylase 1 and 2, and prolyl 4-hydroxylase subunit alpha 1 and 2 levels. Second harmonic generation imaging showed LOXL4 knockdown resulted in thickening of collagen bundles, indicating LOXL4 suppresses collagen synthesis, deposition, and structural changes in the ECM. shRNA knockdown, mouse xenograft model, second harmonic generation imaging, western blotting for collagen-related proteins Oncotarget Medium 28060764
2019 HCC-derived exosomes transfer LOXL4 between HCC cells and to HUVECs. Intracellular (but not extracellular) LOXL4 promotes cell migration by activating the FAK/Src pathway dependent on its amine oxidase activity through a hydrogen peroxide-mediated mechanism. Exosome-transferred LOXL4 promotes angiogenesis via a paracrine mechanism. Exosome isolation and characterization, overexpression/shRNA knockdown, deletion mutants including amine oxidase domain mutants, western blot for FAK/Src, migration assays, in vivo metastasis models Molecular cancer High 30704479
2019 5-azacytidine (5-aza-CR) induces LOXL4 upregulation in liver cancer cells, and LOXL4 subsequently binds the basic domain of p53 via its low-isoelectric point region, inducing reactivation of compromised wild-type p53 and resulting in cell death. The LOXL4-p53 interaction was identified through genome-wide screening. Genome-wide screen, co-immunoprecipitation (LOXL4-p53 binding), domain mapping, xenograft tumor model, cell viability assays Cell death and differentiation High 30728460
2020 EZH2 inhibition enhances miR-30d and miR-29b transcription via promoter binding, reducing LOXL4 expression. LOXL4 was identified as a direct target of miR-29b and miR-30d (validated by dual-luciferase reporter assay and ChIP). EZH2-mediated epigenetic silencing of miR-29b/miR-30d results in elevated LOXL4, promoting breast cancer cell proliferation, migration, and metastasis. Dual-luciferase reporter assay, chromatin immunoprecipitation, qRT-PCR, western blotting, xenograft experiments Theranostics High 32754259
2021 Genetic ablation of LOXL4 in mice did not induce more severe thoracic or abdominal aortic aneurysm compared to wild-type mice under angiotensin II infusion, indicating LOXL4 does not play a major role in angiotensin II-induced aortic aneurysm development. LOXL4 knockout mouse generation, angiotensin II subcutaneous infusion, aortic aneurysm assessment Genes Medium 33807332
2023 Genetic ablation of LOXL4 (but not LOXL2) markedly disrupts pathological collagen cross-linking and fibrosis in the lung. Combined knockout of Loxl2 and Loxl4 does not offer additive antifibrotic effects over Loxl4 deletion alone, and LOXL4 deficiency decreases expression of other LOX family members including Loxl2, establishing LOXL4 as the primary LOX activity underlying pathological collagen cross-linking in lung fibrosis. Genetic knockout mice (Loxl2 KO, Loxl4 KO, double KO), pulmonary fibrosis model, collagen cross-linking analysis, gene expression analysis Science advances High 37235663
2023 LOXL4 shuttled by tumor cell-derived extracellular vesicles is delivered into macrophages, where it activates STAT1 signaling to induce PD-L1 expression, suppressing CD8+ T cell killing activity and promoting immune escape in hepatocellular carcinoma. EV isolation and delivery, in vitro macrophage/CD8+ T cell co-culture assay, in vivo orthotopic xenograft model, western blot for STAT1/PD-L1 Journal of immunotherapy Medium 38047403
2023 ZEB1 (in its Zn2+-bound active form) acts as a transcription factor that drives expression of LOXL1 and LOXL4. Mutation of the Zn-finger motifs of ZEB1 (MutZEB1 ΔZn) leads to significant downregulation of LOXL1 and LOXL4, loss of EMT, and stalled invasion in MDA-MB-231 cells. Stable expression of MutZEB1 (ΔZn) in MDA-MB-231 cells, invasion assays, RNA-Seq analysis Frontiers in oncology Medium 36910659
2025 TGF-β1 decreases LOXL4 protein (but not mRNA) expression in MDA-MB-231 breast cancer cells via proteasomal degradation through MEK/ERK pathway activation. Bortezomib (proteasomal inhibitor) suppresses TGF-β1-mediated LOXL4 reduction and inhibits TGF-β1-induced MEK/ERK pathways. N-glycosylation dysregulation is involved in reduction of LOXL4 secretion. Proteasomal inhibitor treatment, MEK/ERK inhibition, ROS measurement, western blotting for LOXL4 protein vs. mRNA levels, N-glycosylation analysis Journal of receptor and signal transduction research Medium 39862152
2026 LOXL4 promotes ubiquitination and degradation of SOCS3 (suppressor of cytokine signaling 3), relieving SOCS3-mediated inhibition of JAK2 and leading to sustained STAT3 activation. This LOXL4-SOCS3-STAT3 axis enhances DNA damage repair, inhibits apoptosis, and fosters an immunosuppressive tumor microenvironment, driving radiotherapy resistance in glioma. Co-immunoprecipitation, mass spectrometry, stable RT-resistant cell models, functional assays for DNA repair and apoptosis, orthotopic glioma mouse model International immunopharmacology Medium 42134289

Source papers

Stage 0 corpus · 34 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2019 Exosome-mediated secretion of LOXL4 promotes hepatocellular carcinoma cell invasion and metastasis. Molecular cancer 193 30704479
2007 LOXL1 and LOXL4 are epigenetically silenced and can inhibit ras/extracellular signal-regulated kinase signaling pathway in human bladder cancer. Cancer research 94 17456585
2013 LOXL4 is induced by transforming growth factor β1 through Smad and JunB/Fra2 and contributes to vascular matrix remodeling. Molecular and cellular biology 78 23572561
2014 miR-193a-3p regulates the multi-drug resistance of bladder cancer by targeting the LOXL4 gene and the oxidative stress pathway. Molecular cancer 75 25311867
2001 A novel human lysyl oxidase-like gene (LOXL4) on chromosome 10q24 has an altered scavenger receptor cysteine rich domain. Matrix biology : journal of the International Society for Matrix Biology 73 11691588
2020 EZH2-mediated Epigenetic Silencing of miR-29/miR-30 targets LOXL4 and contributes to Tumorigenesis, Metastasis, and Immune Microenvironment Remodeling in Breast Cancer. Theranostics 71 32754259
2014 Lysyl oxidase-like 4 (LOXL4) promotes proliferation and metastasis of gastric cancer via FAK/Src pathway. Journal of cancer research and clinical oncology 56 25216702
2017 LOXL4 knockdown enhances tumor growth and lung metastasis through collagen-dependent extracellular matrix changes in triple-negative breast cancer. Oncotarget 48 28060764
2023 LOXL4, but not LOXL2, is the critical determinant of pathological collagen cross-linking and fibrosis in the lung. Science advances 42 37235663
2019 Derepression of LOXL4 inhibits liver cancer growth by reactivating compromised p53. Cell death and differentiation 42 30728460
2007 Selective upregulation and amplification of the lysyl oxidase like-4 (LOXL4) gene in head and neck squamous cell carcinoma. The Journal of pathology 37 17354256
2019 Downregulation of lysyl oxidase-like 4 LOXL4 by miR-135a-5p promotes lung cancer progression in vitro and in vivo. Journal of cellular physiology 31 30993701
2008 LOXL4 is a selectively expressed candidate diagnostic antigen in head and neck cancer. European journal of cancer (Oxford, England : 1990) 28 18499440
2013 Identification of the involvement of LOXL4 in generation of keratocystic odontogenic tumors by RNA-Seq analysis. International journal of oral science 21 24357854
2010 LOXL4 as a selective molecular marker in primary and metastatic head/neck carcinoma. Anticancer research 17 21115907
2023 LOXL4 Shuttled by Tumor Cells-derived Extracellular Vesicles Promotes Immune Escape in Hepatocellular Carcinoma by Activating the STAT1/PD-L1 Axis. Journal of immunotherapy (Hagerstown, Md. : 1997) 13 38047403
2019 Clinical significance of LOXL4 expression and features of LOXL4-associated protein-protein interaction network in esophageal squamous cell carcinoma. Amino acids 12 30900087
2023 miR-183-5p regulates ECM and EMT to promote non-small cell lung cancer progression by targeting LOXL4. Journal of thoracic disease 11 37197500
2022 Overexpression of miR-328-5p influences cell growth and migration to promote NSCLC progression by targeting LOXL4. Annals of translational medicine 10 35433959
2023 LOXL1 and LOXL4 are novel target genes of the Zn2+-bound form of ZEB1 and play a crucial role in the acceleration of invasive events in triple-negative breast cancer cells. Frontiers in oncology 9 36910659
2021 LOXL4 Abrogation Does Not Exaggerate Angiotensin II-Induced Thoracic or Abdominal Aortic Aneurysm in Mice. Genes 9 33807332
2008 Functional analysis of the 5' flanking domain of the LOXL4 gene in head and neck squamous cell carcinoma cells. International journal of oncology 9 18949373
2022 Long non-coding RNA AGAP2-AS1 promotes cell proliferation and invasion through regulating miR-193a-3p/LOXL4 axis in laryngeal squamous cell carcinoma. Cell cycle (Georgetown, Tex.) 8 35113007
2018 Trans-suppression of host CDH3 and LOXL4 genes during Cryptosporidium parvum infection involves nuclear delivery of parasite Cdg7_FLc_1000 RNA. International journal for parasitology 8 29438669
2024 The dual role of LOXL4 in the pathogenesis and development of human malignant tumors: a narrative review. Translational cancer research 7 38737700
2016 Differential expression of LOXL4 in normal and tumour tissue samples of laryngeal squamous cell carcinoma. Clinical otolaryngology : official journal of ENT-UK ; official journal of Netherlands Society for Oto-Rhino-Laryngology & Cervico-Facial Surgery 7 26138381
2018 Collagen XVIII and LOXL-4 polymorphisms in women with and without advanced pelvic organ prolapse. International urogynecology journal 6 29532123
2025 LOXL4, CREB5 and steroid hormone biosynthesis pathways are involved in type 1 diabetes with polycystic ovary-like changes. European journal of obstetrics, gynecology, and reproductive biology 2 40795623
2025 LNC511 inhibits lung cancer progression by modulating the miR-625/LOXL4/Wnt/β-catenin pathway. Cellular signalling 1 41203182
2026 Multi-Omics Bioinformatic Analyses Linking LOXL4 with Spondylolisthesis. Orthopedic research and reviews 0 41890150
2026 LOXL4 drives radiotherapy resistance and immunosuppression in glioma by targeting SOCS3 for degradation to activate STAT3 signaling. International immunopharmacology 0 42134289
2025 Bortezomib suppresses TGF-β1-mediated LOXL4 reduction through the inhibition of MEK/ERK pathways in MDA-MB-231 cells. Journal of receptor and signal transduction research 0 39862152
2025 Pan-cancer analysis of role of LOXL4 and experiment validation in osteosarcoma. Discover oncology 0 41118012
2021 LAMA2 and LOXL4 are candidate FSGS genes. BMC nephrology 0 34565340

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