Affinage

LXN

Latexin · UniProt Q9BS40

Round 2 corrected
Length
222 aa
Mass
25.8 kDa
Annotated
2026-04-28
36 papers in source corpus 21 papers cited in narrative 21 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

Latexin (LXN) is a vertebrate-specific protein that functions both as a nanomolar-affinity inhibitor of A/B metallocarboxypeptidases and as a pleiotropic regulator of cell proliferation, apoptosis, and inflammatory signaling in diverse tissue contexts. Structurally, LXN comprises two cystatin-like subdomains that bind the active-site funnel of carboxypeptidase A4, occluding a large contact surface to achieve broad-spectrum inhibition of vertebrate metallocarboxypeptidases (PMID:15738388). Independent of its carboxypeptidase-inhibitory activity, LXN negatively regulates hematopoietic stem cell self-renewal and promotes apoptosis through interaction with ribosomal protein Rps3 and inhibition of its nuclear translocation (PMID:29608488, PMID:23028717); in intestinal epithelial cells, LXN forms a complex with the E3 ubiquitin ligase HECTD1 and Rps3 to stabilize IκBα and suppress NF-κB-driven inflammation (PMID:32555320), while in macrophages it restrains M2 polarization and PD-L2 expression by inhibiting JAK1/STAT3 signaling (PMID:36323670). LXN is frequently silenced by promoter CpG hypermethylation across gastric, prostate, melanoma, and hepatocellular cancers, and its re-expression suppresses tumor growth, induces G0/G1 arrest, and sensitizes cancer cells to chemotherapy (PMID:21466706, PMID:24399246, PMID:28087740).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2000 Medium

    Cloning of human LXN established it as a broadly expressed gene mapping to 3q25-q26.2, setting the stage for functional studies beyond the original rat brain context.

    Evidence cDNA cloning from human fetal brain library; Northern blot across 16 tissues; genomic mapping

    PMID:11455960

    Open questions at the time
    • No functional assay performed in this study
    • Protein-level expression across tissues not assessed
  2. 2005 High

    Determination of the LXN–hCPA4 crystal structure resolved the molecular basis of metallocarboxypeptidase inhibition, revealing two cystatin-like subdomains that clamp the enzyme's active-site funnel with nanomolar affinity and explaining why invertebrate and N/E-subfamily MCPs escape inhibition.

    Evidence X-ray crystallography of LXN–hCPA4 complex; structural modeling of non-inhibited MCPs

    PMID:15738388

    Open questions at the time
    • No mutagenesis to validate key contact residues
    • Kinetic parameters for inhibition of individual MCP family members not systematically measured
  3. 2011 Medium

    Reciprocal gain- and loss-of-function experiments in gastric cancer demonstrated that LXN acts as a tumor suppressor whose promoter is silenced by CpG methylation, linking epigenetic regulation to its growth-inhibitory role.

    Evidence Stable overexpression and antisense knockdown in gastric cancer cells; nude mouse xenograft; bisulfite sequencing

    PMID:21466706

    Open questions at the time
    • Downstream targets (Maspin, PDGFRB, etc.) identified by microarray but not validated by loss-of-function
    • Methylation-growth relationship is correlative, no demethylation rescue in vivo
  4. 2012 Medium

    Studies in hematopoietic stem cells and lymphoma cells established that LXN restricts HSC self-renewal and induces apoptosis through a mechanism independent of its carboxypeptidase-inhibitory activity, broadening its functional repertoire beyond enzyme inhibition.

    Evidence LXN-KO mouse HSC colony assays and proteomics; retroviral LXN overexpression in A20 lymphoma cells with apoptosis and xenograft readouts

    PMID:21567403 PMID:23028717

    Open questions at the time
    • The carboxypeptidase-independent mechanism was not molecularly defined at this stage
    • Downstream apoptotic targets (Bcl-2, Pim-2) not validated by rescue experiments
  5. 2013 Medium

    Nuclear localization of LXN in prostate epithelial cells and its role as a mediator of retinoic acid–induced invasion suppression revealed a compartment-specific tumor-suppressive function distinct from its cytosolic enzymatic role.

    Evidence siRNA knockdown; invasion and colony-formation assays; immunofluorescence localization; bisulfite methylation analysis in prostate cells

    PMID:23588494

    Open questions at the time
    • Nuclear binding partners not identified
    • Mechanism linking nuclear LXN to retinoic acid signaling pathway not defined
  6. 2014 Medium

    Identification of LXN-regulated cell cycle arrest via CDK inhibitors (p21, p27, p15) and cyclin D1/E in hepatocellular carcinoma provided a concrete proliferative checkpoint mechanism for its tumor-suppressive activity.

    Evidence LXN overexpression and shRNA knockdown in HCC lines; flow cytometry cell cycle analysis; Western blot for CDK inhibitors

    PMID:24399246

    Open questions at the time
    • Direct versus indirect regulation of CDK inhibitors not distinguished
    • No epistasis experiment to confirm CDK inhibitors are required for LXN-mediated arrest
  7. 2018 Medium

    The discovery that LXN binds Rps3 and inhibits its nuclear translocation provided the first defined signaling partner for LXN's carboxypeptidase-independent functions in HSC regulation and radiation sensitivity.

    Evidence Co-immunoprecipitation of LXN–Rps3; nuclear fractionation; LXN-KO mouse repopulation and radiation sensitivity assays

    PMID:29608488

    Open questions at the time
    • Primary data cited from review; structural basis of LXN–Rps3 interaction unknown
    • Downstream transcriptional targets of nuclear Rps3 in HSCs not comprehensively defined
  8. 2020 High

    Identification of the LXN–HECTD1–Rps3 complex and its role in stabilizing IκBα to suppress NF-κB provided a defined ubiquitin-dependent mechanism through which LXN restrains intestinal inflammation.

    Evidence Proteomics and Co-IP for LXN–HECTD1–Rps3 complex; IκBα ubiquitination assays; LXN-KO mouse DSS colitis model

    PMID:32555320

    Open questions at the time
    • Whether LXN competes with Rps3 for HECTD1 binding or allosterically modulates the complex is unresolved
    • No structural model of the ternary complex
  9. 2021 High

    Discovery that LXN interacts with Filamin A and regulates its cleavage and nuclear translocation extended LXN's mechanistic scope to cytoskeletal and vascular homeostasis, with LXN deletion protecting against atherosclerosis.

    Evidence Co-IP of LXN–FLNA; siRNA knockdown with F-actin imaging; LXN−/− and ApoE−/−LXN−/− double-KO mice with vascular permeability, vasodilation, and atherosclerosis endpoints

    PMID:34085389

    Open questions at the time
    • Binding domain on FLNA not mapped
    • Mechanism by which LXN regulates FLNA proteolytic cleavage not identified
  10. 2022 High

    Demonstration that LXN inhibits JAK1/STAT3 signaling in macrophages to prevent M2 polarization and PD-L2 upregulation established LXN as a checkpoint in anti-tumor immunity, rescued by adoptive transfer of WT macrophages.

    Evidence LXN-KO mouse tumor models; macrophage–T cell co-culture; Western blot for JAK1/STAT3; adoptive macrophage transfer; PD-L2 blockade

    PMID:36323670

    Open questions at the time
    • Direct physical interaction between LXN and JAK1 not demonstrated
    • Mechanism of selective PD-L2 (not PD-L1) regulation unclear
  11. 2024 Medium

    Multiple 2024 studies revealed additional LXN functions: activation of YAP/Wnt in intestinal stem cells upon LXN loss, exosomal LXN secretion by macrophages that inhibits Treg differentiation, and context-dependent roles in endometrial stromal cell migration.

    Evidence LXN-KO mouse intestinal organoids with YAP/Wnt pathway analysis; exosome isolation from macrophages with Treg co-culture; LXN knockdown in endometrial stromal cells

    PMID:39202445 PMID:39208900 PMID:39694381

    Open questions at the time
    • YAP and Wnt activation mechanism (direct target vs. indirect) not resolved
    • Exosomal LXN cargo sorting mechanism unknown
    • Endometrial migration finding lacks pathway-level mechanism
  12. 2025 Medium

    The LXN/Rps3/p53 axis was implicated in oxidative stress–induced cellular senescence in renal tubular cells, linking LXN to SASP-driven macrophage polarization and kidney stone pathogenesis.

    Evidence siRNA and AAV-shLXN knockdown in rat kidney stone model; SA-β-gal senescence staining; SASP cytokine measurement; macrophage co-culture

    PMID:41112268

    Open questions at the time
    • How LXN activates p53 is not defined
    • Whether the Rps3 interaction mediates p53 stabilization or transcriptional activation is untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis of LXN's interactions with Rps3, HECTD1, and FLNA; how a single protein integrates carboxypeptidase inhibition with NF-κB, JAK/STAT, YAP/Wnt, and p53 signaling; and whether these diverse functions are executed by distinct LXN pools (nuclear, cytosolic, secreted/exosomal).
  • No structure of LXN in complex with any non-MCP partner
  • Compartment-specific functions not systematically dissected with domain mutants
  • Relative contribution of carboxypeptidase-dependent vs -independent mechanisms to in vivo phenotypes untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005576 extracellular region 2 GO:0005829 cytosol 2 GO:0005634 nucleus 1 GO:0031410 cytoplasmic vesicle 1
Pathway
R-HSA-1643685 Disease 4 R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 3 R-HSA-5357801 Programmed Cell Death 3
Partners
CPA4FLNAHECTD1RPS3
Complex memberships
LXN-HECTD1-Rps3

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2005 Crystal structure of human latexin (LXN) in complex with human carboxypeptidase A4 (hCPA4) revealed that LXN consists of two topologically equivalent subdomains structurally reminiscent of cystatins, each comprising an alpha-helix enveloped by a curved beta-sheet; the enzyme is bound at the interface of these subdomains. The complex occludes a large contact surface with relatively few contacts, explaining the nanomolar inhibition constant and the broad inhibitory spectrum across all vertebrate A/B metallocarboxypeptidases. Modeling studies explained why N/E subfamily MCPs and invertebrate A/B MCPs are not inhibited, due to differences in loop segments shaping the active-site access funnel. X-ray crystallography of LXN–hCPA4 complex; structural modeling for non-inhibited MCPs Proceedings of the National Academy of Sciences of the United States of America High 15738388
2000 Human LXN encodes a 222-amino-acid protein with 84% sequence identity to rat and mouse latexin. Northern blot analysis demonstrated broad expression in 15 of 16 tissues examined (absent in peripheral blood leukocytes), with highest levels in heart, prostate, ovary, kidney, pancreas, and colon. The LXN gene spans ~5.9 kb, contains at least 6 exons, and maps to chromosome 3q25-q26.2. cDNA cloning from human fetal brain library; Northern blot analysis; genomic mapping Molecular biology reports Medium 11455960
2013 In human prostate epithelial cells, LXN localizes to the nucleus (distinct from RARRES1, which localizes to the endoplasmic reticulum). siRNA-mediated knockdown of LXN enhanced colony-forming ability (stem cell properties) and increased invasive capacity of primary prostate cultures. Inhibition of LXN fully rescued the anti-invasive effect induced by all-trans retinoic acid (atRA), establishing LXN as a downstream mediator of atRA's anti-invasion activity. LXN expression was co-ordinately repressed by DNA methylation in prostate cancer cell lines. siRNA knockdown; colony formation assay; invasion assay; subcellular localization by immunofluorescence; bisulfite methylation analysis Oncogenesis Medium 23588494
2011 Overexpression of LXN in LXN-negative gastric cancer cells (MGC803) inhibited colony formation and suppressed tumor growth in nude mice, while antisense-mediated knockdown in LXN-positive BGC823 cells enhanced tumor growth and colony formation. LXN overexpression differentially regulated tumor-related genes including Maspin, WFDC1, SLPI, S100P, and PDGFRB. CpG hypermethylation of the LXN promoter correlated with silenced LXN expression in cancer cell lines. Stable transfection (overexpression and antisense knockdown); colony formation assay; nude mouse xenograft; microarray gene expression; bisulfite sequencing BMC cancer Medium 21466706
2012 Retrovirus-mediated overexpression of LXN in A20 mouse lymphoma cells inhibited in vitro growth ~16-fold and in vivo tumor volume ~2-fold. LXN-induced growth inhibition was associated with increased apoptosis and downregulation of anti-apoptotic genes Bcl-2 and Pim-2. Importantly, this tumor-suppressive mechanism was not dependent on LXN's canonical carboxypeptidase inhibitor activity. Retroviral overexpression; in vitro proliferation assay; mouse xenograft; RT-PCR for Bcl-2 and Pim-2; apoptosis assay PloS one Medium 23028717
2012 Proteomic analysis of Sca-1+ bone marrow cells from LXN-knockout mice demonstrated that latexin ablation reduced the abundance of multiple proteins involved in HSC niche interaction, including N-cadherin, Tie2, and Roundabout 4. LXN was found to co-localize with these niche molecules in hematopoietic stem/progenitor cells. LXN-deficient KSL cells showed enhanced self-renewal in methylcellulose colony assays, and LXN knockout increased KSL cell numbers in vivo. LXN-knockout mouse model; proteomics of Sca-1+ cells; immunofluorescence co-localization; methylcellulose colony assay; flow cytometry Journal of cellular physiology Medium 21567403
2013 Exogenous LXN expression in melanoma cell lines significantly inhibited tumor cell proliferation and correlated with reduced expression of stem cell transcription factors OCT4, NANOG, SOX2, KLF4, and MYCN, suggesting LXN suppresses the stem cell-like properties of melanoma cells. The LXN CpG island promoter was hypermethylated in melanoma cell lines and tumors; 5-aza-2'-deoxycytidine treatment restored LXN expression. Exogenous LXN expression; proliferation assay; RT-PCR/Western blot for stem cell factors; bisulfite sequencing; demethylation drug treatment The Journal of investigative dermatology Medium 23364479
2014 LXN overexpression in hepatocellular carcinoma cells (SK-hep-1) promoted G0/G1 cell cycle arrest, while LXN silencing in YY-8103 cells promoted transition from G0/G1 to S phase. These effects were associated with differential expression of CDK inhibitors p21Cip1, p27Kip1, and p15INK4B, as well as cyclin D1 and cyclin E. LXN overexpression and shRNA knockdown; flow cytometry cell cycle analysis; Western blot for cell cycle regulators; colony formation; nude mouse xenograft Oncology reports Medium 24399246
2014 LXN protein treatment of CD133+ MiaPaCa-2 pancreatic cancer stem-like cells increased apoptosis and inhibited proliferation in a dose-dependent manner, associated with downregulation of Bcl-2 and c-myc and upregulation of Bax. Exogenous LXN protein treatment; CCK-8 proliferation assay; flow cytometry apoptosis assay; Western blot for Bcl-2, Bax, c-myc World journal of surgical oncology Medium 25551472
2017 LXN knockdown conferred docetaxel resistance to prostate cancer cells in vitro and in vivo, while LXN overexpression sensitized cells to docetaxel. Bone stromal cells decreased LXN expression through promoter methylation, inducing chemoresistance in co-cultured prostate cancer cells. In a mouse model, prostate cancer cells developed docetaxel resistance specifically in the bone microenvironment, coinciding with decreased LXN expression compared to the soft tissue microenvironment. siRNA knockdown; LXN overexpression; docetaxel resistance assays in vitro and in vivo; mouse xenograft; co-culture with bone stromal cells; bisulfite methylation analysis Molecular cancer research : MCR Medium 28087740
2019 LXN protein is both cytosolic and secreted by normal prostate luminal cells. LXN overexpression in the luminal prostate cancer line LNCaP reduced plating efficiency. Transcriptome analysis showed LXN overexpression had significant indirect effects on genes involved in retinoid metabolism and IFN-associated inflammatory responses, without direct transcriptional effects, suggesting a post-transcriptional or signaling mechanism. LXN overexpression; colony/plating efficiency assay; transcriptome analysis (RNA-seq); Western blot; conditioned medium analysis for secretion Scientific reports Medium 30914656
2020 LXN was identified as a suppressor of colitis. Proteomics revealed LXN physically interacts with HECTD1 (an E3 ubiquitin ligase) and ribosomal protein subunit Rps3, forming a functional complex. LXN expression promotes IκBα accumulation in intestinal epithelial cells; LXN knockdown enhances the HECTD1-Rps3 interaction, leading to ubiquitination and degradation of IκBα, and thereby activating NF-κB-driven inflammatory response. LXN deficiency aggravated DSS-induced colitis in mice. Proteomics/co-immunoprecipitation to identify LXN–HECTD1–Rps3 complex; Western blot for IκBα ubiquitination; LXN knockout mouse model (DSS colitis); ectopic LXN expression Scientific reports High 32555320
2021 LXN interacts with Filamin A (FLNA) and regulates FLNA proteolytic cleavage and nuclear translocation in vascular endothelial cells. Laminar shear stress (LSS) reduces LXN expression in ECs; LXN knockdown recapitulates LSS-induced morphological changes and F-actin remodeling. LXN-/- and ApoE-/-LXN-/- double-knockout mice showed improved vascular permeability, vasodilation, and reduced atherosclerosis, establishing LXN as a regulator of endothelial morphology and vascular homeostasis. Co-immunoprecipitation (LXN–FLNA interaction); siRNA knockdown; F-actin imaging; LXN-/- and double-KO mouse models; vascular permeability and vasodilation assays; atherosclerosis assessment Journal of cellular and molecular medicine High 34085389
2022 LXN deficiency in macrophages promotes M2 polarization and upregulates PD-L2 expression (but not PD-L1), inhibiting T cell function in the tumor microenvironment. Mechanistically, LXN inhibits STAT3 transcriptional activity by targeting inhibition of JAK1 in macrophages. Adoptive transfer of wild-type macrophages rescued T cell function in LXN-deficient mice. Targeted inhibition of PD-L2 ameliorated cancer growth in LXN-deficient mice. LXN-knockout mouse model; subcutaneous tumor and AOM/DSS colorectal cancer models; flow cytometry for immune cell populations and polarization; co-culture macrophage-T cell systems; Western blot for JAK1/STAT3; adoptive macrophage transfer; PD-L2 inhibition Cell death discovery High 36323670
2024 LXN colocalizes with Lgr5+ intestinal stem cells (ISCs) in crypts. LXN deletion upregulates Lgr5 expression and enhances ISC proliferation, promoting intestinal organoid development. Mechanistically, LXN deficiency activates both the YAP and Wnt signaling pathways in ISCs, accelerating normal intestinal growth and regeneration post-injury. LXN-knockout mouse model; immunofluorescence co-localization with Lgr5; intestinal organoid culture; Western blot for YAP and Wnt pathway components; DSS-induced injury model International journal of biological macromolecules Medium 39208900
2024 LXN is secreted by macrophages via exosomes. LXN-enriched macrophage-derived exosomes inhibit CD4+ T cell differentiation into Treg cells both in vitro and in vivo, enhancing tumor immune surveillance. Biomimetic nanoparticles loaded with LXN protein (MØ@LXN-NPS) recapitulated this Treg-inhibitory and anti-tumor activity. Macrophage-T cell co-culture system; exosome isolation and characterization; flow cytometry for Treg differentiation; in vivo tumor models; biomimetic nanoparticle engineering International journal of biological macromolecules Medium 39694381
2024 LXN knockdown in endometrial stromal cells reduced their migratory capacity while promoting cell viability, indicating LXN positively regulates migration and negatively regulates proliferation in this cell type. LXN knockdown; Transwell migration assay; MTT viability assay Genes Low 39202445
2025 In renal tubular epithelial cells (RTECs), oxalate-induced oxidative stress activates the LXN/Rps3/p53 signaling pathway, promoting premature cellular senescence and SASP factor secretion, which in turn drives M1-like macrophage polarization and increased calcium oxalate crystal deposition. siRNA knockdown of LXN, or AAV-shLXN in a rat kidney stone model, reduced RTEC senescence, decreased SASP, reversed M1 macrophage polarization, and diminished intrarenal CaOx crystal deposition. siRNA knockdown of LXN; AAV-shLXN in rat model; SA-β-gal senescence staining; SASP cytokine measurement; macrophage co-culture; immunohistochemistry; Von Kossa staining Frontiers in immunology Medium 41112268
2026 LXN knockdown in mice (AAV9-shLXN) reduced CCl4-induced liver injury and suppressed hepatic stellate cell (HSC) activation, inhibiting α-SMA and collagen I expression. LXN expression showed a substantial positive correlation with THBS2 (thrombospondin-2), and LXN knockdown downregulated THBS2, suggesting LXN promotes liver fibrosis via a LXN-THBS2 signaling axis that drives HSC activation. AAV9-mediated LXN knockdown in mouse CCl4 liver fibrosis model; siLXN in LX-2 cells; qPCR; Western blot; immunohistochemistry; immunofluorescence Frontiers in bioscience (Landmark edition) Medium 41761978
2024 In smooth muscle cells (SMCs), LXN deficiency significantly attenuated SMC proliferation and migration by inhibiting PDGF receptor expression. In macrophages, LXN deficiency inhibited MCP-1-induced macrophage migration by suppressing ERK phosphorylation. Global, SMC-specific, and myeloid-specific LXN knockout (but not endothelial-specific KO) markedly prevented neointimal hyperplasia after carotid artery ligation in mice. Cell-type-specific LXN KO mouse models (global, SMC-specific, EC-specific, myeloid-specific); carotid artery ligation model; Western blot for PDGF receptors and ERK phosphorylation; immunofluorescence; proliferation and migration assays bioRxivpreprint Medium bio_10.1101_2024.10.03.616555
2018 LXN acts endogenously in hematopoietic stem cells (HSCs) to negatively regulate their population size by enhancing apoptosis and decreasing self-renewal. LXN interacts with ribosomal protein Rps3 and inhibits its nuclear translocation, sensitizing hematopoietic cells to radiation-induced cell death. LXN inactivation downregulates thrombospondin 1 (Thbs1), connecting the LXN-Rps3 axis to downstream transcriptional effects. LXN knockout mouse model; repopulation assays; apoptosis assays; co-immunoprecipitation (LXN-Rps3); nuclear fractionation for Rps3 localization; radiation sensitivity assays (review summarizing primary experimental data) Current opinion in hematology Medium 29608488

Source papers

Stage 0 corpus · 36 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2014 A proteome-scale map of the human interactome network. Cell 977 25416956
2020 A reference map of the human binary protein interactome. Nature 849 32296183
2007 Large-scale mapping of human protein-protein interactions by mass spectrometry. Molecular systems biology 733 17353931
2012 A census of human soluble protein complexes. Cell 689 22939629
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2007 hORFeome v3.1: a resource of human open reading frames representing over 10,000 human genes. Genomics 222 17207965
2013 Proteomic analysis of podocyte exosome-enriched fraction from normal human urine. Journal of proteomics 126 23376485
2005 Structure of human carboxypeptidase A4 with its endogenous protein inhibitor, latexin. Proceedings of the National Academy of Sciences of the United States of America 85 15738388
2013 Retinoic acid represses invasion and stem cell phenotype by induction of the metastasis suppressors RARRES1 and LXN. Oncogenesis 50 23588494
2000 Cloning, tissue expression pattern and genomic organization of latexin, a human homologue of rat carboxypeptidase A inhibitor. Molecular biology reports 40 11455960
2018 BAP1 regulation of the key adaptor protein NCoR1 is critical for γ-globin gene repression. Genes & development 32 30463901
2011 Latexin expression is downregulated in human gastric carcinomas and exhibits tumor suppressor potential. BMC cancer 30 21466706
2013 The hematopoietic stem cell regulatory gene latexin has tumor-suppressive properties in malignant melanoma. The Journal of investigative dermatology 29 23364479
2020 Latexin deficiency in mice up-regulates inflammation and aggravates colitis through HECTD1/Rps3/NF-κB pathway. Scientific reports 27 32555320
2012 Latexin regulates the abundance of multiple cellular proteins in hematopoietic stem cells. Journal of cellular physiology 23 21567403
2014 Latexin exhibits tumor suppressor potential in hepatocellular carcinoma. Oncology reports 22 24399246
2018 Alterations in the brain interactome of the intrinsically disordered N-terminal domain of the cellular prion protein (PrPC) in Alzheimer's disease. PloS one 21 29791485
2012 Latexin is down-regulated in hematopoietic malignancies and restoration of expression inhibits lymphoma growth. PloS one 19 23028717
2019 The putative tumour suppressor protein Latexin is secreted by prostate luminal cells and is downregulated in malignancy. Scientific reports 18 30914656
2017 Bone Microenvironment Changes in Latexin Expression Promote Chemoresistance. Molecular cancer research : MCR 13 28087740
2013 Clinical significance of CD146 and latexin during different stages of thyroid cancer. Molecular and cellular biochemistry 13 23712706
2022 Loss of LXN promotes macrophage M2 polarization and PD-L2 expression contributing cancer immune-escape in mice. Cell death discovery 11 36323670
2015 Latexin exhibits tumor-suppressor potential in pancreatic ductal adenocarcinoma. Oncology reports 11 26530530
2014 Latexin inhibits the proliferation of CD133+ miapaca-2 pancreatic cancer stem-like cells. World journal of surgical oncology 10 25551472
2021 LXN deficiency regulates cytoskeleton remodelling by promoting proteolytic cleavage of Filamin A in vascular endothelial cells. Journal of cellular and molecular medicine 9 34085389
2024 The comprehensive SARS-CoV-2 'hijackome' knowledge base. Cell discovery 7 39653747
2024 Therapeutic potential of ADSC-EV-derived lncRNA DLEU2: A novel molecular pathway in alleviating sepsis-induced lung injury via the miR-106a-5p/LXN axis. International immunopharmacology 6 38442573
2023 Circ_0002715 promotes the development of osteoarthritis through regulating LXN by sponging miR-127-5p. Journal of orthopaedic surgery and research 6 36949500
2018 Latexin and hematopoiesis. Current opinion in hematology 6 29608488
2024 Carboxypeptidase Inhibitor LXN Expression in Endometrial Tissue Is Menstrual Cycle Phase-Dependent and Is Upregulated in Endometriotic Lesions. Genes 2 39202445
2025 Premature renal epithelial cell senescence promoted by LXN/Rps3/p53 signaling pathway activation increases calcium oxalate crystal deposition by altering macrophage polarization. Frontiers in immunology 1 41112268
2024 Carboxypeptidase inhibitor Latexin (LXN) regulates intestinal organogenesis and intestinal remodeling involved in intestinal injury repair in mice. International journal of biological macromolecules 1 39208900
2024 Latexin (LXN) enhances tumor immune surveillance in mice by inhibiting Treg cells through the macrophage exosome pathway. International journal of biological macromolecules 1 39694381
2026 LXN-THBS2 Signaling Axis Regulates Hepatic Stellate Cell Activation and Promotes the Development of Liver Fibrosis. Frontiers in bioscience (Landmark edition) 0 41761978