Affinage

LAPTM5

Lysosomal-associated transmembrane protein 5 · UniProt Q13571

Length
262 aa
Mass
29.9 kDa
Annotated
2026-06-10
39 papers in source corpus 22 papers cited in narrative 22 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

LAPTM5 is a pentaspanning lysosomal integral membrane protein of hematopoietic cells that governs lysosomal trafficking and degradation of selected cargo, thereby tuning immune receptor signaling and lysosomal homeostasis (PMID:8661146, PMID:36037365). Its own Golgi-to-lysosome delivery requires three PY motifs that recruit the Nedd4 ubiquitin ligase through WW-domain contacts and a UIM that engages ubiquitinated GGA3, a route that operates independently of LAPTM5 ubiquitination itself (PMID:17116753). Through this lysosomal sorting machinery LAPTM5 drives degradation of intracellular cargo including newly synthesized CD3ζ (PMID:24638062), the E3 ligase WWP2 (PMID:36037365), the deubiquitinase USP10 (PMID:42149696), and HIV-1 envelope glycoproteins, the last restricting macrophage HIV-1 infectivity until antagonized by Vpr acting via DCAF1 (PMID:34140527). In lymphocytes LAPTM5 is a negative regulator of activation: BCR engagement upregulates LAPTM5, which promotes BCR internalization and degrades WWP2 to cause PTEN accumulation and AKT suppression, restraining autoreactive B cells (PMID:36037365), a PTEN/PI3K-AKT-mTOR axis it also engages via USP10 in renal epithelial fibrosis (PMID:42149696). In macrophages LAPTM5 positively sustains proinflammatory NF-κB and MAPK signaling by maintaining RIP1 ubiquitination and limiting A20 (PMID:22733818), and it stabilizes STING by blocking both K48- and K63-linked polyubiquitination (PMID:41087666). LAPTM5 protein abundance is itself set by ubiquitin ligases—ITCH binds its PPxY motif and targets it for proteasomal degradation (PMID:22009753)—and its accumulation can trigger lysosomal membrane permeabilization and cathepsin-dependent, caspase-independent or apoptotic cell death (PMID:19787053, PMID:28464033). Its expression is transcriptionally controlled by activators including RUNX2 (PMID:31545469) and repressors including FOXP3 (PMID:36799186). LAPTM5 additionally preserves lysosomal membrane stability and autophagic flux, in part by competing with LAMP1 for WWP2 binding to block LAMP1 degradation (PMID:40280227).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1996 Medium

    Establishing LAPTM5 as a multispanning lysosomal membrane protein of hematopoietic cells defined the organelle and cell types where it acts.

    Evidence Immunocytology and subcellular fractionation with a specific antibody

    PMID:8661146

    Open questions at the time
    • No molecular function assigned at this stage
    • Trafficking route to lysosome not yet defined
  2. 2006 High

    Defining the trafficking code resolved how LAPTM5 reaches the lysosome, showing it depends on PY-motif recruitment of Nedd4 and UIM binding of ubiquitinated GGA3 rather than on its own ubiquitination.

    Evidence Co-IP, RNAi knockdown of Nedd4/GGA3, and site-directed mutagenesis of PY/UIM motifs with subcellular localization

    PMID:17116753

    Open questions at the time
    • Cargo carried along this route not yet identified
    • Structural basis of UIM-GGA3 recognition not resolved
  3. 2009 Medium

    Linking LAPTM5 accumulation to lysosomal membrane permeabilization established that excess protein is cytotoxic through a non-apoptotic lysosomal death program.

    Evidence LAPTM5 restoration in neuroblastoma cells with autophagic flux and LMP assays

    PMID:19787053

    Open questions at the time
    • Molecular trigger of LMP unknown
    • Relationship to physiological LAPTM5 levels unclear
  4. 2011 Medium

    Identifying ITCH as a ligase for LAPTM5 explained how its abundance is restrained post-translationally and how this controls its cytotoxicity.

    Evidence Co-IP, bidirectional ITCH gain/loss-of-function, ubiquitination and cell death assays

    PMID:22009753

    Open questions at the time
    • Single lab
    • Ubiquitination site on LAPTM5 not mapped in this study
  5. 2012 High

    Genetic dissection placed LAPTM5 as a positive regulator of macrophage proinflammatory signaling acting at the RIP1 ubiquitination/A20 step.

    Evidence LAPTM5-/- macrophages and RAW264.7 knockdown with NF-κB/MAPK and RIP1 ubiquitination readouts

    PMID:22733818

    Open questions at the time
    • Direct biochemical mechanism linking lysosomal LAPTM5 to RIP1/A20 unclear
    • Whether effect requires cargo degradation untested
  6. 2014 Medium

    Showing LAPTM5 degrades intracellular but not surface CD3ζ defined cargo selectivity and separated it from the SLAP/c-Cbl downregulation pathway.

    Evidence Localization kinetics of newly synthesized CD3ζ, Golgi-targeting and ITAM mutants, genetic epistasis

    PMID:24638062

    Open questions at the time
    • Direct LAPTM5-CD3ζ binding interface not defined
    • Single lab
  7. 2021 High

    Demonstrating LAPTM5-mediated lysosomal degradation of HIV-1 envelope glycoproteins identified an antiviral restriction function and its Vpr/DCAF1 antagonism, explaining macrophage-specific Vpr effects.

    Evidence Silencing/reconstitution, Vpr expression, HIV-1 infection and envelope trafficking assays in macrophages and CD4+ T cells

    PMID:34140527

    Open questions at the time
    • Whether envelope is direct LAPTM5 cargo not biochemically resolved
    • Breadth across other enveloped viruses untested
  8. 2022 High

    Mechanistic work in immature B cells defined a dual pathway by which LAPTM5 restrains lymphocyte activation: BCR internalization plus WWP2 degradation leading to PTEN/AKT suppression.

    Evidence BCR stimulation, LAPTM5 overexpression/KO, internalization and phospho-signaling assays, WWP2/PTEN measurement, LAPTM5-/- mice

    PMID:36037365

    Open questions at the time
    • How LAPTM5 selects WWP2 for degradation not detailed
    • Relative contribution of the two arms in vivo unquantified
  9. 2022 Medium

    Identifying hnRNP K/LCDR-mediated stabilization of LAPTM5 mRNA added a post-transcriptional control layer tying LAPTM5 levels to lysosomal stability.

    Evidence RNA-protein binding, knockdown, mRNA stability and LMP assays, rescue in vitro and PDX

    PMID:35091468

    Open questions at the time
    • Direct hnRNP K binding site on LAPTM5 mRNA not mapped
    • Single lab
  10. 2023 Medium

    Multiple studies positioned LAPTM5 within transcriptional circuits, identifying FOXP3 as a direct repressor and Myc as a dual transcriptional/post-transcriptional suppressor.

    Evidence ChIP and dual-luciferase reporter assays (FOXP3); promoter E-box and 3'UTR reporter analysis (Myc/miR-17-3p)

    PMID:36799186 PMID:37713124

    Open questions at the time
    • Myc/miR-17-3p regulation rests on limited methodological detail
    • Tissue specificity of these regulators not integrated
  11. 2025 Medium

    Two studies extended LAPTM5 to ubiquitin-balance control of partner proteins: stabilizing STING by blocking its polyubiquitination, and preserving LAMP1 by competing with WWP2.

    Evidence Co-IP, linkage-specific ubiquitination assays, knockdown with downstream readouts, in vivo rosacea and NSCLC models

    PMID:40280227 PMID:41087666

    Open questions at the time
    • Whether STING stabilization is direct or via cargo trafficking unclear
    • Structural basis of LAPTM5-WWP2-LAMP1 competition unresolved
  12. 2026 Medium

    Further work mapped ubiquitination sites K86/K122 controlling LAPTM5 stability via Ube3c and linked LAPTM5 to autophagy-mediated TBK1 degradation and to USP10/PTEN-driven fibrosis.

    Evidence Site-directed mutagenesis, biotin pulldown/MS/DARTS, autophagic flux and TBK1 assays; co-IP and PTEN rescue in a progeroid model

    PMID:41666511 PMID:42149696

    Open questions at the time
    • Single lab for each finding
    • Integration of ubiquitination-site control with Nedd4/ITCH inputs not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • A unifying biochemical mechanism explaining how one lysosomal trafficking protein can both promote and suppress signaling in a cell-type- and cargo-specific manner remains undefined.
  • No structural model of cargo recognition
  • Rules determining which cargo are degraded vs which partners are stabilized unknown
  • How LAPTM5 mechanistically modulates RIP1/A20 and STING ubiquitination not resolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 4 GO:0060089 molecular transducer activity 2 GO:0005198 structural molecule activity 1
Localization
GO:0005764 lysosome 2 GO:0005794 Golgi apparatus 2 GO:0005768 endosome 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 3 R-HSA-9609507 Protein localization 2 R-HSA-9612973 Autophagy 2
Partners
CD1EGGA3ITCHNEDD4STING1USP10WDFY4WWP2

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 LAPTM5 transport from the Golgi to the lysosome requires binding to the ubiquitin ligase Nedd4 via three PY motifs (L/PPxY) on LAPTM5 interacting with Nedd4 WW domains, and a LAPTM5 UIM motif that binds ubiquitinated GGA3; this trafficking is independent of LAPTM5 ubiquitination itself. Mutation of PY motifs or UIM retains LAPTM5 in the Golgi; Nedd4 or GGA3 knockdown produces the same retention. Co-immunoprecipitation, RNAi knockdown, site-directed mutagenesis of PY/UIM motifs, fluorescence microscopy/subcellular localization The Journal of cell biology High 17116753
1996 LAPTM5 is a pentaspanning (5 transmembrane domain) integral membrane protein that localizes to lysosomes in hematopoietic cells, as determined by immunocytology and cell fractionation with a specific antibody. Immunocytology, subcellular fractionation, antibody-based detection Genomics Medium 8661146
2012 LAPTM5 acts as a positive regulator of proinflammatory signaling in macrophages: LAPTM5-deficient macrophages show reduced NF-κB and MAPK activation downstream of TNF receptor and pattern recognition receptors, reduced RIP1 ubiquitination upon TNF stimulation, and up-regulated A20 (a deubiquitinase that terminates NF-κB by deubiquitinating RIP1). LAPTM5 knockdown in RAW264.7 cells, LAPTM5-/- mouse macrophages, cytokine secretion assays, NF-κB/MAPK pathway activation assays, RIP1 ubiquitination assays The Journal of biological chemistry High 22733818
2014 LAPTM5 promotes lysosomal degradation of intracellular (newly synthesized, Golgi-localizing) CD3ζ but not of cell-surface CD3ζ in the mature TCR complex; this is independent of TCR signaling-triggered tyrosine phosphorylation of CD3ζ. LAPTM5 and the SLAP/c-Cbl pathway operate in genetically distinct pathways to downregulate TCR expression. Subcellular localization kinetics of newly synthesized CD3ζ, Golgi-targeting mutant CD3ζ, CD3ζ YF (ITAM tyrosine-to-phenylalanine) mutant, genetic epistasis with SLAP/c-Cbl Immunology and cell biology Medium 24638062
2009 Accumulation of LAPTM5 protein in neuroblastoma cells induces non-apoptotic, caspase-independent lysosomal cell death characterized by lysosomal membrane permeabilization (LMP), interruption of autophagic flux, and accumulation of autophagic vacuoles, p62/SQSTM1, and ubiquitinated proteins. LAPTM5 restoration/overexpression in NB cells, cell death assays (non-apoptotic), autophagic flux analysis, lysosomal membrane permeabilization assays PloS one Medium 19787053
2011 ITCH (an HECT-type E3 ubiquitin ligase) directly binds the PPxY motif of LAPTM5 via its WW domains and ubiquitinates LAPTM5, leading to its proteasomal degradation; ITCH overexpression degrades LAPTM5 and conversely ITCH knockdown stabilizes LAPTM5 protein. Inhibition of ITCH enhances LAPTM5-mediated cell death in neuroblastoma cells. Co-immunoprecipitation, ITCH overexpression and siRNA knockdown, ubiquitination assays, cell death assays The Journal of biological chemistry Medium 22009753
2021 LAPTM5 restricts HIV-1 infectivity in macrophages by transporting HIV-1 envelope glycoproteins to lysosomes for degradation, thereby reducing virion infectivity. HIV-1 Vpr counteracts this restriction by triggering LAPTM5 degradation via DCAF1. LAPTM5 is highly expressed in macrophages but not CD4+ T cells, explaining the macrophage-specific effect of Vpr; re-expressing LAPTM5 in CD4+ T cells reconstitutes Vpr-dependent enhancement of infection. LAPTM5 silencing/reconstitution, Vpr expression, HIV-1 infection assays in macrophages and CD4+ T cells, envelope glycoprotein trafficking assays, DCAF1-dependent degradation assays Nature communications High 34140527
2022 BCR stimulation up-regulates LAPTM5, which then triggers immature B cell apoptosis via two mechanisms: (1) promoting BCR internalization and reducing SYK and ERK phosphorylation; (2) targeting the E3 ubiquitin ligase WWP2 for lysosomal degradation, causing accumulation of its substrate PTEN, suppressing AKT phosphorylation, increasing FOXO1/p27Kip1/BIM expression. In vivo, LAPTM5 deficiency exacerbates autoreactive B cell survival and autoantibody production. BCR stimulation assays, LAPTM5 overexpression/knockout, BCR internalization assays, phospho-SYK/ERK/AKT measurement, WWP2/PTEN protein level assays, LAPTM5-/- mice Proceedings of the National Academy of Sciences of the United States of America High 36037365
2022 hnRNP K binds to and stabilizes LAPTM5 mRNA, and this is regulated upstream by the lncRNA LCDR; knockdown of hnRNP K destabilizes LAPTM5 transcript, reduces LAPTM5 protein, and promotes lysosomal membrane permeabilization and cell death. LAPTM5 overexpression or cathepsin B inhibition partially rescues LMP induced by LCDR/hnRNP K knockdown. RNA-protein binding assays, siRNA knockdown of hnRNP K and LAPTM5, LAPTM5 mRNA stability assays, lysosomal membrane permeabilization assays, rescue experiments in vitro and in vivo (PDX) Proceedings of the National Academy of Sciences of the United States of America Medium 35091468
2012 LAPTM5 physically associates with CD1e (a lipid antigen presentation protein) in trans-Golgi and late endosomal compartments; the interaction is detectable under physiological conditions and is enhanced when lysosomal acidification is blocked by bafilomycin. However, LAPTM5 does not control CD1e ubiquitination or the generation of soluble lysosomal CD1e. Co-immunoprecipitation, co-localization by fluorescence microscopy, bafilomycin treatment PloS one Medium 22880058
2017 Ectopic overexpression of LAPTM5 in HeLa cells causes lysosomal targeting of LAPTM5, down-regulation of Mcl-1 and Bid, Bak activation, mitochondrial membrane potential loss, and caspase-9/-8/-3-dependent apoptosis; cathepsin inhibition (but not pan-caspase inhibition) blocks LAPTM5-induced mitochondrial depolarization, indicating a cathepsin-dependent lysosomal pathway upstream of mitochondria. GFP-LAPTM5 overexpression in HeLa cells, flow cytometry (apoptosis, ΔΨm), caspase activity assays, cathepsin inhibitor and pan-caspase inhibitor rescue experiments, Mcl-1 co-overexpression rescue PloS one Medium 28464033
2019 RUNX2 directly transactivates the LAPTM5 gene by binding the LAPTM5 promoter at position -1176 to -1171 (confirmed by ChIP and dual-luciferase reporter assay). LAPTM5 in turn is involved in trafficking of RANKL: LAPTM5 knockdown increases RANKL protein in cytoplasm and culture media and enhances osteoclastic differentiation of co-cultured cells. ChIP, dual-luciferase reporter assay, RUNX2 overexpression/silencing, LAPTM5 knockdown, RANKL ELISA/quantification, osteoclast differentiation co-culture assay Molecular medicine reports Medium 31545469
2020 LAPTM5 suppresses CD40-mediated NF-κB activation in glioblastoma cells; LAPTM5 knockdown unleashes CD40-driven NF-κB signaling, increasing invasiveness, clonogenicity, and temozolomide resistance, all of which are reversed by NF-κB inhibition. LAPTM5 knockdown in glioma cell lines, expression array, NF-κB inhibition rescue, invasion/clonogenicity/chemosensitivity assays in vitro and in vivo Frontiers in oncology Medium 32582531
2025 LAPTM5 competes with LAMP1 for binding to the E3 ubiquitin ligase WWP2, thereby inhibiting LAMP1 ubiquitination and degradation, preserving lysosomal membrane stability and autophagic flux, and conferring cisplatin resistance in NSCLC. LAPTM5 knockdown increases lysosomal membrane permeability, releases cathepsin D, elevates ROS, and accelerates cell death. Co-immunoprecipitation (LAPTM5-WWP2-LAMP1 interactions), LAPTM5 knockdown, lysosomal membrane permeability assays, cathepsin D release, ROS measurement, cell viability assays Cellular signalling Medium 40280227
2025 LAPTM5 associates with STING and represses both K48- and K63-linked polyubiquitination of STING, preventing its proteasomal and lysosomal degradation and thereby stabilizing STING protein levels; LAPTM5 knockdown reduces STING protein, its downstream signaling (including inflammatory responses), and alleviates LL-37-induced rosacea-like phenotypes in mice. Co-immunoprecipitation (LAPTM5-STING), LAPTM5 knockdown in macrophages, ubiquitination assays (K48/K63-linkage specific), STING protein stability assays, in vivo LL-37 rosacea model Communications biology Medium 41087666
2026 Ginkgetin (GK) inhibits K48-linked ubiquitination of Laptm5 at sites K86 and K122 (identified by site mutation assays) by targeting Ube3c (identified by biotin pulldown and DARTS), stabilizing Laptm5 protein. Increased Laptm5 promotes autophagosome-lysosome fusion and autophagy-mediated degradation of TBK1, reducing downstream inflammatory signaling in macrophages. Co-immunoprecipitation, site mutation of Laptm5 (K86, K122), biotin pulldown with mass spectrometry, DARTS, ubiquitination assays, autophagic flux assays, TBK1 degradation assays Phytomedicine Medium 41666511
2026 LAPTM5 promotes renal tubular epithelial cell EMT and fibrosis by interacting with USP10 and facilitating its lysosomal degradation, thereby reducing PTEN levels and relieving PTEN-mediated inhibition of the PI3K/AKT/mTOR-autophagy pathway. PTEN overexpression rescues LAPTM5-induced EMT. Co-immunoprecipitation (LAPTM5-USP10), LAPTM5 overexpression, PTEN rescue experiments, D-galactose progeroid mouse model, Western blot for pathway components FASEB journal Medium 42149696
2023 c-Myc transcriptionally represses LAPTM5 by binding to two E-boxes in the LAPTM5 promoter. Additionally, Myc transactivates miR-17-3p, which binds 11 sites in the LAPTM5 3'UTR to inhibit LAPTM5 protein synthesis, providing a dual transcriptional and post-transcriptional suppression mechanism. Promoter binding assays (E-box mutagenesis implied), miRNA-target site analysis with 3'UTR reporter, B-lymphoma growth assays with CDS vs CDS+3'UTR constructs Annals of hematology Low 37713124
2023 FOXP3 directly binds the LAPTM5 promoter and negatively regulates LAPTM5 expression, as confirmed by dual-luciferase reporter and chromatin immunoprecipitation assays. LAPTM5 promotes breast cancer malignant phenotypes (proliferation, migration, invasion, EMT) partly through activation of the Wnt/β-catenin signaling pathway. ChIP, dual-luciferase reporter assay, LAPTM5 overexpression/knockdown, Wnt/β-catenin pathway analysis, xenograft tumor assay Oncology reports Medium 36799186
2025 WDFY4 interacts with LAPTM5 (validated by co-immunoprecipitation and immunofluorescence co-localization), and WDFY4 knockdown inhibits LAPTM5 expression; elevated LAPTM5 activates the downstream CDC42/mTOR/4EBP1/SLC7A11 pathway, promoting ferroptosis and inflammation in endothelial cells. LAPTM5 overexpression rescues the anti-ferroptotic effect of WDFY4 knockdown. Co-immunoprecipitation, immunofluorescence co-localization, WDFY4 knockdown, LAPTM5 overexpression rescue, pathway analysis (CDC42/mTOR/4EBP1/SLC7A11), in vivo ApoE-/- mouse model Journal of cellular and molecular medicine Low 40755163
2023 ZKSCAN5 and SETD7 both bind the LAPTM5 promoter and form a complex; ZKSCAN5 recruits SETD7 to promote LAPTM5 transcription in pancreatic ductal adenocarcinoma cells. LAPTM5 knockdown reverses the pro-metastatic effect of ZKSCAN5 overexpression. ChIP (ZKSCAN5 and SETD7 binding to LAPTM5 promoter), co-immunoprecipitation (ZKSCAN5-SETD7 complex), LAPTM5 knockdown rescue of ZKSCAN5-driven metastasis, in vivo liver metastasis model Histology and histopathology Low 38018874
2026 In AML, LAPTM5 promotes autophagic flux by upregulating LAMP1 and LAMP2 expression, facilitating autophagolysosome formation; LAPTM5 knockdown impairs lysosomal biogenesis and disrupts autophagolysosome formation, sensitizing resistant AML cells to cytarabine. LAPTM5 knockdown, autophagic flux assays, LAMP1/LAMP2 expression analysis, in vivo tumor growth assays with cytarabine combination Cell death & disease Low 41912486

Source papers

Stage 0 corpus · 39 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 Transport of LAPTM5 to lysosomes requires association with the ubiquitin ligase Nedd4, but not LAPTM5 ubiquitination. The Journal of cell biology 87 17116753
1996 LAPTM5: a novel lysosomal-associated multispanning membrane protein preferentially expressed in hematopoietic cells. Genomics 81 8661146
2022 Genome-Scale CRISPR screen identifies LAPTM5 driving lenvatinib resistance in hepatocellular carcinoma. Autophagy 80 36037300
2012 LAPTM5 protein is a positive regulator of proinflammatory signaling pathways in macrophages. The Journal of biological chemistry 80 22733818
2022 LCDR regulates the integrity of lysosomal membrane by hnRNP K-stabilized LAPTM5 transcript and promotes cell survival. Proceedings of the National Academy of Sciences of the United States of America 48 35091468
2009 Lysosomal-associated protein multispanning transmembrane 5 gene (LAPTM5) is associated with spontaneous regression of neuroblastomas. PloS one 48 19787053
2016 Downregulation of LAPTM5 suppresses cell proliferation and viability inducing cell cycle arrest at G0/G1 phase of bladder cancer cells. International journal of oncology 39 27922670
2021 Vpr counteracts the restriction of LAPTM5 to promote HIV-1 infection in macrophages. Nature communications 36 34140527
2022 LAPTM5 mediates immature B cell apoptosis and B cell tolerance by regulating the WWP2-PTEN-AKT pathway. Proceedings of the National Academy of Sciences of the United States of America 29 36037365
2003 Stage-specific expression of Clast6/E3/LAPTM5 during B cell differentiation: elevated expression in human B lymphomas. International journal of oncology 27 12527926
2003 Inactivation of the E3/LAPTm5 gene by chromosomal rearrangement and DNA methylation in human multiple myeloma. Leukemia 26 12886255
2016 Down-regulation of LAPTM5 in human cancer cells. Oncotarget 23 27058622
2014 LAPTM5 promotes lysosomal degradation of intracellular CD3ζ but not of cell surface CD3ζ. Immunology and cell biology 23 24638062
2011 HECT-type ubiquitin ligase ITCH targets lysosomal-associated protein multispanning transmembrane 5 (LAPTM5) and prevents LAPTM5-mediated cell death. The Journal of biological chemistry 21 22009753
2020 LAPTM5-CD40 Crosstalk in Glioblastoma Invasion and Temozolomide Resistance. Frontiers in oncology 18 32582531
2024 The function and mechanism of LAPTM5 in diseases. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 13 39096616
2017 Ectopic overexpression of LAPTM5 results in lysosomal targeting and induces Mcl-1 down-regulation, Bak activation, and mitochondria-dependent apoptosis in human HeLa cells. PloS one 13 28464033
2022 Levofloxacin exerts broad-spectrum anticancer activity via regulation of THBS1, LAPTM5, SRD5A3, MFAP5 and P4HA1. Anti-cancer drugs 10 34419964
2022 Spine‑specific downregulation of LAPTM5 expression promotes the progression and spinal metastasis of estrogen receptor‑positive breast cancer by activating glutamine‑dependent mTOR signaling. International journal of oncology 10 35294039
2019 LAPTM5 is transactivated by RUNX2 and involved in RANKL trafficking in osteoblastic cells. Molecular medicine reports 10 31545469
2023 LAPTM5 regulated by FOXP3 promotes the malignant phenotypes of breast cancer through activating the Wnt/β‑catenin pathway. Oncology reports 9 36799186
2012 Lysosomal-associated transmembrane protein 5 (LAPTM5) is a molecular partner of CD1e. PloS one 8 22880058
2015 Expression and Polymorphisms of Lysosome-Associated Protein Transmembrane 5 (LAPTM5) in Patients with Systemic Lupus Erythematosus in a Chinese Population. Biochemical genetics 7 25998573
2025 LAPTM5 Confers the Resistance to Venetoclax via Promoting the Autophagosome-Lysosome Fusion in Multiple Myeloma. Journal of cellular and molecular medicine 5 39753521
2025 LAPTM5 confers cisplatin resistance in NSCLC by suppressing LAMP1 ubiquitination to stabilize lysosomal membranes and sustain autophagic flux. Cellular signalling 5 40280227
2023 c-Myc inhibits LAPTM5 expression in B-cell lymphomas. Annals of hematology 5 37713124
2022 Expression of RUNX2/LAPTM5 in the Induction of MC3T3-e1 Mineralization and Its Possible Relationship with Autophagy. Tissue engineering and regenerative medicine 5 36121636
2021 [Expression of RUNX2/LAPTM5 in MC3T3-E1 osteoblastic cells with induced mineralization]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University 4 34658355
2025 LINC02888 promotes HGSOC progression and immune evasion via PPIB-mediated stabilization of LAPTM5 mRNA and inhibition of RIG-I-like receptor signaling. Journal of translational medicine 3 40495222
2023 ZKSCAN5 activates LAPTM5 expression by recruiting SETD7 to promote metastasis in pancreatic ductal adenocarcinoma. Histology and histopathology 3 38018874
2025 WDFY4 Promotes the Progression of Atherosclerosis by Regulating Ferroptosis Mediated by the LAPTM5/CDC42/mTOR/4EBP1/SLC7A11 Pathway. Journal of cellular and molecular medicine 2 40755163
2025 COL6A1, LAPTM5, and ZFAND2A as Crucial Biomolecules Driving Immunoregulation in Human Nucleus Pulposus Degeneration. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2 41124083
2026 Ginkgetin alleviates sepsis-induced acute lung injury by promoting autophagy via inhibiting ubiquitination of Laptm5 in macrophages. Phytomedicine : international journal of phytotherapy and phytopharmacology 1 41666511
2025 LAPTM5 exacerbates STING-mediated inflammation induced by LL-37 through stabilizing STING in rosacea. Communications biology 1 41087666
2026 LAPTM5 potentiates airway remodeling by regulating MAPKs-mediated airway smooth muscle cells' dysfunction. Mammalian genome : official journal of the International Mammalian Genome Society 0 41699322
2026 Targeting LAPTM5 enhances AML sensitivity to cytarabine through autophagy inhibition. Cell death & disease 0 41912486
2026 LAPTM5-dependent lipophagy enhances ferroptosis sensitivity in glioma cells. Translational cancer research 0 41969478
2026 LAPTM5 Promotes Age-Related Renal Fibrosis via USP10/PTEN-Mediated Autophagy Inhibition. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 0 42149696
2025 LAPTM5 drives omental metastasis in high-grade serous ovarian cancer via TGF-β/Smad-mediated epithelial plasticity. Journal of translational medicine 0 41462255

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