Affinage

LAMA5

Laminin subunit alpha-5 · UniProt O15230

Length
3695 aa
Mass
399.7 kDa
Annotated
2026-06-10
33 papers in source corpus 19 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

LAMA5 encodes laminin α5, a secreted basement-membrane glycoprotein that assembles with laminin β1 and γ1 chains into laminin-511/521 heterotrimers and acts as a master regulator of cell adhesion, proliferation, polarity, and morphogenesis across epithelial, vascular, neuromuscular, and skeletal tissues (PMID:34774562, PMID:35419533, PMID:21915268). A recurrent theme is that laminin α5 transduces basement-membrane attachment into intracellular signaling that balances WNT and PI3K/AKT outputs: it restrains canonical Wnt while activating PI3K/Akt in intestinal cells (PMID:22666383), and its loss disrupts β1 integrin signaling through the kinases PYK2 and FYN, destabilizes vinculin localization and the actin cytoskeleton, and impairs WNT signaling to produce a bent-bone skeletal dysplasia (PMID:33242826); WNT-dependent control of laminin α5 levels in turn governs branching morphogenesis and chondrogenesis (PMID:33629734). Laminin α5 supports tissue integrity through receptor partners including SV2A at the neuromuscular junction, where a binding-disrupting variant causes presynaptic transmission failure (PMID:28544784, PMID:29377152), and integrin α6b, with which it acts redundantly or in a shared pathway to maintain collective migration and apicobasal polarity. In disease, pathogenic LAMA5 variants impair heterotrimer assembly or secretion and cause nephrotic syndrome and FSGS-like glomerulopathy with reduced laminin α5 and increased glomerular vinculin (PMID:34774562, PMID:35419533, PMID:36173685). In cancer, laminin α5 mediates KRAS-mutant tumor-cell adhesion to endothelium via BCAM (PMID:27143691), drives hepatic metastasis and tumor angiogenesis downstream of TNFα/NFκB (PMID:31064120), and promotes proliferation and migration through integrin α4/STAT3 signaling, with MAZ acting as a transcriptional activator of LAMA5 (PMID:38154529, PMID:40072648). Beyond intact trimers, MMP1 cleaves laminin α5 into fragments that drive VEGF-independent angiogenesis via integrin αvβ3 (PMID:27324842), and its transcription is also activated by glucocorticoid receptor in stress-induced cardiomyocyte hypertrophy (PMID:40642838).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2011 Medium

    Established that human laminin α5 incorporates into basement membranes of multiple organs in vivo and that kidney enforces a feedback control on laminin α5 abundance.

    Evidence BAC transgenic mice with human LAMA5; immunoelectron microscopy and quantitative mRNA analysis

    PMID:21915268

    Open questions at the time
    • Molecular basis of the proposed kidney expression-monitoring/feedback mechanism unidentified
    • Did not resolve which receptors mediate deposition into specific basement membranes
  2. 2012 Medium

    Connected laminin α5 to interconnected intracellular signaling by showing it suppresses Wnt while activating PI3K, framing it as a signaling hub rather than a passive structural protein.

    Evidence Lama5 knockout mouse intestinal RNA profiling plus in vitro knockdown and pathway modulation

    PMID:22666383

    Open questions at the time
    • Receptor linking laminin α5 to Wnt/PI3K crosstalk not defined
    • Direct versus indirect contribution to each pathway not separated
  3. 2016 Medium

    Defined two distinct extracellular activities of laminin α5 in cancer: a BCAM-dependent adhesion substrate for tumor-endothelial attachment, and an MMP1-generated fragment that drives angiogenesis through integrin αvβ3.

    Evidence Adhesion assays with genetic/biochemical inhibition of BCAM and LAMA5; MMP1 knockdown/secretome with endothelial angiogenesis and integrin αvβ3 antibody blockade

    PMID:27143691 PMID:27324842

    Open questions at the time
    • Cleavage site mapping of MMP1 fragments incomplete
    • In vivo relevance of BCAM/LAMA5 adhesion in metastasis not directly tested
  4. 2017 Medium

    Linked LAMA5 variants to human disease through two mechanisms: an SV2A-binding-disrupting variant causing presynaptic neuromuscular failure, and a cleavage-altering variant perturbing epithelial-mesenchymal SHH/GLI signaling.

    Evidence WES/RNAseq of affected families; patient-derived cell expression; neuronal adhesion and endplate electrophysiology; knock-in mouse generation

    PMID:28544784 PMID:28735299

    Open questions at the time
    • Structural basis of laminin α5–SV2A interaction unresolved
    • Mechanism connecting LAMA5 cleavage to SHH/GLI1 upregulation not dissected
  5. 2018 Medium

    Replicated and extended the SV2A-binding deficit at the neuromuscular junction and placed laminin α5 upstream of endothelial PI3K-AKT-mTOR signaling.

    Evidence Repeat neuronal culture binding/adhesion and endplate EM/electrophysiology; HUVEC siRNA knockdown with p-AKT/p-mTOR immunoblotting and tube formation

    PMID:29377152 PMID:30200802

    Open questions at the time
    • Endothelial pathway assignment rests on protein-level changes without epistasis
    • How laminin α5 engages the PI3K axis (which receptor) untested
  6. 2019 Medium

    Showed LAMA5 is an inducible, microenvironment-regulated gene in metastasis, induced by myeloid-derived TNFα/NFκB signaling and required for hepatic metastatic growth and tumor vascularization.

    Evidence shRNA knockdown in cancer cells; orthotopic hepatic metastasis model; conditioned-medium and Notch gene expression analysis

    PMID:31064120

    Open questions at the time
    • Direct NFκB binding to LAMA5 regulatory regions not shown
    • Mechanism of Notch modulation in metastatic endothelia unresolved
  7. 2020 Medium

    Resolved the intracellular signaling complex through which laminin α5 loss acts, defining a β1 integrin–PYK2–FYN–vinculin–actin–WNT axis underlying a skeletal dysplasia.

    Evidence Exome sequencing of patients; western blot, IHC, WNT luciferase, and migration/wound-healing assays on patient-derived material

    PMID:33242826

    Open questions at the time
    • Direct biochemical chain from integrin engagement to PYK2/FYN activation not reconstituted
    • Tissue specificity of the bent-bone phenotype unexplained
  8. 2021 Medium

    Established the structural disease mechanism in kidney by showing that LAMA5 variants reduce protein levels and heterotrimer assembly (or retain trimer formation despite truncation), causing nephrotic syndrome, and connected WNT to control of Lama5 in branching morphogenesis.

    Evidence In vitro heterotrimer assembly assays; knock-in mouse nephrotic models with proteomics/ultrastructure; embryonic SMG organ culture with Wnt/FGF manipulation

    PMID:33629734 PMID:34774562 PMID:35419533

    Open questions at the time
    • Why truncated trimer-competent laminin α5 still causes disease unresolved
    • Genetic background modifiers of nephrotic progression unmapped
  9. 2022 Medium

    Linked a glomerulopathy variant to defective LG4-5 domain secretion and impaired cell adhesion (increased glomerular vinculin), reinforcing adhesion failure as a unifying disease mechanism.

    Evidence In vitro LG4-5 secretion assay; heterozygous/homozygous knockin mice with IHC; WES

    PMID:36173685

    Open questions at the time
    • Cell-type dependence of secretion defect mechanistically unexplained
    • Causal link between vinculin elevation and FSGS not directly demonstrated
  10. 2023 Medium

    Defined laminin α5 as a stromal driver of tumor cell-state transitions, acting through integrin α4/STAT3 to drive acinar-to-ductal metaplasia and upstream of Notch-mediated EMT in ovarian cancer.

    Evidence CAF coculture organoid/explant models with LAMA5/ITGA4 depletion; proteomic-transcriptomic integration; ovarian cancer shRNA knockdown with EMT/Notch marker analysis and xenografts

    PMID:37527216 PMID:38154529

    Open questions at the time
    • Ovarian Notch placement is marker-based without mechanistic dissection
    • Whether integrin α4/STAT3 axis operates in non-pancreatic contexts untested
  11. 2023 Medium

    Extended SHH/GLI1 control of palatogenesis, showing laminin α5 silencing reduces proliferation and increases apoptosis via the SHH/GLI1 axis to cause cleft palate, distinct from an EMT mechanism.

    Evidence LAMA5-shRNA adenovirus in embryonic mouse palatal organ culture; PCR, western blot, fusion imaging with EMT-marker negative controls

    PMID:37390938

    Open questions at the time
    • How laminin α5 signals to SHH/GLI1 not defined
    • Receptor mediating the proliferation/apoptosis response unidentified
  12. 2025 Medium

    Identified transcriptional activators of LAMA5 (MAZ in gastric cancer via STAT3; glucocorticoid receptor in stress cardiomyocyte hypertrophy), tying laminin α5 induction to defined upstream transcription factors and downstream effectors.

    Evidence ChIP and luciferase for MAZ promoter binding plus STAT3-activator rescue and tumor models; animal stress models with GR manipulation in vivo and in vitro

    PMID:40072648 PMID:40642838

    Open questions at the time
    • Whether MAZ/GR regulation of LAMA5 generalizes across tissues unknown
    • Direct GR-LAMA5 promoter occupancy versus indirect activation not fully separated
  13. 2025 Medium

    Genetic dissection in zebrafish and mice clarified laminin α5–integrin α6b relationships and vascular zonation: redundancy with itga6b in collective migration, a shared pathway maintaining epithelial polarity, and a laminin α4/α5 ratio controlling cerebrovascular functional identity.

    Evidence Zebrafish single and lama5/itga6b double mutants with live imaging and polarity markers; endothelial-specific and global mouse KO with scRNA-seq and functional validation (preprints)

    Open questions at the time
    • Preprints not yet peer-reviewed
    • Molecular signal distinguishing redundant versus same-pathway integrin α6b interactions unresolved
    • How laminin α4/α5 ratio is sensed by endothelium unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how a single basement-membrane laminin reconciles its opposing regulatory outputs (WNT suppression versus PI3K/STAT3 activation) across tissues, and what receptor logic selects between adhesion, proliferation, and polarity programs in each context.
  • No unified receptor-to-pathway map across tissues
  • Structural basis of SV2A and BCAM binding unsolved
  • Direct in vivo reconstitution of the integrin-PYK2-FYN-vinculin module lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 3 GO:0060089 molecular transducer activity 3 GO:0098631 cell adhesion mediator activity 3
Localization
GO:0005576 extracellular region 3 GO:0031012 extracellular matrix 2
Pathway
R-HSA-1643685 Disease 5 R-HSA-162582 Signal Transduction 4 R-HSA-1266738 Developmental Biology 3 R-HSA-1474244 Extracellular matrix organization 3
Partners
BCAMFYNITGA4ITGA6ITGAVITGB1PYK2SV2A
Complex memberships
laminin-511/521 heterotrimer (laminin α5/β1/γ1)

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2016 LAMA5 (laminin α5) acts as a substrate for BCAM (basal cell adhesion molecule) on endothelial cells, and the BCAM/LAMA5 interaction mediates adhesion of KRAS-mutant colorectal cancer cells specifically to endothelial cells (but not pericytes or hepatocytes); genetic suppression or biochemical inhibition of either BCAM or LAMA5 impaired this adhesion. Adhesion assays with genetic suppression (siRNA/shRNA) and biochemical inhibition of BCAM and LAMA5; immunohistochemistry validation in preclinical models and human specimens; phage display screen Clinical Cancer Research Medium 27143691
2016 MMP1 cleaves LAMA5 to generate internal and C-terminal proteolytic fragments that are secreted by oncogenically transformed (H-Ras) epithelial cells; these fragments promote endothelial cell angiogenesis (vessel length and branching) in a VEGF-independent manner via integrin αvβ3 on endothelial cells. In vitro MMP1 knockdown/secretome analysis; endothelial angiogenesis assays; antibody-based integrin αvβ3 inhibition; in vivo xenograft tumor growth assay Scientific Reports Medium 27324842
2012 Laminin α5 (encoded by Lama5) inhibits Wnt signaling and activates PI3K signaling in intestinal epithelial and mesenchymal cells; loss of Lama5 in mice causes conflicting Wnt/PI3K signals, altering cell adhesion, migration, and differentiation, establishing laminin-511 as a regulator of interconnected PI3K/Akt and Wnt pathways. RNA profiling of lama5 knockout mouse embryonic intestinal tissue; cell culture knockdown experiments; epistasis via signaling pathway modulation PLoS One Medium 22666383
2017 The LAMA5 missense mutation p.V3140M alters the amount of LAMA5 peptides derived from protein cleavage, perturbs epithelial-mesenchymal signaling, causes upregulation of Sonic Hedgehog and GLI1, and strongly inhibits ECM proteins COL1A1, MMP1, and MMP3 in cells from affected individuals; skin biopsies showed alteration of dermal papilla with reduction of germinative layer. WES and RNAseq of affected human family; expression studies in patient-derived cells; skin biopsy histology; knock-in mouse model generation Journal of Medical Genetics Medium 28735299
2017 The LAMA5 variant p.Arg2659Trp causes decreased binding of laminin α5 to SV2A (synaptic vesicle glycoprotein 2A) and impairs laminin-521 cell adhesion and cell projection support in primary neuronal cultures, resulting in presynaptic failure with reduced endplate potential quantal content and denuded nerve terminals. Expression studies in primary neuronal cultures; cell adhesion assays; electrophysiological endplate studies; electron microscopy; repetitive nerve stimulation American Journal of Medical Genetics Part A Medium 28544784
2018 The LAMA5 variant p.Arg2659Trp causes decreased binding of laminin α5 to SV2A and impairs laminin-521 cell adhesion and cell projection support in primary neuronal cultures, contributing to presynaptic neuromuscular transmission failure; endplates showed normal postsynaptic folding but denuded or partially occupied nerve terminals. Expression studies; cell adhesion and projection assays in primary neuronal cultures; endplate electrophysiology; electron microscopy Annals of the New York Academy of Sciences Medium 29377152
2019 LAMA5 expression in colorectal cancer cells is induced by TNFα/NFκB pathway signaling activated by tumour-derived CD11b+ myeloid cell-conditioned medium; shRNA-mediated downregulation of LAMA5 in cancer cells impaired hepatic metastatic growth, reduced intratumoural vessel branching, and increased Notch pathway gene expression in metastasis-derived endothelia. shRNA knockdown in cancer cells; orthotopic hepatic metastasis mouse model; qPCR with human-specific primers; Notch pathway gene expression analysis; conditioned medium experiments with TNFα/NFκB pathway Cancers Medium 31064120
2020 Biallelic loss-of-function mutations in LAMA5 disrupt a focal adhesion signaling complex: loss of LAMA5 alters β1 integrin signaling through non-canonical kinase PYK2 and skeletal-enriched SRC kinase FYN, negatively impacts the actin cytoskeleton, disrupts vinculin localization, and impairs WNT signaling in cartilage, producing a bent bone skeletal dysplasia. Exome sequencing; Sanger sequencing; qPCR; western blot; immunohistochemistry; luciferase assay for WNT signaling; migration and wound healing assays EBioMedicine Medium 33242826
2021 A missense mutation (E884G) in the L4a domain of LAMA5 reduces LAMA5 protein levels in vivo and significantly reduces assembly of the laminin 521 heterotrimer in vitro; homozygous mice develop nephrotic syndrome with proteinuria and glomerular changes; genetic background modifies disease progression. In vitro heterotrimer assembly assay; mouse knockin model; proteomic analysis of glomerular extracellular fraction; histology; ultrastructure analysis Kidney International Medium 34774562
2021 Canonical Wnt/β-catenin signaling negatively regulates submandibular gland branching morphogenesis through regulation of Lama5 levels; FGF signaling acts upstream as a negative regulator of Wnt, whose effect is partially reversed by Wnt3a; inhibition of Wnt promotes branching while overactivation suppresses it via Lama5. Embryonic mouse SMG organ culture; branching morphogenesis assay; gene expression analysis; pharmacological manipulation of Wnt and FGF pathways The International Journal of Developmental Biology Medium 33629734
2021 LAMA5 biallelic truncating variants produce smaller laminin α5 proteins that nevertheless form trimers with laminin β1 and γ1 chains, demonstrating that truncated LAMA5 retains heterotrimer formation capacity but causes infantile nephrotic syndrome in patients. In vitro heterotrimer formation assays; targeted next-generation sequencing; clinical characterization Kidney360 Medium 35419533
2022 A heterozygous LAMA5 variant (p.Val3687Met) causes cell-type-dependent changes in secretion of variant laminin α5 LG4-5 domain; heterozygous and homozygous knockin mice develop FSGS-like pathology with reduced laminin α5 and increased glomerular vinculin levels, suggesting impaired cell adhesion underlies the glomerulopathy. In vitro secretion assay of LG4-5 domain; heterozygous and homozygous knockin mouse model; immunohistochemistry; whole-exome sequencing JCI Insight Medium 36173685
2023 CAF-secreted LAMA5 activates integrin α4/STAT3 signaling axis in acinar cells to drive acinar-to-ductal metaplasia (ADM); depletion of LAMA5 or ITGA4 in acinar cells abolishes CAF-mediated transdifferentiation. Proteomic (LC-MS/MS) and transcriptomic (RNA-seq) data integration; confocal microscopy; immunoblotting; qRT-PCR; acinar cell organoids, explants, and CAF cocultures; mCAF coculture models Gastroenterology Medium 38154529
2023 LAMA5 knockdown in ovarian cancer cell lines inhibits cell proliferation, migration, and invasion in vitro and in vivo, and reduces expression of EMT markers and Notch signaling pathway-related markers, placing LAMA5 upstream of Notch-mediated EMT. Lentiviral shRNA knockdown; in vitro proliferation, migration, invasion assays; in vivo tumor xenograft; IHC; western blot for EMT and Notch markers FASEB Journal Low 37527216
2018 LAMA5 knockdown in HUVECs or hypoxia/reoxygenation reduces HUVEC proliferation, migration, and vascular formation, and downregulates PI3K downstream targets p-AKT and p-mTOR, placing LAMA5 upstream of PI3K-AKT-mTOR signaling in endothelial cells. siRNA knockdown; CCK-8 proliferation assay; transwell migration assay; tube formation assay; western blot for p-AKT and p-mTOR The Journal of Maternal-Fetal & Neonatal Medicine Low 30200802
2011 Human laminin α5 expressed transgenically in mice deposits into basement membranes of heart, liver, spleen, and kidney; high-level transgenic human LAMA5 expression suppresses endogenous mouse Lama5 mRNA and laminin α5 protein in kidney, suggesting a laminin expression monitoring/feedback mechanism in kidney. Transgenic mouse (BAC-based human LAMA5 locus); immunoelectron microscopy; quantitative mRNA analysis; immunofluorescence PLoS One Medium 21915268
2023 LAMA5 silencing in the palatal process inhibits proliferation (reduced ki67, cyclin D1) and promotes apoptosis (increased caspase 3) in mouse palatal cells via the SHH/GLI1 axis (reduced gli1), causing failure of palate fusion; E-cadherin, vimentin, Shh, and ptch1 were not significantly changed, indicating the mechanism is proliferation/apoptosis rather than EMT. LAMA5-shRNA adenovirus transfection into embryonic mouse palatal process in vitro organ culture; PCR; western blot; fluorescence microscopy for fusion assessment Biomedical Journal Medium 37390938
2025 MAZ transcription factor binds the LAMA5 promoter to activate its transcription; LAMA5 promotes gastric cancer cell proliferation and migration through STAT3 signaling; Colivelin (STAT3 activator) reverses the anti-tumor effects of LAMA5 knockdown. ChIP assay; luciferase reporter assay; siRNA knockdown of LAMA5 and MAZ; CCK-8, colony formation, EdU, wound healing, Transwell assays; in vivo tumor model Functional & Integrative Genomics Medium 40072648
2025 Corticosterone activates glucocorticoid receptor (GR), which directly targets and activates the Lama5 gene; the corticosterone-GR-LAMA5 axis mediates chronic psychological stress-induced cardiomyocyte hypertrophy in vivo and in vitro. Animal stress models; in vitro corticosterone treatment; GR manipulation; in vivo and in vitro confirmation of GR-Lama5 regulatory axis; multiple independent animal experiment batches Advanced Science Medium 40642838
2025 CRISPR/Cas9 knockout of LAMA5 in urine-derived stem cells impairs chondrogenesis and disrupts cell–cell junction programs; loss of LAMA5 attenuates canonical WNT signaling (reduced WNT7A expression); pharmacological WNT activation with LiCl partially restores WNT7A, FLI1, TFAP2A, GRHL2, and PITX1 expression toward wild-type levels. CRISPR/Cas9 KO; 2D and 3D chondrogenic differentiation; bulk RNA sequencing; WGCNA; pharmacological WNT activation (LiCl); qPCR bioRxivpreprint Medium
2025 In zebrafish, laminin α5 (lama5) is a key basement membrane component underlying the migrating posterior lateral line primordium; loss of lama5 alone compromises basement membrane integrity without blocking migration, but simultaneous depletion of lama5 and integrin α6b (itga6b) markedly decreases migration velocity and ultimately blocks collective migration, indicating functional redundancy between these adhesion components. Zebrafish loss-of-function genetics; live imaging of pLLP migration; combinatorial lama5/itga6b double mutant analysis bioRxivpreprint Medium
2025 In zebrafish epidermis, loss of laminin α5 reduces E-cadherin localization and increases cell spreading with dynamic cell boundaries and increased cell proliferation (mesenchymal traits); this phenotype is recapitulated by integrin α6b mutation and is not exacerbated in the double mutant, indicating that laminin α5 and integrin α6b function in the same pathway to maintain epithelial apicobasal polarity. Zebrafish lama5 and itga6b loss-of-function mutants; immunofluorescence for E-cadherin, aPKC, Lgl; double mutant epistasis analysis bioRxivpreprint Low
2025 Endothelial-specific loss of laminin α5 (Tek-cre:Lama5-/-) in mice alters cerebrovascular transcriptional identity; compensatory upregulation of laminin α5 in Lama4-/- vessels enhances expression of junctional proteins (Ocln, Cldn5) and promotes vessel contractility, demonstrating that the laminin α4/α5 ratio in vascular basement membranes regulates functional zonation between arterioles, capillaries, and postcapillary venules. Single-cell RNA sequencing of cerebral blood vessels from Lama4-/-, Tek-cre:Lama5-/-, and wild-type mice; in vitro and in vivo functional studies; immunohistochemistry bioRxivpreprint Medium

Source papers

Stage 0 corpus · 33 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2019 Tumour-Derived Laminin α5 (LAMA5) Promotes Colorectal Liver Metastasis Growth, Branching Angiogenesis and Notch Pathway Inhibition. Cancers 70 31064120
2016 BCAM and LAMA5 Mediate the Recognition between Tumor Cells and the Endothelium in the Metastatic Spreading of KRAS-Mutant Colorectal Cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 59 27143691
2017 Identification of the first dominant mutation of LAMA5 gene causing a complex multisystem syndrome due to dysfunction of the extracellular matrix. Journal of medical genetics 39 28735299
2018 COL4A5 and LAMA5 variants co-inherited in familial hematuria: digenic inheritance or genetic modifier effect? BMC nephrology 37 29764427
2023 Cancer-Associated Fibroblast Induces Acinar-to-Ductal Cell Transdifferentiation and Pancreatic Cancer Initiation Via LAMA5/ITGA4 Axis. Gastroenterology 33 38154529
2017 Presynaptic congenital myasthenic syndrome with a homozygous sequence variant in LAMA5 combines myopia, facial tics, and failure of neuromuscular transmission. American journal of medical genetics. Part A 31 28544784
2023 LAMA5 promotes cell proliferation and migration in ovarian cancer by activating Notch signaling pathway. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 28 37527216
2016 Transformed MDCK cells secrete elevated MMP1 that generates LAMA5 fragments promoting endothelial cell angiogenesis. Scientific reports 28 27324842
2019 Genetic variants in the LAMA5 gene in pediatric nephrotic syndrome. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 27 29534211
2012 Abnormal Wnt and PI3Kinase signaling in the malformed intestine of lama5 deficient mice. PloS one 25 22666383
2022 Recessive LAMA5 Variants Associated With Partial Epilepsy and Spasms in Infancy. Frontiers in molecular neuroscience 24 35663266
2018 LAMA5 promotes human umbilical vein endothelial cells migration, proliferation, and angiogenesis and is decreased in preeclampsia. The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians 18 30200802
2021 Clear Evidence of LAMA5 Gene Biallelic Truncating Variants Causing Infantile Nephrotic Syndrome. Kidney360 13 35419533
2018 Early posterior vitreous detachment is associated with LAMA5 dominant mutation. Ophthalmic genetics 11 30589377
2020 Biallelic mutations in LAMA5 disrupts a skeletal noncanonical focal adhesion pathway and produces a distinct bent bone dysplasia. EBioMedicine 10 33242826
2021 A novel model of nephrotic syndrome results from a point mutation in Lama5 and is modified by genetic background. Kidney international 9 34774562
2018 A presynaptic congenital myasthenic syndrome attributed to a homozygous sequence variant in LAMA5. Annals of the New York Academy of Sciences 8 29377152
2010 Association of a common LAMA5 variant with anthropometric and metabolic traits in an Italian cohort of healthy elderly subjects. Experimental gerontology 7 20951195
2016 Association of the Laminin, Alpha 5 (LAMA5) rs4925386 with height and longevity in an elderly population from Southern Italy. Mechanisms of ageing and development 6 26968355
2022 A heterozygous LAMA5 variant may contribute to slowly progressive, vinculin-enhanced familial FSGS and pulmonary defects. JCI insight 5 36173685
2016 Rare Variants in LAMA5 Gene associated with FLT4 and FOXC2 Mutations in Primary Lymphedema May Contribute to Severity. Lymphology 5 29908552
2011 Transgenic expression of human LAMA5 suppresses murine Lama5 mRNA and laminin α5 protein deposition. PloS one 5 21915268
2023 Congenital nephrotic syndrome with diffuse mesangial sclerosis caused by compound heterozygous mutation in LAMA5 gene. Pediatric nephrology (Berlin, Germany) 4 37985485
2021 Canonical Wnt signaling regulates branching morphogenesis of submandibular gland by modulating levels of lama5. The International journal of developmental biology 4 33629734
2020 Gene-based association analysis reveals involvement of LAMA5 and cell adhesion pathways in nicotine dependence in African- and European-American samples. Addiction biology 3 32281736
2025 Chronic Psychological Stress Induces Cardiomyocyte Hypertrophy Through Corticosterone-Glucocorticoid Receptor-LAMA5 Axis. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2 40642838
2025 The role of LAMA5 in breast cancer progression and its potential in immunotherapy. Discover oncology 2 40694271
2023 LAMA5-inspired adhesive dodecapeptide facilitates efficient dentine regeneration: An in vitro and in vivo study. International endodontic journal 2 37632694
2012 Common variants in the LAMA5 gene associate with fasting plasma glucose and serum triglyceride levels in a cohort of pre-and early pubertal children. Journal of pediatric genetics 2 23264881
2023 LAMA5: A new pathogenic gene for non-syndromic cleft lip with or without cleft palate. Biomedical journal 1 37390938
1998 Evaluation of Lama5 as a candidate for the mouse ragged (Ra) mutation. Biochemical and biophysical research communications 1 9735344
2025 MAZ-mediated LAMA5 transcription activation promotes gastric cancer progression through the STAT3 signaling. Functional & integrative genomics 0 40072648
2025 Integrated Mendelian randomization analysis reveals causal relationship between LAMA5 and bladder cancer and its metabolic mechanisms. Contemporary oncology (Poznan, Poland) 0 41098863

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