ArticleThe Journal of biological chemistry2009
Scaffold-forming and Adhesive Contributions of Synthetic Laminin-binding Proteins to Basement Membrane Assembly.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 63 citations in OpenAlex.
- Aligned basement membrane-modified collagen scaffolds for skeletal muscle tissue engineering.bioRxiv : the preprint server for biology · 2026Article
- Dual AAV gene therapy using laminin-linking proteins ameliorates muscle and nerve defects in LAMA2-related muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Glomerular basement membrane structural integrity dictates trans-tissue deposition of laminin in the kidney.Cell reports · 2026Article
- Vemurafenib improves muscle histopathology in a mouse model of LAMA2-related congenital muscular dystrophy.Disease models & mechanisms · 2023Article
- Dual transgene amelioration of Lama2-null muscular dystrophy.Matrix biology : journal of the International Society for Matrix Biology · 2023Article
- Exogenous laminin exhibits a unique vascular pattern in the brain via binding to dystroglycan and integrins.Fluids and barriers of the CNS · 2022Article
- Amelioration of muscle and nerve pathology of Lama2-related dystrophy by AAV9-laminin-αLN linker protein.JCI insight · 2022Article
- Peripheral Nerve Development and the Pathogenesis of Peripheral Neuropathy: the Sorting Point.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- Retinal capillary basement membrane thickening: Role in the pathogenesis of diabetic retinopathy.Progress in retinal and eye research · 2021Review
- Organization of the laminin polymer node.Matrix biology : journal of the International Society for Matrix Biology · 2021Article
- Laminin Polymerization and Inherited Disease: Lessons From Genetics.Frontiers in genetics · 2021Review
- A deletion in the N-terminal polymerizing domain of laminin β2 is a new mouse model of chronic nephrotic syndrome.Kidney international · 2020Article
- A mutation affecting laminin alpha 5 polymerisation gives rise to a syndromic developmental disorder.Development (Cambridge, England) · 2020Article
- Structural biology of laminins.Essays in biochemistry · 2019Review
- α-Integrins dictate distinct modes of type IV collagen recruitment to basement membranes.The Journal of cell biology · 2019Article
- The laminin binding α3 and α6 integrins cooperate to promote epithelial cell adhesion and growth.Matrix biology : journal of the International Society for Matrix Biology · 2019Article
- Linker Protein Repair of LAMA2 Dystrophic Neuromuscular Basement Membranes.Frontiers in molecular neuroscience · 2019Review
- Current understanding and treatment of cardiac and skeletal muscle pathology in laminin-α2 chain-deficient congenital muscular dystrophy.The application of clinical genetics · 2019Article
- Laminin-deficient muscular dystrophy: Molecular pathogenesis and structural repair strategies.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- Chimeric protein identification of dystrophic, Pierson and other laminin polymerization residues.Matrix biology : journal of the International Society for Matrix Biology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Laminins that possess three short arms contribute to basement membrane assembly by anchoring to cell surfaces, polymerizing, and binding to nidogen and collagen IV. Although laminins containing the alpha4 and alpha5 subunits are expressed in alpha2-deficient congenital muscular dystrophy, they may be ineffective substitutes because they bind weakly to cell surfaces and/or because they lack the third arm needed for polymerization. We asked whether linker proteins engineered to bind to deficient laminins that provide such missing activities would promote basement membrane assembly in a Schwann cell model. A chimeric fusion protein (alphaLNNd) that adds a short arm terminus to laminin through the nidogen binding locus was generated and compared with the dystrophy-ameliorating protein miniagrin (mAgrin) that binds to the laminin coiled-coil dystroglycan and sulfatides. alphaLNNd was found to mediate laminin binding to collagen IV, to bind to galactosyl sulfatide, and to selectively convert alpha-short arm deletion-mutant laminins LmDeltaalphaLN and LmDeltaalphaLN-L4b into polymerizing laminins. This protein enabled polymerization-deficient laminin but not an adhesion-deficient laminin lacking LG domains (LmDeltaLG) to assemble an extracellular matrix on Schwann cell surfaces. mAgrin, on the other hand, enabled LmDeltaLG to form an extracellular matrix on cell surfaces without increasing accumulation of non-polymerizing laminins. These gain-of-function studies reveal distinct polymerization and anchorage contributions to basement membrane assembly in which the three different LN domains mediate the former, and the LG domains provide primary anchorage with secondary contributions from the alphaLN domain. These findings may be relevant for an understanding of the pathogenesis and treatment of laminin deficiency states.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.