ArticleBiochemical and biophysical research communications2015
LMAN1 (ERGIC-53) is a potential carrier protein for matrix metalloproteinase-9 glycoprotein secretion.
Article in Biochemical and biophysical research communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Glycosylation modification: a trigger for obesity and its complications?Molecular medicine (Cambridge, Mass.) · 2026Review
- Immunomodulation by glycosylation: bridging glycobiology to adaptive immunity and therapeutic innovation.Frontiers in immunology · 2026Review
- Molecular tag for promotingiScience · 2024Article
- Glycosylation: mechanisms, biological functions and clinical implications.Signal transduction and targeted therapy · 2024Review
- Effect of Acupuncture on Tear Proteomics in Patients with Video Display Terminal-Related Dry Eye.Journal of proteome research · 2024Article
- The Influence of Lysosomal Stress on Dental Pulp Stem Cell-Derived Schwann Cells.Biomolecules · 2024Article
- Structure of full-length ERGIC-53 in complex with MCFD2 for cargo transport.Nature communications · 2024Article
- Identification of LMAN1- and SURF4-Dependent Secretory Cargoes.Journal of proteome research · 2023Article
- Mammalian cargo receptors for endoplasmic reticulum-to-Golgi transport: mechanisms and interactions.Biochemical Society transactions · 2023Review
- Separate roles of LMAN1 and MCFD2 in ER-to-Golgi trafficking of FV and FVIII.Blood advances · 2023Article
- Cargo selection in endoplasmic reticulum-to-Golgi transport and relevant diseases.The Journal of clinical investigation · 2023Review
- LMAN1-MCFD2 complex is a cargo receptor for the ER-Golgi transport of α1-antitrypsin.The Biochemical journal · 2022Article
- Altered phenotype in LMAN1-deficient mice with low levels of residual LMAN1 expression.Blood advances · 2020Article
- Amyotrophic lateral sclerosis-linked UBQLN2 mutants inhibit endoplasmic reticulum to Golgi transport, leading to Golgi fragmentation and ER stress.Cellular and molecular life sciences : CMLS · 2020Article
- Article
- How to Avoid a No-Deal ER Exit.Cells · 2019Review
- LMAN1 (ERGIC-53) promotes trafficking of neuroreceptors.Biochemical and biophysical research communications · 2019Article
- Type 2 deiodinase polymorphism causes ER stress and hypothyroidism in the brain.The Journal of clinical investigation · 2019Article
- Article
- Functional Roles of N-Linked Glycosylation of Human Matrix Metalloproteinase 9.Traffic (Copenhagen, Denmark) · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Matrix metalloproteinase-9 (MMP-9) is a secreted glycoprotein with a major role in shaping the extracellular matrix and a detailed understanding of the secretory mechanism could help identify methods to correct diseases resulting from dysregulation of secretion. MMP-9 appears to follow a canonical secretory pathway through a quality control cycle in the endoplasmic reticulum (ER) before transport of the properly folded protein to the Golgi apparatus and beyond for secretion. Through a complementation assay, we determined that LMAN1, a well-studied lectin-carrier protein, interacts with a secretion-competent N-glycosylated MMP-9 in the ER while N-glycosylation-deficient secretion-compromised MMP-9 does not. In contrast, co-immunoprecipitation demonstrated protein interaction between LMAN1 and secretion-compromised N-glycosylation-deficient MMP-9. MMP-9 secretion was reduced in the LMAN1 knockout cell line compared to control cells confirming the functional role of LMAN1. These observations support the role of LMAN1 as a lectin-carrier protein mediating efficient MMP-9 secretion.
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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.