ArticleInvestigative ophthalmology & visual science2011
Olfactomedin 2: expression in the eye and interaction with other olfactomedin domain-containing proteins.
Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 15 citations in OpenAlex.
- Olfactomedin-2 at the Crossroads of Smooth Muscle Cell Plasticity.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Evolution of the Nonvisual and Visual Opsin Gene Repertoire in Ray-Finned Fishes.Genome biology and evolution · 2025Article
- Article
- Coinheritance ofWorld journal of clinical cases · 2021Article
- Pathological molecular mechanism of symptomatic late-onset Fuchs endothelial corneal dystrophy by bioinformatic analysis.PloS one · 2018Article
- Impaired AMPA receptor trafficking by a double knockout of zebrafish olfactomedin1a/b.Journal of neurochemistry · 2017Article
- Olfactomedin 2 Regulates Smooth Muscle Phenotypic Modulation and Vascular Remodeling Through Mediating Runt-Related Transcription Factor 2 Binding to Serum Response Factor.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- Identification and functional characterisation of genetic variants in OLFM2 in children with developmental eye disorders.Human genetics · 2017Article
- Olfactomedin-like 2 A and B (OLFML2A and OLFML2B) expression profile in primates (human and baboon).Biological research · 2016Article
- Olfactomedin-1 Has a V-shaped Disulfide-linked Tetrameric Structure.The Journal of biological chemistry · 2015Article
- Olfactomedin 2, a novel regulator for transforming growth factor-β-induced smooth muscle differentiation of human embryonic stem cell-derived mesenchymal cells.Molecular biology of the cell · 2014Article
- Deletion of olfactomedin 2 induces changes in the AMPA receptor complex and impairs visual, olfactory, and motor functions in mice.Experimental neurology · 2014Article
- Deletion in the N-terminal half of olfactomedin 1 modifies its interaction with synaptic proteins and causes brain dystrophy and abnormal behavior in mice.Experimental neurology · 2013Article
- Olfactomedin 1 interacts with the Nogo A receptor complex to regulate axon growth.The Journal of biological chemistry · 2012Article
- Article
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4 authors at 1 institution in 1 country.
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Abstract
purposeOlfactomedin 2 (OLFM2) belongs to the family of olfactomedin domain-containing proteins. Genetic data suggest its association with glaucoma in Japanese patients. However, its functions are still elusive. In this study, the properties of mammalian OLFM2 were investigated.
methodsExpression of the rat and mouse Olfm2 gene was studied by using real-time PCR and in situ hybridization. Substitutions were introduced into OLFM2 by mutagenesis in vitro. Intracellular localization of OLFM2 was studied by confocal microscopy after transient transfection in HEK293 cells. Interaction of OLFM2 with olfactomedin 1 (Olfm1), olfactomedin 3 (Olfm3), myocilin, and gliomedin was studied by using co-immunoprecipitation.
resultsTwo major human OLFM2 mRNAs encode secreted proteins with a length of 454 and 478 amino acids. OLFM2 is more closely related to OLFM1 and -3 than to any other family members. Olfm2 showed the most dynamic expression pattern compared with Olfm1 and -3 during mouse eye development and was expressed preferentially in the developing retinal ganglion cell layer. Among three OLFM2 substitutions tested (T86M, R144Q, and L420S), only L420S completely blocked secretion of the protein. OLFM2 interacted with Olfm1 and -3, but not with myocilin and gliomedin. Co-transfection of the L420S mutant with wild-type Olfm1 and -3 significantly inhibited secretion of Olfm1 and -3.
conclusionsHighly conserved OLFM2 protein may play an important role in the course of retinal and eye development. Severe mutations in one of the closely related olfactomedin domain-containing proteins (Olfm1-3) may block the secretion and probably the activity of all three family members, leading to more pronounced diseases of the retina than the knockout of individual genes.
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