ArticlePloS one2016
Gpnmb Is a Potential Marker for the Visceral Pathology in Niemann-Pick Type C Disease.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 59 citations in OpenAlex.
- Identification of serum protein biomarkers in individuals with Niemann-Pick disease, type C1.Biomarker research · 2026Article
- Identification of serum protein biomarkers in individuals with Niemann-Pick disease, type C1.Research square · 2026Article
- Identification of serum protein biomarkers in individuals with Niemann-Pick disease, type C1.medRxiv : the preprint server for health sciences · 2026Article
- GBA1 Gene-Associated Transcriptomic Signatures Reveal Risk Genes in Parkinson's Disease.Biomedicines · 2025Article
- Regulation of lipoprotein processing by GPNMB in foamy macrophages: potential therapeutic targets for atherosclerosis.Nature communications · 2025Article
- Glycoprotein non-metastatic melanoma protein B is a biomarker of inflammation in individuals with Gaucher disease: relationship to clinico-pathological subtypes.Orphanet journal of rare diseases · 2025Article
- Proteomic landscape of Alzheimer's disease: emerging technologies, advances and insights (2021 - 2025).Molecular neurodegeneration · 2025Review
- Increased plasma GPNMB levels in patients with parkinson's disease and cognitive impairment.Scientific reports · 2025Article
- Glucosylated cholesterol accumulates in atherosclerotic lesions and impacts macrophage immune response.Journal of lipid research · 2025Article
- Potential Use of the Cholesterol Transfer Inhibitor U18666A as a Potent Research Tool for the Study of Cholesterol Mechanisms in Neurodegenerative Disorders.Molecular neurobiology · 2024Review
- Regional Differences in the Small Intestinal Proteome of Control Mice and of Mice Lacking Lysosomal Acid Lipase.Journal of proteome research · 2024Article
- Fructose regulates the pentose phosphate pathway and induces an inflammatory and resolution phenotype in Kupffer cells.Scientific reports · 2024Article
- Glycoprotein Non-Metastatic Protein B (GPNMB): The Missing Link Between Lysosomes and Obesity.Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association · 2023Review
- Progranulin and GPNMB: interactions in endo-lysosome function and inflammation in neurodegenerative disease.Journal of neuroinflammation · 2023Review
- Peripheral immune system modulates Purkinje cell degeneration in Niemann-Pick disease type C1.Life science alliance · 2023Article
- Glycolipids in Parkinson's disease: beyond neuronal function.FEBS open bio · 2023Review
- Identification of cerebral spinal fluid protein biomarkers in Niemann-Pick disease, type C1.Biomarker research · 2023Article
- The physiological and pathophysiological roles of the autophagy lysosomal system in the conventional aqueous humor outflow pathway: More than cellular clean up.Progress in retinal and eye research · 2022Review
- Glycoprotein nonmetastatic melanoma protein B regulates lysosomal integrity and lifespan of senescent cells.Scientific reports · 2022Article
- Correlation of age of onset and clinical severity in Niemann-Pick disease type C1 with lysosomal abnormalities and gene expression.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Impaired function of NPC1 or NPC2 lysosomal proteins leads to the intracellular accumulation of unesterified cholesterol, the primary defect underlying Niemann-Pick type C (NPC) disease. In addition, glycosphingolipids (GSLs) accumulate in lysosomes as well. Intralysosomal lipid accumulation triggers the activation of a set of genes, including potential biomarkers. Transcript levels of Gpnmb have been shown to be elevated in various tissues of an NPC mouse model. We speculated that Gpnmb could serve as a marker for visceral lipid accumulation in NPC disease. We report that Gpnmb expression is increased at protein level in macrophages in the viscera of Npc1nih/nih mice. Interestingly, soluble Gpnmb was also found to be increased in murine and NPC patient plasma. Exposure of RAW264.7 macrophages to the NPC-phenotype-inducing drug U18666A also upregulated Gpnmb expression. Inhibition of GSL synthesis with the glucosylceramide synthase (GCS) inhibitor N-butyl-1-deoxynojirimycin prevented U18666A-induced Gpnmb induction and secretion. In summary, we show that Gpnmb is upregulated in NPC mice and patients, most likely due to GSL accumulation.
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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.