ArticleNeurogenetics2017
Increased brain expression of GPNMB is associated with genome wide significant risk for Parkinson's disease on chromosome 7p15.3.
Article in Neurogenetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Pooled it
- 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
- The Relationship of Peripheral Glycoprotein Nonmetastatic Melanoma Protein B and Parkinson's Disease: Insights From a Mendelian Randomization Study.International journal of genomics · 2026Article
- GPNMB, LRRK2, and lysosome exocytosis in Parkinson's.Science advances · 2025Review
- GPNMB is a biomarker for lysosomal dysfunction and is secreted via LRRK2-modulated lysosomal exocytosis.Science advances · 2025Article
- Bidirectional regulation of glycoprotein nonmetastatic melanoma protein B by β-glucocerebrosidase deficiency inbioRxiv : the preprint server for biology · 2025Article
- Identification of pivotal genes and regulatory networks associated with SAH based on multi-omics analysis and machine learning.Scientific reports · 2025Article
- Malignant mesothelioma-associated inflammatory microenvironment promotes tumor progression via GPNMB.Journal of translational medicine · 2025Article
- The janus-faced biology of GPNMB: from tissue homeostasis to cancer pathogenesis.Frontiers in molecular biosciences · 2025Review
- Human VCP mutant ALS/FTD microglia display immune and lysosomal phenotypes independently of GPNMB.Molecular neurodegeneration · 2024Article
- CSF GPNMB in Parkinson's disease: A potential association with age and microglial activation.Journal of Parkinson's disease · 2024Article
- SR-TWAS: leveraging multiple reference panels to improve transcriptome-wide association study power by ensemble machine learning.Nature communications · 2024Article
- GPNMB Biomarker Levels in GBA1 Carriers with Lewy Body Disorders.Movement disorders : official journal of the Movement Disorder Society · 2024Article
- Common genetic risk for Parkinson's disease and dysfunction of the endo-lysosomal system.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- Investigating the role and regulation of GPNMB in progranulin-deficient macrophages.Frontiers in immunology · 2024Article
- Epigenetic associations ofFrontiers in psychiatry · 2024Article
- Article
- Progranulin and GPNMB: interactions in endo-lysosome function and inflammation in neurodegenerative disease.Journal of neuroinflammation · 2023Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
Abstract
Genome wide association studies (GWAS) for Parkinson's disease (PD) have previously revealed a significant association with a locus on chromosome 7p15.3, initially designated as the glycoprotein non-metastatic melanoma protein B (GPNMB) locus. In this study, the functional consequences of this association on expression were explored in depth by integrating different expression quantitative trait locus (eQTL) datasets (Braineac, CAGEseq, GTEx, and Phenotype-Genotype Integrator (PheGenI)). Top risk SNP rs199347 eQTLs demonstrated increased expressions of GPNMB, KLHL7, and NUPL2 with the major allele (AA) in brain, with most significant eQTLs in cortical regions, followed by putamen. In addition, decreased expression of the antisense RNA KLHL7-AS1 was observed in GTEx. Furthermore, rs199347 is an eQTL with long non-coding RNA (AC005082.12) in human tissues other than brain. Interestingly, transcript-specific eQTLs in immune-related tissues (spleen and lymphoblastoid cells) for NUPL2 and KLHL7-AS1 were observed, which suggests a complex functional role of this eQTL in specific tissues, cell types at specific time points. Significantly increased expression of GPNMB linked to rs199347 was consistent across all datasets, and taken in combination with the risk SNP being located within the GPNMB gene, these results suggest that increased expression of GPNMB is the causative link explaining the association of this locus with PD. However, other transcript eQTLs and subsequent functional roles cannot be excluded. This highlights the importance of further investigations to understand the functional interactions between the coding genes, antisense, and non-coding RNA species considering the tissue and cell-type specificity to understand the underlying biological mechanisms in PD.
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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.