Chen Gong
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Chen Gong has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
Amy W Butler
Department of Medical & Molecular Genetics, King’s College London , St Thomas Street, London , SE1 9RT
1 shared publicationAriella Amar
Department of Medical & Molecular Genetics, King’s College London , St Thomas Street, London , SE1 9RT
1 shared publication- David Lester Morris
Concordia University
1 shared publication Lu Liu
Department of Dermatology, The First Affiliated Hospital of Anhui Medical University , Hefei, Anhui
1 shared publication- Nick Dand
Department of Medical and Molecular Genetics, King’s College London , London
1 shared publication - Pinelopi Maria Triantafyllou
Department of Medical & Molecular Genetics, King’s College London , St Thomas Street, London , SE1 9RT
1 shared publication
Latest Publications
- Open Access
- 11 September 2026
- Published by Oxford University Press (OUP) in Human Molecular Genetics
- Vol. 35 (20)
Shared genetic architecture of schizophrenia and lupus identifies pleiotropic loci with distinct downstream mechanisms
Schizophrenia (SCZ) and systemic lupus erythematosus (SLE) exhibit epidemiological overlap, suggesting shared genetic underpinnings. Using the largest SLE genome-wide association study (GWAS) to date, we identified a significant genetic correlation between SCZ and SLE (rg = 0.25, p = 9.0 × 10−4). Cross-trait analysis nominated multiple candidate shared loci outside the major histocompatibility complex (MHC), most with aligned effects. The strongest candidate shared association was found at the FURIN-FES locus, previously implicated in SCZ and newly associated with SLE. In addition to FURIN-FES, FCGR2A, DOT1L and an intergenic noncoding RNA locus on chromosome 2 showed additional evidence consistent with shared association. Functional annotation showed that this locus modulated the expression of FURIN, which encodes a proprotein convertase involved in diverse biological processes, and FES, which encodes a tyrosine kinase important in innate immune signalling. The shared risk allele was also associated with altered plasma levels of FURIN, FES, and their functional partners (GDF2, BMP10, NTF4, FER). Tissue- and cell-type-specific eQTL analysis revealed distinct regulatory effects: FURIN expression was perturbed in neuronal and immune cells, while FES expression was altered in immune cells. Mendelian randomisation supported a causal role for FES protein in both disorders. These findings highlight that pleiotropy at the FURIN-FES locus for SCZ and SLE is compatible with disease-specific mechanisms. This underscores that shared genetics across traits does not necessarily mean shared biology.
- 11 September 2026
- Published by Oxford University Press (OUP) in Human Molecular Genetics
- Vol. 35 (20)
Open AccessShared genetic architecture of schizophrenia and lupus identifies pleiotropic loci with distinct downstream mechanisms
Schizophrenia (SCZ) and systemic lupus erythematosus (SLE) exhibit epidemiological overlap, suggesting shared genetic underpinnings. Using the largest SLE genome-wide association study (GWAS) to date, we identified a significant genetic correlation between SCZ and SLE (rg = 0.25, p = 9.0 × 10−4). Cross-trait analysis nominated multiple candidate shared loci outside the major histocompatibility complex (MHC), most with aligned effects. The strongest candidate shared association was found at the FURIN-FES locus, previously implicated in SCZ and newly associated with SLE. In addition to FURIN-FES, FCGR2A, DOT1L and an intergenic noncoding RNA locus on chromosome 2 showed additional evidence consistent with shared association. Functional annotation showed that this locus modulated the expression of FURIN, which encodes a proprotein convertase involved in diverse biological processes, and FES, which encodes a tyrosine kinase important in innate immune signalling. The shared risk allele was also associated with altered plasma levels of FURIN, FES, and their functional partners (GDF2, BMP10, NTF4, FER). Tissue- and cell-type-specific eQTL analysis revealed distinct regulatory effects: FURIN expression was perturbed in neuronal and immune cells, while FES expression was altered in immune cells. Mendelian randomisation supported a causal role for FES protein in both disorders. These findings highlight that pleiotropy at the FURIN-FES locus for SCZ and SLE is compatible with disease-specific mechanisms. This underscores that shared genetics across traits does not necessarily mean shared biology.