rs1147367 - RN7SL159P - LINC00963

Magnitude 2.0 · 2 studies on file

Reported associations

• Refining antipsychotic treatment strategies in schizophrenia: discovery of genetic biomarkers for enhanced drug response prediction. - Molecular psychiatry (2025) · Chen L, Huai C, Song C, Wu S, Xu Y, Yi Z, Tang J, Fan L, Wu X, Ge Z, Liu C, Jiang D, Weng S, Wang G, Zhang X, Zhao X, Shen L, Zhang N, Wu H, Wang Y, Guo Z, Zhang S, Jiang B, Zhou W, Ma J, Li M, Chu Y, Zhou C, Lv Q, Xu Q, Zhu W, Zhang Y, Lian W, Liu S, Li X, Gao S, Liu A, He L, Yang Z, Dai B, Ye J, Lin R, Lu Y, Yan Q, Hu Y, Xing Q, Huang H, Qin S · PubMed 39562719

  Schizophrenia (SCZ) is a severe mental disorder affecting around 1% of individuals worldwide. The variability in response to antipsychotic drugs (APDs) among SCZ patients presents a significant challenge for clinicians in determining the most effective medication. In this study, we investigated the biological markers and established a predictive model for APD response based on a large-scale genome-wide association study using 3269 Chinese schizophrenia patients. Each participant underwent an 8-week treatment regimen with one of five mono-APDs: olanzapine, risperidone, aripiprazole, quetiapine, or amisulpride. By dividing the response into ordinal groups of "high", "medium", and "low", we mitigated the bias of unclear treatment outcome and identified three novel significantly associated gen

• A genome-wide association study identifies key modulators of complement factor H binding to malondialdehyde-epitopes - Proceedings of the National Academy of Sciences of the United States of America (2020) · Alic L, Papac-Milicevic N, Czamara D, Rudnick RB, Ozsvar-Kozma M, Hartmann A, Gurbisz M, Hoermann G, Haslinger-Hutter S, Zipfel PF, Skerka C, Binder EB, Binder CJ · PubMed 32321835

  ABSTRACT: Significance Dysregulation of the alternative complement pathway due to impaired binding of complement factor H (CFH) to self-ligands or altered self-ligands (e.g. malondialdehyde [MDA]-modified molecules) involved in homeostasis can promote the development of complement-related diseases, such as age-related macular degeneration (AMD). We identified, in an unbiased GWAS approach, that common genetic variants within the CFH gene family (rs1061170 and the deletion of the complement factor H-related protein 1 and 3 genes [CFHR3 and CFHR1]) act as major modulators of CFH recruitment and its ability to regulate complement on MDA-epitopes. These findings demonstrate the importance of the genetic status within the CFH/CFHR3/CFHR1 locus in tissue homeostasis and provide a mechanistic exp

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