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154. Theoretical Prediction and Experimental Verification of ees Versus Time in Biocatalytic Resolution and its Application in a Bioresolution-inversion Process

Author

Xu Yi, Zhou Dan, and Chen Jianbo

Subjects
theoretical prediction, bioresolution-inversion, epoxide hydrolase, lipase, Engineering (General). Civil engineering (General), TA1-2040
Abstract

A systematic theoretical derivation of bioresolution-inversion process was made. An equation was derived between the maximum ee value of final product (eef(max)) and enantiomeric ratio (E) of a reaction. The corresponding equations of conv.(max), eep(max), ees(max) versus E-value were also derivative and the interrelationships among eef(max), conv.(max), eep(max) and ees(max) were deduced. Furthermore, a simple equation was de-veloped to predict the enantiomeric excess of substrate (ees) at any other time of the whole reaction course based on the ees value which was determined at a certain reaction time. This equation of ees versus time was verified by three different experiments. Based on the equation of ees versus time, a new equation for predicting the time (t(max)) needed to reach the maximum enantiomeric excess of the final product (eef (max)) after the resolution-inversion was developed.

Published
2015
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185. Co‐occurrence of BAP1 and SF3B1 mutations in uveal melanoma induces cellular senescence

Author

Yu, Le, Zhou, Dan, Zhang, Guiming, Ren, Zhonglu, Luo, Xin, Liu, Peng, Plouffe, Steven W, Meng, Zhipeng, Moroishi, Toshiro, Li, Yilei, Zhang, Yiyue, Brown, Joan Heller, Liu, Shuwen, and Guan, Kun‐Liang

Subjects
Cancer, Biotechnology, Eye Disease and Disorders of Vision, Rare Diseases, Genetics, 2.1 Biological and endogenous factors, Aetiology, Animals, Cellular Senescence, DNA Mutational Analysis, Humans, Melanoma, Mice, Mice, Nude, Mutation, Phosphoproteins, RNA Splicing Factors, Tumor Suppressor Proteins, Ubiquitin Thiolesterase, Uveal Neoplasms, Zebrafish, BAP1, mutually exclusive pattern, recurrent mutations, senescence, uveal melanoma, SF3B1, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Uveal melanoma (UM) is the most common intraocular tumor in adults. Recurrent mutations in BRCA1-associated protein 1 (BAP1) and splicing factor 3B subunit 1 (SF3B1) display a mutually exclusive pattern in UM, but the underlying mechanism is unknown. We show that combined BAP1 deficiency and SF3B1 hotspot mutation lead to senescence and growth arrest in human UM cells. Although p53 protein expression is induced, deletion of TP53 (encoding p53) only modestly rescues the observed senescent phenotype. UM cells with BAP1 loss or SF3B1 mutation are more sensitive to chemotherapeutic drugs compared with their isogenic parental cells. Transcriptome analysis shows that DNA-repair genes are downregulated upon co-occurrence of BAP1 deletion and SF3B1 mutation, thus leading to impaired DNA damage response and the induction of senescence. The co-occurrence of these two mutations reduces invasion of UM cells in zebrafish xenograft models and suppresses growth of melanoma xenografts in nude mice. Our findings provide a mechanistic explanation for the mutual exclusivity of BAP1 and SF3B1 mutations in human UM.

Published
2022

186. Integration of genetic, transcriptomic, and clinical data provides insight into 16p11.2 and 22q11.2 CNV genes

Author

Vysotskiy, Mikhail, Zhong, Xue, Miller-Fleming, Tyne W, Zhou, Dan, Cox, Nancy J, and Weiss, Lauren A

Subjects
Biological Sciences, Genetics, Human Genome, Brain Disorders, Intellectual and Developmental Disabilities (IDD), Mental Health, Genetic Testing, Schizophrenia, Autism, Biotechnology, Clinical Research, 2.1 Biological and endogenous factors, Aetiology, Mental health, Good Health and Well Being, Autism Spectrum Disorder, Autistic Disorder, Chromosome Deletion, Chromosome Disorders, Chromosomes, Human, Pair 16, DNA Copy Number Variations, DiGeorge Syndrome, Genotype, Humans, Intellectual Disability, Phenotype, Psychotic Disorders, Scavenger Receptors, Class F, Transcriptome, Tumor Suppressor Proteins, Copy number variants, Transcriptome imputation, Electronic health records, Psychiatric traits, Phenome-wide association studies, Autism Working Group of the Psychiatric Genomics Consortium^, Bipolar Disorder Working Group of the Psychiatric Genomics Consortium^, Schizophrenia Working Group of the Psychiatric Genomics Consortium^, Clinical Sciences
Abstract

BackgroundDeletions and duplications of the multigenic 16p11.2 and 22q11.2 copy number variant (CNV) regions are associated with brain-related disorders including schizophrenia, intellectual disability, obesity, bipolar disorder, and autism spectrum disorder (ASD). The contribution of individual CNV genes to each of these identified phenotypes is unknown, as well as the contribution of these CNV genes to other potentially subtler health implications for carriers. Hypothesizing that DNA copy number exerts most effects via impacts on RNA expression, we attempted a novel in silico fine-mapping approach in non-CNV carriers using both GWAS and biobank data.MethodsWe first asked whether gene expression level in any individual gene in the CNV region alters risk for a known CNV-associated behavioral phenotype(s). Using transcriptomic imputation, we performed association testing for CNV genes within large genotyped cohorts for schizophrenia, IQ, BMI, bipolar disorder, and ASD. Second, we used a biobank containing electronic health data to compare the medical phenome of CNV carriers to controls within 700,000 individuals in order to investigate the full spectrum of health effects of the CNVs. Third, we used genotypes for over 48,000 individuals within the biobank to perform phenome-wide association studies between imputed expressions of individual 16p11.2 and 22q11.2 genes and over 1500 health traits.ResultsUsing large genotyped cohorts, we found individual genes within 16p11.2 associated with schizophrenia (TMEM219, INO80E, YPEL3), BMI (TMEM219, SPN, TAOK2, INO80E), and IQ (SPN), using conditional analysis to identify upregulation of INO80E as the driver of schizophrenia, and downregulation of SPN and INO80E as increasing BMI. We identified both novel and previously observed over-represented traits within the electronic health records of 16p11.2 and 22q11.2 CNV carriers. In the phenome-wide association study, we found seventeen significant gene-trait pairs, including psychosis (NPIPB11, SLX1B) and mood disorders (SCARF2), and overall enrichment of mental traits.ConclusionsOur results demonstrate how integration of genetic and clinical data aids in understanding CNV gene function and implicates pleiotropy and multigenicity in CNV biology.

Published
2021

187. Novel ancestry-specific primary open-angle glaucoma loci and shared biology with vascular mechanisms and cell proliferation

Author

Lo Faro, Valeria, Bhattacharya, Arjun, Zhou, Wei, Zhou, Dan, Wang, Ying, Läll, Kristi, Kanai, Masahiro, Lopera-Maya, Esteban, Straub, Peter, Pawar, Priyanka, Tao, Ran, Zhong, Xue, Namba, Shinichi, Sanna, Serena, Nolte, Ilja M., Okada, Yukinori, Ingold, Nathan, MacGregor, Stuart, Snieder, Harold, Surakka, Ida, Shortt, Jonathan, Gignoux, Chris, Rafaels, Nicholas, Crooks, Kristy, Verma, Anurag, Verma, Shefali S., Guare, Lindsay, Rader, Daniel J., Willer, Cristen, Martin, Alicia R., Brantley, Milam A., Jr., Gamazon, Eric R., Jansonius, Nomdo M., Joos, Karen, Cox, Nancy J., and Hirbo, Jibril

Published
2024
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