Esco2 and Cohesin Regulate CRL4 Ubiquitin Ligaseddb1Expression and Thalidomide Teratogenicity
Copyright policy )Esco2 and Cohesin Regulate CRL4 Ubiquitin Ligaseddb1Expression and Thalidomide Teratogenicity
ABSTRACTCornelia de Lange syndrome (CdLS) and Roberts syndrome (RBS) are severe developmental maladies that arise from mutation of cohesin (including SMC3, CdLS) and ESCO2 (RBS). Though ESCO2 activate cohesin, CdLS and RBS etiologies are currently considered non-synonymous and for which pharmacological treatments are unavailable. Here, we identify a unifying mechanism that integrates these genetic maladies to pharmacologically-induced teratogenicity via thalidomide. Our results reveal that Esco2 and cohesin co-regulate a component of CRL4 ubiquitin ligase through which thalidomide exerts teratogenic effects. These findings are the first to link RBS and CdLS to thalidomide teratogenicity and offers new insights into treatments.
Receptors, Interleukin-17, Hypertelorism, Chromosomal Proteins, Non-Histone, Ectromelia, Ubiquitin, Ubiquitin-Protein Ligases, Cell Cycle Proteins, Thalidomide, Craniofacial Abnormalities, DNA-Binding Proteins, Ligases, Acetyltransferases, De Lange Syndrome, Mutation, Humans, Cohesins, Research Paper
Receptors, Interleukin-17, Hypertelorism, Chromosomal Proteins, Non-Histone, Ectromelia, Ubiquitin, Ubiquitin-Protein Ligases, Cell Cycle Proteins, Thalidomide, Craniofacial Abnormalities, DNA-Binding Proteins, Ligases, Acetyltransferases, De Lange Syndrome, Mutation, Humans, Cohesins, Research Paper
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