Research Topics
Genomes and Genes
Species | Catherine CoffinierSummaryAffiliation: University of California Country: USA Publications
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Detail Information
Publications
Abnormal development of the cerebral cortex and cerebellum in the setting of lamin B2 deficiencyCatherine Coffinier
Departments of Medicine and Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
Proc Natl Acad Sci U S A 107:5076-81. 2010..These studies establish an essential function for lamin B2 in neuronal migration and brain development...- Deficiencies in lamin B1 and lamin B2 cause neurodevelopmental defects and distinct nuclear shape abnormalities in neuronsCatherine Coffinier
Department of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA
Mol Biol Cell 22:4683-93. 2011.... - HIV protease inhibitors block the zinc metalloproteinase ZMPSTE24 and lead to an accumulation of prelamin A in cellsCatherine Coffinier
Department of Medicine Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
Proc Natl Acad Sci U S A 104:13432-7. 2007..6 microM; tipranavir, 1.2 +/- 0.4 microM). We conclude that the HIV-PIs inhibit ZMPSTE24, leading to an accumulation of farnesyl-prelamin A. The inhibition of ZMPSTE24 by HIV-PIs could play a role in the side effects of these drugs... - LINCing lamin B2 to neuronal migration: growing evidence for cell-specific roles of B-type laminsCatherine Coffinier
Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
Nucleus 1:407-11. 2010.... - Direct synthesis of lamin A, bypassing prelamin a processing, causes misshapen nuclei in fibroblasts but no detectable pathology in miceCatherine Coffinier
Department of Medicine, University of California, Los Angeles, CA 90095, USA
J Biol Chem 285:20818-26. 2010..We conclude that prelamin A processing is dispensable in mice and that direct synthesis of mature lamin A has little if any effect on the targeting of lamin A to the nuclear rim in mouse tissues... - A potent HIV protease inhibitor, darunavir, does not inhibit ZMPSTE24 or lead to an accumulation of farnesyl-prelamin A in cellsCatherine Coffinier
Department of Medicine and Human Genetics, David Geffen School of Medicine, University of California Los Angeles, 695 Charles E Young Drive South, Los Angeles, CA 90095, USA
J Biol Chem 283:9797-804. 2008..Ritonavir, like lopinavir, inhibits ZMPSTE24 and leads to an accumulation of prelamin A... - Understanding the roles of nuclear A- and B-type lamins in brain developmentStephen G Young
Department of Medicine, UCLA, Los Angeles, California 90095, USA
J Biol Chem 287:16103-10. 2012..The relevance of lamins A and C in the brain remains unclear, but it is intriguing that prelamin A expression in the brain is low and is regulated by miR-9, a brain-specific microRNA... - A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutationShao H Yang
Department of Medicine, Division of Cardiology, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA, and Department of Medicine, Wallenberg Laboratory, Sahlgrenska University Hospital, Goteborg, Sweden
J Clin Invest 116:2115-21. 2006..These studies suggest that FTIs could be useful for treating humans with HGPS... - The posttranslational processing of prelamin A and diseaseBrandon S J Davies
Department of Medicine, University of California, Los Angeles, California 90095, USA
Annu Rev Genomics Hum Genet 10:153-74. 2009..In this review, we discuss the posttranslational modifications of prelamin A and their relevance to the pathogenesis and treatment of progeroid syndromes... - Activating the synthesis of progerin, the mutant prelamin A in Hutchinson-Gilford progeria syndrome, with antisense oligonucleotidesLoren G Fong
Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
Hum Mol Genet 18:2462-71. 2009..Thus, different ASOs can be used to increase or decrease 'HGPS splicing'. ASOs represent a new and powerful tool for recreating HGPS pathophysiology in wild-type cells... - Investigating the purpose of prelamin A processingBrandon Sj Davies
Department of Medicine, University of California, Los Angeles, USA
Nucleus 2:4-9. 2011.... - Regulation of prelamin A but not lamin C by miR-9, a brain-specific microRNAHea Jin Jung
Molecular Biology Institute and Department of Medicine and Human Genetics, University of California, Los Angeles, CA 90095, USA
Proc Natl Acad Sci U S A 109:E423-31. 2012..The down-regulation of prelamin A expression in the brain could explain why mouse models of Hutchinson-Gilford progeria syndrome are free of central nervous system pathology... - Are B-type lamins essential in all mammalian cells?Shao H Yang
Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA
Nucleus 2:562-9. 2011..The absence of either lamin B1 or lamin B2, or the absence of both B-type lamins, results in severe neurodevelopmental abnormalities... 
A protein farnesyltransferase inhibitor ameliorates disease in a mouse model of progeriaLoren G Fong
Department of Medicine Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
Science 311:1621-3. 2006..The FTI-treated mice exhibited improved body weight, grip strength, bone integrity, and percent survival at 20 weeks of age. These results suggest that FTIs may have beneficial effects in humans with progeria...- Development of the vertebral morphogenetic field in the mouse: interactions between Crossveinless-2 and Twisted GastrulationLise Zakin
Howard Hughes Medical Institute and Department of Biological Chemistry, University of California, Los Angeles, CA 90095 1662, USA
Dev Biol 323:6-18. 2008..We propose a model in which CV2 and Tsg participate in the generation of a BMP signaling morphogenetic field during vertebral formation in which CV2 serves to concentrate diffusible Tsg/BMP4 complexes in the vertebral body cartilage... - Mouse Crossveinless-2 is the vertebrate homolog of a Drosophila extracellular regulator of BMP signalingCatherine Coffinier
Howard Hughes Medical Institute and Department of Biological Chemistry, University of California, Los Angeles, CA 90095 1662, USA
Mech Dev 119:S179-84. 2002..We conclude that CV-2 is an evolutionarily conserved extracellular regulator of the Dpp/BMP signaling pathway... - Crossveinless-2 Is a BMP feedback inhibitor that binds Chordin/BMP to regulate Xenopus embryonic patterningAndrea L Ambrosio
Howard Hughes Medical Institute, Department of Biological Chemistry, University of California, Los Angeles, Los Angeles, CA 90095, USA
Dev Cell 15:248-60. 2008..We propose that the CV2/Chordin interaction may help coordinate BMP diffusion to the ventral side of the embryo, ensuring that BMPs liberated from Chordin inhibition by tolloid proteolysis cause peak signaling levels... - Chordin-like CR domains and the regulation of evolutionarily conserved extracellular signaling systemsJose Garcia Abreu
Howard Hughes Medical Institute and Department of Biological Chemistry, University of California, Los Angeles, CA 90095 1662, USA
Gene 287:39-47. 2002..We discuss how the study of CR domains may provide a general mechanism for the regulation of growth factor signaling in the extracellular space... - HIV-protease inhibitors block the enzymatic activity of purified Ste24pSarah E Hudon
Department of Chemistry and the Purdue Cancer Center, Purdue University, 560 Oval Drive, West Lafayette, IN 47907 2084, USA
Biochem Biophys Res Commun 374:365-8. 2008.... - Selective deletion of the Hnf1beta (MODY5) gene in beta-cells leads to altered gene expression and defective insulin releaseLi Wang
Pediatric Endocrine Unit, MassGeneral Hospital for Children, Boston, Massachusetts 02114 2696, USA
Endocrinology 145:3941-9. 2004..These results indicate that HNF1beta is involved in regulating the beta-cell transcription factor network and is necessary for glucose sensing or glycolytic signaling...