Catherine Coffinier

Summary

Affiliation: University of California
Country: USA

Publications

  1. pmc Abnormal development of the cerebral cortex and cerebellum in the setting of lamin B2 deficiency
    Catherine 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
  2. pmc Deficiencies in lamin B1 and lamin B2 cause neurodevelopmental defects and distinct nuclear shape abnormalities in neurons
    Catherine Coffinier
    Department of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA
    Mol Biol Cell 22:4683-93. 2011
  3. pmc HIV protease inhibitors block the zinc metalloproteinase ZMPSTE24 and lead to an accumulation of prelamin A in cells
    Catherine 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
  4. pmc LINCing lamin B2 to neuronal migration: growing evidence for cell-specific roles of B-type lamins
    Catherine Coffinier
    Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
    Nucleus 1:407-11. 2010
  5. pmc A potent HIV protease inhibitor, darunavir, does not inhibit ZMPSTE24 or lead to an accumulation of farnesyl-prelamin A in cells
    Catherine 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
  6. pmc Direct synthesis of lamin A, bypassing prelamin a processing, causes misshapen nuclei in fibroblasts but no detectable pathology in mice
    Catherine Coffinier
    Department of Medicine, University of California, Los Angeles, CA 90095, USA
    J Biol Chem 285:20818-26. 2010
  7. pmc Understanding the roles of nuclear A- and B-type lamins in brain development
    Stephen G Young
    Department of Medicine, UCLA, Los Angeles, California 90095, USA
    J Biol Chem 287:16103-10. 2012
  8. pmc A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation
    Shao 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
  9. pmc Activating the synthesis of progerin, the mutant prelamin A in Hutchinson-Gilford progeria syndrome, with antisense oligonucleotides
    Loren 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
  10. pmc The posttranslational processing of prelamin A and disease
    Brandon S J Davies
    Department of Medicine, University of California, Los Angeles, California 90095, USA
    Annu Rev Genomics Hum Genet 10:153-74. 2009

Collaborators

Detail Information

Publications21

  1. pmc Abnormal development of the cerebral cortex and cerebellum in the setting of lamin B2 deficiency
    Catherine 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...
  2. pmc Deficiencies in lamin B1 and lamin B2 cause neurodevelopmental defects and distinct nuclear shape abnormalities in neurons
    Catherine Coffinier
    Department of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA
    Mol Biol Cell 22:4683-93. 2011
    ....
  3. pmc HIV protease inhibitors block the zinc metalloproteinase ZMPSTE24 and lead to an accumulation of prelamin A in cells
    Catherine 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...
  4. pmc LINCing lamin B2 to neuronal migration: growing evidence for cell-specific roles of B-type lamins
    Catherine Coffinier
    Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
    Nucleus 1:407-11. 2010
    ....
  5. pmc A potent HIV protease inhibitor, darunavir, does not inhibit ZMPSTE24 or lead to an accumulation of farnesyl-prelamin A in cells
    Catherine 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...
  6. pmc Direct synthesis of lamin A, bypassing prelamin a processing, causes misshapen nuclei in fibroblasts but no detectable pathology in mice
    Catherine 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...
  7. pmc Understanding the roles of nuclear A- and B-type lamins in brain development
    Stephen 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...
  8. pmc A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation
    Shao 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...
  9. pmc Activating the synthesis of progerin, the mutant prelamin A in Hutchinson-Gilford progeria syndrome, with antisense oligonucleotides
    Loren 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...
  10. pmc The posttranslational processing of prelamin A and disease
    Brandon 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...
  11. pmc Farnesylation of lamin B1 is important for retention of nuclear chromatin during neuronal migration
    Hea Jin Jung
    Molecular Biology Institute, Department of Medicine, and Department of Human Genetics, University of California, Los Angeles, CA 90095, USA
    Proc Natl Acad Sci U S A 110:E1923-32. 2013
    ..Thus, farnesylation of lamin B1--but not lamin B2--is crucial for brain development and for retaining chromatin within the bounds of the nuclear lamina during neuronal migration...
  12. pmc Investigating the purpose of prelamin A processing
    Brandon Sj Davies
    Department of Medicine, University of California, Los Angeles, USA
    Nucleus 2:4-9. 2011
    ....
  13. pmc Regulation of prelamin A but not lamin C by miR-9, a brain-specific microRNA
    Hea 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...
  14. pmc 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...
  15. ncbi request reprint A protein farnesyltransferase inhibitor ameliorates disease in a mouse model of progeria
    Loren 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...
  16. pmc Development of the vertebral morphogenetic field in the mouse: interactions between Crossveinless-2 and Twisted Gastrulation
    Lise 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...
  17. pmc Mouse Crossveinless-2 is the vertebrate homolog of a Drosophila extracellular regulator of BMP signaling
    Catherine 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...
  18. pmc Crossveinless-2 Is a BMP feedback inhibitor that binds Chordin/BMP to regulate Xenopus embryonic patterning
    Andrea 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...
  19. ncbi request reprint Chordin-like CR domains and the regulation of evolutionarily conserved extracellular signaling systems
    Jose 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...
  20. pmc HIV-protease inhibitors block the enzymatic activity of purified Ste24p
    Sarah 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
    ....
  21. ncbi request reprint Selective deletion of the Hnf1beta (MODY5) gene in beta-cells leads to altered gene expression and defective insulin release
    Li 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...