M O Bergo

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi Targeted inactivation of the isoprenylcysteine carboxyl methyltransferase gene causes mislocalization of K-Ras in mammalian cells
    M O Bergo
    Gladstone Institute of Cardiovascular Disease, Cardiovascular Research Institute, and Department of Medicine, University of California, San Francisco, California 94141 9100, USA
    J Biol Chem 275:17605-10. 2000
  2. ncbi Genetic and pharmacologic analyses of the role of Icmt in Ras membrane association and function
    Annika W Svensson
    Wallenberg Laboratory, Department of Internal Medicine, Sahlgrenska University Hospital, Sweden
    Methods Enzymol 407:144-59. 2006
  3. ncbi Defining the importance of phosphatidylserine synthase 2 in mice
    Martin O Bergo
    Gladstone Institute of Cardiovascular Disease, San Francisco, CA 94141 9100, USA
    J Biol Chem 277:47701-8. 2002
  4. pmc Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect
    Martin O Bergo
    Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, CA 94141 9100, USA
    Proc Natl Acad Sci U S A 99:13049-54. 2002
  5. pmc Inactivation of Icmt inhibits transformation by oncogenic K-Ras and B-Raf
    Martin O Bergo
    Gladstone Institute of Cardiovascular Disease, San Francisco, California 94141 9100, USA
    J Clin Invest 113:539-50. 2004
  6. ncbi Isoprenylcysteine carboxyl methyltransferase deficiency in mice
    M O Bergo
    Gladstone Institute of Cardiovascular Disease, The Cardiovascular Research Institute, University of California, San Francisco, California 94141 9100, USA
    J Biol Chem 276:5841-5. 2001
  7. pmc Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmpste24-deficient mice
    Loren G Fong
    Department of Medicine, University of California, Los Angeles, CA 90095, USA
    Proc Natl Acad Sci U S A 101:18111-6. 2004
  8. ncbi Biochemical studies of Zmpste24-deficient mice
    G K Leung
    Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, California 94141 9100, USA
    J Biol Chem 276:29051-8. 2001
  9. pmc Prelamin A and lamin A appear to be dispensable in the nuclear lamina
    Loren G Fong
    Department of Medicine Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA
    J Clin Invest 116:743-52. 2006
  10. pmc Absence of the CAAX endoprotease Rce1: effects on cell growth and transformation
    Martin O Bergo
    Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, California 94141 9100, USA
    Mol Cell Biol 22:171-81. 2002

Collaborators

Detail Information

Publications30

  1. ncbi Targeted inactivation of the isoprenylcysteine carboxyl methyltransferase gene causes mislocalization of K-Ras in mammalian cells
    M O Bergo
    Gladstone Institute of Cardiovascular Disease, Cardiovascular Research Institute, and Department of Medicine, University of California, San Francisco, California 94141 9100, USA
    J Biol Chem 275:17605-10. 2000
    ..We conclude that carboxyl methylation of the isoprenylcysteine is important for proper K-Ras localization in mammalian cells...
  2. ncbi Genetic and pharmacologic analyses of the role of Icmt in Ras membrane association and function
    Annika W Svensson
    Wallenberg Laboratory, Department of Internal Medicine, Sahlgrenska University Hospital, Sweden
    Methods Enzymol 407:144-59. 2006
    ....
  3. ncbi Defining the importance of phosphatidylserine synthase 2 in mice
    Martin O Bergo
    Gladstone Institute of Cardiovascular Disease, San Francisco, CA 94141 9100, USA
    J Biol Chem 277:47701-8. 2002
    ..We conclude that Pss2 is responsible for the majority of serine exchange activity in in vitro assays, but a deficiency in this enzyme does not cause perturbations in phospholipid content or severe developmental abnormalities...
  4. pmc Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect
    Martin O Bergo
    Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, CA 94141 9100, USA
    Proc Natl Acad Sci U S A 99:13049-54. 2002
    ..Muscle weakness in Zmpste24(-/-) mice can be reasonably ascribed to defective processing of prelamin A, but the brittle bone phenotype suggests a broader role for Zmpste24 in mammalian biology...
  5. pmc Inactivation of Icmt inhibits transformation by oncogenic K-Ras and B-Raf
    Martin O Bergo
    Gladstone Institute of Cardiovascular Disease, San Francisco, California 94141 9100, USA
    J Clin Invest 113:539-50. 2004
    ..These studies identify Icmt as a potential target for reducing the growth of K-Ras- and B-Raf-induced malignancies...
  6. ncbi Isoprenylcysteine carboxyl methyltransferase deficiency in mice
    M O Bergo
    Gladstone Institute of Cardiovascular Disease, The Cardiovascular Research Institute, University of California, San Francisco, California 94141 9100, USA
    J Biol Chem 276:5841-5. 2001
    ..g. N-acetyl-S-geranylgeranyl-l-cysteine). In addition, Icmt-/- cells lacked the ability to methylate Rab proteins. Thus, Icmt appears to be the only enzyme participating in the carboxyl methylation of isoprenylated proteins...
  7. pmc Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmpste24-deficient mice
    Loren G Fong
    Department of Medicine, University of California, Los Angeles, CA 90095, USA
    Proc Natl Acad Sci U S A 101:18111-6. 2004
    ..These data suggest that prelamin A is toxic and that reducing its levels by as little as 50% provides striking protection from disease...
  8. ncbi Biochemical studies of Zmpste24-deficient mice
    G K Leung
    Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, California 94141 9100, USA
    J Biol Chem 276:29051-8. 2001
    ..Thus, both enzymatic activities of yeast Ste24p are conserved in mouse Zmpste24, but these enzymatic activities are not essential for mouse development or for fertility...
  9. pmc Prelamin A and lamin A appear to be dispensable in the nuclear lamina
    Loren G Fong
    Department of Medicine Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA
    J Clin Invest 116:743-52. 2006
    ..These studies suggest a new therapeutic strategy for treating progeria and other lamin A diseases...
  10. pmc Absence of the CAAX endoprotease Rce1: effects on cell growth and transformation
    Martin O Bergo
    Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, California 94141 9100, USA
    Mol Cell Biol 22:171-81. 2002
    ..These studies support the idea that interference with postisoprenylation processing retards cell growth, limits Ras-induced transformation, and sensitizes tumor cells to a farnesyltransferase inhibitor...
  11. ncbi N-myristoyltransferase 1 is essential in early mouse development
    Shao H Yang
    Department of Medicine, University of California, Los Angeles, California 90095, USA
    J Biol Chem 280:18990-5. 2005
    ..We conclude that Nmt1 is not essential for the viability of mammalian cells but is required for development, likely because it is the principal N-myristoyltransferase in early embryogenesis...
  12. ncbi Blocking the secretion of hepatic very low density lipoproteins renders the liver more susceptible to toxin-induced injury
    Johan Björkegren
    Gladstone Institute of Cardiovascular Disease, Cardiovascular Research Institute, University of California, San Francisco 94110, USA
    J Biol Chem 277:5476-83. 2002
    ..Our results suggest that blocking lipoprotein secretion in the liver may increase the susceptibility of the liver to certain toxic challenges...
  13. ncbi On the physiological importance of endoproteolysis of CAAX proteins: heart-specific RCE1 knockout mice develop a lethal cardiomyopathy
    Martin O Bergo
    Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, California 94141 9100, USA
    J Biol Chem 279:4729-36. 2004
    ..These studies indicate that the endoproteolytic processing of CAAX proteins is essential for cardiac function but is less important for the liver...
  14. pmc Blocking protein farnesyltransferase improves nuclear blebbing in mouse fibroblasts with a targeted Hutchinson-Gilford progeria syndrome mutation
    Shao H Yang
    Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
    Proc Natl Acad Sci U S A 102:10291-6. 2005
    ..0001 by chi2 statistic). These studies suggest a possible treatment strategy for HGPS...
  15. ncbi Protein farnesyltransferase inhibitors and progeria
    Margarita Meta
    Department of Medicine, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
    Trends Mol Med 12:480-7. 2006
    ..In addition, recent data showing that FTIs ameliorate disease phenotypes in a pair of mouse models of progeria are discussed...
  16. pmc Genetic studies on the functional relevance of the protein prenyltransferases in skin keratinocytes
    Roger Lee
    Department of Medicine, David Geffen School of Medicine, University of California, LA, Los Angeles, CA 90095, USA
    Hum Mol Genet 19:1603-17. 2010
    ..Like Fntb-deficient keratinocytes, Pggt1b-deficient keratinocytes did not proliferate in culture. Thus, both FTase and GGTase-I are required for the homeostasis of skin keratinocytes...
  17. pmc Lamin B1 is required for mouse development and nuclear integrity
    Laurent Vergnes
    Veterans Affairs Greater Los Angeles Healthcare System, David Geffen School of Medicine, University of California, Los Angeles, CA 90073, USA
    Proc Natl Acad Sci U S A 101:10428-33. 2004
    ..These mutant mice and cell lines derived from them will be useful models for studying the role of the nuclear lamina in various cellular processes...
  18. 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...
  19. pmc Caution! Analyze transcripts from conditional knockout alleles
    Shao H Yang
    Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
    Transgenic Res 18:483-9. 2009
    ..With thousands of new conditional knockout alleles under construction within mouse mutagenesis consortiums, the protein farnesyltransferase allele holds an important lesson-to characterize knockout alleles at both the DNA and RNA levels...
  20. pmc Inactivating Icmt ameliorates K-RAS-induced myeloproliferative disease
    Annika M Wahlstrom
    Wallenberg Laboratory, Institute of Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden
    Blood 112:1357-65. 2008
    ..Finally, inactivating Icmt reduced lung tumor development and myeloproliferation phenotypes in a mouse model of K-RAS-induced cancer. We conclude that inactivation of Icmt ameliorates phenotypes of K-RAS-induced malignancies in vivo...
  21. pmc Filamin B deficiency in mice results in skeletal malformations and impaired microvascular development
    Xianghua Zhou
    Sahlgrenska Center for Cardiovascular and Metabolic Research, Wallenberg Laboratory, Goteborg University, SE 413 45 Goteborg, Sweden
    Proc Natl Acad Sci U S A 104:3919-24. 2007
    ..These mice died or had to be euthanized before 4 weeks of age. Thus, the phenotypes of Flnb-deficient mice closely resemble those of human skeletal disorders with mutations in FLNB...
  22. pmc Rce1 deficiency accelerates the development of K-RAS-induced myeloproliferative disease
    Annika M Wahlstrom
    Wallenberg Laboratory, Department of Medicine, Sahlgrenska University Hospital, S 413 45 Gothenburg, Sweden
    Blood 109:763-8. 2007
    ..We conclude that the inactivation of Rce1 worsens the myeloproliferative disease caused by oncogenic K-RAS...
  23. pmc Targeting Ras signaling through inhibition of carboxyl methylation: an unexpected property of methotrexate
    Ann M Winter-Vann
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    Proc Natl Acad Sci U S A 100:6529-34. 2003
    ..These results suggest that inhibition of Icmt is a critical component of the antiproliferative effect of methotrexate, expanding our understanding of this widely used drug and identifying Icmt as a target for drug discovery...
  24. pmc Endoproteolytic processing of RhoA by Rce1 is required for the cleavage of RhoA by Yersinia enterocolitica outer protein T
    Florian Fueller
    Institute for Experimental and Clinical Pharmacology and Toxicology, Albert Ludwigs University of Freiburg, Albert Str 25, 79104 Freiburg, Germany
    Infect Immun 74:1712-7. 2006
    ..Our data demonstrate that Rce1-mediated removal of -aaX from isoprenylated Rho GTPases is required for the proteolytic activity of YopT in living cells, whereas carboxyl methylation by Icmt is not...
  25. ncbi Tumor necrosis factor alpha stimulation of Rac1 activity. Role of isoprenylcysteine carboxylmethyltransferase
    Christopher Papaharalambus
    Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia 30322, USA
    J Biol Chem 280:18790-6. 2005
    ..These results suggest that ICMT regulates Rac1 activity by controlling the interaction of Rac1 with RhoGDI. We hypothesize that ICMT regulates the release of Rac1 from RhoGDI...
  26. pmc A small-molecule inhibitor of isoprenylcysteine carboxyl methyltransferase with antitumor activity in cancer cells
    Ann M Winter-Vann
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    Proc Natl Acad Sci U S A 102:4336-41. 2005
    ..These findings provide a compelling rationale for development of Icmt inhibitors as another approach to anticancer drug development...
  27. pmc Genetic analyses of the role of RCE1 in RAS membrane association and transformation
    Martin O Bergo
    Wallenberg Laboratory, Department of Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden
    Methods Enzymol 438:367-89. 2008
    ..Here, we will review methods that have been used to define the physiologic importance of the endoproteolytic processing step of CAAX protein processing...
  28. pmc GGTase-I deficiency reduces tumor formation and improves survival in mice with K-RAS-induced lung cancer
    Anna Karin M Sjogren
    Wallenberg Laboratory, Institute of Medicine, Sahlgrenska University Hospital, S 413 45 Goteborg, Sweden
    J Clin Invest 117:1294-304. 2007
    ..Interestingly, several cell types remained viable in the absence of GGTase-I, and myelopoiesis appeared to function normally. These findings suggest that inhibiting GGTase-I may be a useful strategy to treat K-RAS-induced malignancies...
  29. pmc A carboxyl-terminal interaction of lamin B1 is dependent on the CAAX endoprotease Rce1 and carboxymethylation
    Christopher P Maske
    Sir William Dunn School of Pathology, University of Oxford, Oxford, OX1 3RE, UK
    J Cell Biol 162:1223-32. 2003
    ..These data show that the organization of the nuclear envelope and lamina is dependent on a mechanism involving the methylation of lamin B1, and they identify a potential mechanism of laminopathy involving a B-type lamin...
  30. ncbi Extra Rabs unsnarl a lipid traffic jam
    Martin O Bergo
    Nat Med 8:662-4. 2002