David Ginsburg

Summary

Affiliation: University of Michigan
Country: USA

Publications

  1. ncbi request reprint The molecular biology of von Willebrand disease
    D Ginsburg
    Department of Internal Medicine, Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arbor, MI 48109 9650, USA
    Haemophilia 5:19-27. 1999
  2. ncbi request reprint Identifying novel genetic determinants of hemostatic balance
    D Ginsburg
    Department of Internal Medicine, Howard Hughes Medical Institute, University of Michigan, Life Sciences Institute, Ann Arbor, MI 48109 2216, USA
    J Thromb Haemost 3:1561-8. 2005
  3. doi request reprint Genetics and genomics to the clinic: a long road ahead
    David Ginsburg
    Howard Hughes Medical Institute, Department of Internal Medicine, and the Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA
    Cell 147:17-9. 2011
  4. pmc Combined deficiency of factor V and factor VIII is due to mutations in either LMAN1 or MCFD2
    Bin Zhang
    Life Sciences Institute, Department of Internal Medicine, 210 Washtenaw Ave, Ann Arbor, MI 48109 0650, USA
    Blood 107:1903-7. 2006
  5. pmc Reduced thrombin generation increases host susceptibility to group A streptococcal infection
    Hongmin Sun
    Department of Internal Medicine, University of Missouri Columbia, USA
    Blood 113:1358-64. 2009
  6. ncbi request reprint LMAN1 and MCFD2 form a cargo receptor complex and interact with coagulation factor VIII in the early secretory pathway
    Bin Zhang
    Life Sciences Institute, the Departments of Biological Chemistry, Internal Medicine, Human Genetics Howard Hughes Medical Institute, University of Michigan, Ann Arbor, Michigan 48109, USA
    J Biol Chem 280:25881-6. 2005
  7. pmc Modifiers of von Willebrand factor identified by natural variation in inbred strains of mice
    Jordan A Shavit
    Department of Pediatrics, University of Michigan, Ann Arbor, MI 48109, USA
    Blood 114:5368-74. 2009
  8. ncbi request reprint The murine platelet and plasma factor V pools are biosynthetically distinct and sufficient for minimal hemostasis
    Hongmin Sun
    Department of Internal Medicine, Division of Molecular Medicine and Genetics, University of Michigan, Ann Arbor, 48109, USA
    Blood 102:2856-61. 2003
  9. pmc Linkage analysis identifies a locus for plasma von Willebrand factor undetected by genome-wide association
    Karl C Desch
    Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, MI 48109, USA
    Proc Natl Acad Sci U S A 110:588-93. 2013
  10. pmc Selection on cis-regulatory variation at B4galnt2 and its influence on von Willebrand factor in house mice
    JILL M JOHNSEN
    Department of Internal Medicine, University of Michigan, USA
    Mol Biol Evol 26:567-78. 2009

Research Grants

Collaborators

Detail Information

Publications54

  1. ncbi request reprint The molecular biology of von Willebrand disease
    D Ginsburg
    Department of Internal Medicine, Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arbor, MI 48109 9650, USA
    Haemophilia 5:19-27. 1999
    ..However, the complex genetic factors determining the clinical severity of type 1 von Willebrand disease, the most common variant, still remain largely unknown and are the subject of current investigation...
  2. ncbi request reprint Identifying novel genetic determinants of hemostatic balance
    D Ginsburg
    Department of Internal Medicine, Howard Hughes Medical Institute, University of Michigan, Life Sciences Institute, Ann Arbor, MI 48109 2216, USA
    J Thromb Haemost 3:1561-8. 2005
    ..Ongoing studies in mice genetically engineered to carry the factor V Leiden mutation may similarly identify novel genes contributing to thrombosis risk in humans...
  3. doi request reprint Genetics and genomics to the clinic: a long road ahead
    David Ginsburg
    Howard Hughes Medical Institute, Department of Internal Medicine, and the Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA
    Cell 147:17-9. 2011
    ..This perspective will take brief stock of what genetics/genomics have brought to clinical practice to date and what we might expect for the future...
  4. pmc Combined deficiency of factor V and factor VIII is due to mutations in either LMAN1 or MCFD2
    Bin Zhang
    Life Sciences Institute, Department of Internal Medicine, 210 Washtenaw Ave, Ann Arbor, MI 48109 0650, USA
    Blood 107:1903-7. 2006
    ....
  5. pmc Reduced thrombin generation increases host susceptibility to group A streptococcal infection
    Hongmin Sun
    Department of Internal Medicine, University of Missouri Columbia, USA
    Blood 113:1358-64. 2009
    ....
  6. ncbi request reprint LMAN1 and MCFD2 form a cargo receptor complex and interact with coagulation factor VIII in the early secretory pathway
    Bin Zhang
    Life Sciences Institute, the Departments of Biological Chemistry, Internal Medicine, Human Genetics Howard Hughes Medical Institute, University of Michigan, Ann Arbor, Michigan 48109, USA
    J Biol Chem 280:25881-6. 2005
    ..MCFD2 may function to specifically recruit factor V and factor VIII to sites of transport vesicle budding within the endoplasmic reticulum lumen...
  7. pmc Modifiers of von Willebrand factor identified by natural variation in inbred strains of mice
    Jordan A Shavit
    Department of Pediatrics, University of Michigan, Ann Arbor, MI 48109, USA
    Blood 114:5368-74. 2009
    ..Mvwf6 displays conservation of synteny with potential VWF modifier loci identified in human pedigrees, suggesting that its ortholog may modify VWF in human populations...
  8. ncbi request reprint The murine platelet and plasma factor V pools are biosynthetically distinct and sufficient for minimal hemostasis
    Hongmin Sun
    Department of Internal Medicine, Division of Molecular Medicine and Genetics, University of Michigan, Ann Arbor, 48109, USA
    Blood 102:2856-61. 2003
    ..In addition, these findings indicate that the murine platelet and plasma FV pools are biosynthetically distinct, in contrast to a previous report demonstrating a plasma origin for platelet FV in humans...
  9. pmc Linkage analysis identifies a locus for plasma von Willebrand factor undetected by genome-wide association
    Karl C Desch
    Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, MI 48109, USA
    Proc Natl Acad Sci U S A 110:588-93. 2013
    ..These results raise the possibility that similar loci could explain a significant portion of the "missing heritability" for other complex genetic traits...
  10. pmc Selection on cis-regulatory variation at B4galnt2 and its influence on von Willebrand factor in house mice
    JILL M JOHNSEN
    Department of Internal Medicine, University of Michigan, USA
    Mol Biol Evol 26:567-78. 2009
    ..Similar mechanisms may account for the variability in VWF levels and high prevalence of VWD in other mammals, including humans...
  11. pmc Spontaneous Irs1 passenger mutation linked to a gene-targeted SerpinB2 allele
    Randal J Westrick
    Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA
    Proc Natl Acad Sci U S A 107:16904-9. 2010
    ..When linked to a targeted allele, such mutations could lead to incorrect assignment of phenotype and may account for a subset of markedly discordant results from experiments independently targeting the same gene...
  12. pmc Enhanced VWF biosynthesis and elevated plasma VWF due to a natural variant in the murine Vwf gene
    Heidi L Lemmerhirt
    Howard Hughes Medical Institute, University of Michigan, 210 Washtenaw, Life Sciences Institute, Rm 5028, Ann Arbor, MI 48109, USA
    Blood 108:3061-7. 2006
    ..The identification of a natural Vwf gene variant among inbred mice affecting biosynthesis suggests that similar genetic variation may contribute to the wide range of VWF levels observed in humans...
  13. pmc Inhibitor of streptokinase gene expression improves survival after group A streptococcus infection in mice
    Hongmin Sun
    Department of Internal Medicine, University of Missouri Hospital and Clinics, Columbia, MO 65212, USA
    Proc Natl Acad Sci U S A 109:3469-74. 2012
    ..These data suggest that the class of compounds represented by CCG-2979 may be of therapeutic value for the treatment of GAS and potentially other gram-positive infections in humans...
  14. pmc The endothelial-specific regulatory mutation, Mvwf1, is a common mouse founder allele
    JILL M JOHNSEN
    Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, 48109 2216, USA
    Mamm Genome 19:32-40. 2008
    ..Similar selective pressures could contribute to the high prevalence of von Willebrand disease in humans...
  15. ncbi request reprint Plasminogen is a critical host pathogenicity factor for group A streptococcal infection
    Hongmin Sun
    Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA
    Science 305:1283-6. 2004
    ..In addition, local fibrin clot formation may be implicated in host defense against microbial pathogens...
  16. ncbi request reprint Atherosclerosis progression in LDL receptor-deficient and apolipoprotein E-deficient mice is independent of genetic alterations in plasminogen activator inhibitor-1
    H Sjöland
    Division of Cardiology, Department of Internal Medicine, Howard Hughes Medical Institute, University of Michigan Medical Center, Ann Arbor 48109 0644, USA
    Arterioscler Thromb Vasc Biol 20:846-52. 2000
    ....
  17. pmc Fatal hemorrhage in mice lacking gamma-glutamyl carboxylase
    Aihua Zhu
    Howard Hughes Medical Institute, University of Michigan, Ann Arbor, MI 48109, USA
    Blood 109:5270-5. 2007
    ....
  18. pmc pak2a mutations cause cerebral hemorrhage in redhead zebrafish
    David A Buchner
    Howard Hughes Medical Institute and Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA
    Proc Natl Acad Sci U S A 104:13996-4001. 2007
    ..These data provide in vivo evidence for a critical function of Pak2 in vascular integrity and demonstrate a severe disease phenotype resulting from loss of Pak2 function...
  19. pmc The COPII pathway and hematologic disease
    Rami Khoriaty
    Department of Hematology and Oncology, University of Michigan, Ann Arbor, MI, USA
    Blood 120:31-8. 2012
    ..These diseases and their molecular pathogenesis are the focus of this review...
  20. ncbi request reprint Homozygosity for factor V Leiden leads to enhanced thrombosis and atherosclerosis in mice
    Daniel T Eitzman
    Division of Cardiology, University of Michigan Medical Center, Ann Arbor 48109 0644, USA
    Circulation 111:1822-5. 2005
    ..Although the impact of FVL on the development of venous thrombosis is well established, its effect on arterial thrombosis and atherosclerosis is controversial...
  21. pmc Vitronectin is not essential for normal mammalian development and fertility
    X Zheng
    Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109 0650, USA
    Proc Natl Acad Sci U S A 92:12426-30. 1995
    ..These observations demonstrate that VN is not essential for cell adhesion and migration during normal mouse development and suggest that its role in these processes may partially overlap with other adhesive matrix components...
  22. ncbi request reprint Vitronectin inhibits the thrombotic response to arterial injury in mice
    W P Fay
    Departments of Internal Medicine and Human Genetics and the Howard Hughes Medical Institute, University of Michigan, Ann Arbor, MI, USA
    Blood 93:1825-30. 1999
    ....
  23. ncbi request reprint Plasminogen activator inhibitor-1 and vitronectin promote vascular thrombosis in mice
    D T Eitzman
    Cardiovascular Research Center and Division of Molecular Medicine and Human Genetics, Department of Internal Medicine, and the Howard Hughes Medical Institute, University of Michigan Medical Center, Ann Arbor, MI 49109 0644, USA
    Blood 95:577-80. 2000
    ..01 compared to WT mice). These results suggest that endogenous fibrinolysis and its regulation by PAI-1 and VN have important roles in the development of occlusive vascular thrombosis after vascular injury. (Blood. 2000;95:577-580)..
  24. ncbi request reprint Plasminogen activator inhibitor-1 deficiency protects against atherosclerosis progression in the mouse carotid artery
    D T Eitzman
    Divisions of Cardiology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI, USA
    Blood 96:4212-5. 2000
    ..Blood. 2000;96:4212-4215)..
  25. ncbi request reprint Hyperlipidemia promotes thrombosis after injury to atherosclerotic vessels in apolipoprotein E-deficient mice
    D T Eitzman
    Cardiovascular Research Center, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109 0644, USA
    Arterioscler Thromb Vasc Biol 20:1831-4. 2000
    ....
  26. doi request reprint Targeted gene sequencing identifies variants in the protein C and endothelial protein C receptor genes in patients with unprovoked venous thromboembolism
    Cynthia Wu
    From the Department of Clinical Hematology, University of Alberta, Edmonton, Alberta, Canada C W Departments of Medicine D J D, J I W, C K, P C L, Department of Medical Sciences L P, Z L, Department of Pathology and Molecular Medicine J W, and Oncology J J, Thrombosis and Atherosclerosis Research Institute D J D, L P, Z L, J I W, P C L, McMaster University, Hamilton, Ontario, Canada and Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, Michigan K D, D G
    Arterioscler Thromb Vasc Biol 33:2674-81. 2013
    ....
  27. doi request reprint Exocyst function is regulated by effector phosphorylation
    Xiao Wei Chen
    Life Sciences Institute, University of Michigan Medical Center, Ann Arbor, Michigan 48109, USA
    Nat Cell Biol 13:580-8. 2011
    ..The exocyst thus serves as a 'gatekeeper' for exocytic vesicles through a circuit of engagement, disengagement and re-engagement with G proteins...
  28. pmc Transgenic overexpression of a stable Plasminogen Activator Inhibitor-1 variant
    Abigail T Fahim
    Department of Human Genetics, University of Michigan, Ann Arbor, MI, United States
    Thromb Res 123:785-92. 2009
    ..This study aimed to engineer transgenic overexpression of a stable murine PAI-1 variant to examine the physiologic effects in vivo from delayed transition of PAI-1 to latency...
  29. ncbi request reprint Mvwf, a dominant modifier of murine von Willebrand factor, results from altered lineage-specific expression of a glycosyltransferase
    K L Mohlke
    Howard Hughes Medical Institute, The University of Michigan, Ann Arbor 48109 0650, USA
    Cell 96:111-20. 1999
    ..These findings identify alterations in glycosyltransferase function as a potential general mechanism for the genetic modification of plasma protein levels...
  30. pmc The plasminogen activator inhibitor-2 gene is not required for normal murine development or survival
    K M Dougherty
    Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arbor, MI 48109 0650, USA
    Proc Natl Acad Sci U S A 96:686-91. 1999
    ..Finally, crossing PAI-2 -/- with PAI-1 -/- mice to generate animals deficient in both plasminogen activator inhibitors failed to uncover an overlap in function between these two related proteins...
  31. ncbi request reprint Fatal haemorrhage and incomplete block to embryogenesis in mice lacking coagulation factor V
    J Cui
    Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arbor, USA
    Nature 384:66-8. 1996
    ....
  32. ncbi request reprint Mutations in the ER-Golgi intermediate compartment protein ERGIC-53 cause combined deficiency of coagulation factors V and VIII
    W C Nichols
    Department of Internal Medicine, University of Michigan, Ann Arbor 48109 0650, USA
    Cell 93:61-70. 1998
    ..These findings suggest that ERGIC-53 may function as a molecular chaperone for the transport from ER to Golgi of a specific subset of secreted proteins, including coagulation factors V and VIII...
  33. pmc Shigatoxin triggers thrombotic thrombocytopenic purpura in genetically susceptible ADAMTS13-deficient mice
    David G Motto
    Department of Pediatrics, University of Michigan, Ann Arbor, Michigan 48109, USA
    J Clin Invest 115:2752-61. 2005
    ..These data suggest that microbe-derived toxins (or possibly other sources of endothelial injury), together with additional genetic susceptibility factors, are required to trigger TTP in the setting of ADAMTS13 deficiency...
  34. pmc Functional display of platelet-binding VWF fragments on filamentous bacteriophage
    Andrew Yee
    Life Sciences Institute, University of Michigan, Ann Arbor, Michigan, United States of America
    PLoS ONE 8:e73518. 2013
    ..These findings also point to key structural elements within the A1 domain that regulate VWF-platelet adhesion. ..
  35. pmc SEC24A deficiency lowers plasma cholesterol through reduced PCSK9 secretion
    Xiao Wei Chen
    Life Sciences Institute, University of Michigan, Ann Arbor, United States
    elife 2:e00444. 2013
    ..DOI:http://dx.doi.org/10.7554/eLife.00444.001...
  36. ncbi request reprint Bleeding due to disruption of a cargo-specific ER-to-Golgi transport complex
    Bin Zhang
    Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109 0650, USA
    Nat Genet 34:220-5. 2003
    ..MCFD2 is localized to the ERGIC through a direct, calcium-dependent interaction with LMAN1. These findings suggest that the MCFD2-LMAN1 complex forms a specific cargo receptor for the ER-to-Golgi transport of selected proteins...
  37. ncbi request reprint Getting secretory granules ready for prime time
    Bin Zhang
    Howard Hughes Medical Institute and Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA
    Cell 115:372-3. 2003
    ..identify mutations in Munc13-4 as a cause of familial hemophagocytic lymphohistiocytosis. Munc13-4 appears to be involved in the priming of cytotoxic granules prior to fusion with the plasma membrane...
  38. pmc Analysis of informed consent document utilization in a minimal-risk genetic study
    Karl Desch
    University of Michigan, Ann Arbor, USA
    Ann Intern Med 155:316-22. 2011
    ..Despite efforts to optimize the informed consent document, only limited data are available about the actual use of consent documents by participants in biomedical research...
  39. ncbi request reprint Biosynthetic origin and functional significance of murine platelet factor V
    Tony L Yang
    Department of Human Genetics, University of Michigan, Ann Arbor, MI 48109, USA
    Blood 102:2851-5. 2003
    ....
  40. ncbi request reprint Distant conserved sequences flanking endothelial-specific promoters contain tissue-specific DNase-hypersensitive sites and over-represented motifs
    John A Bernat
    Department of Human Genetics, Howard Hughes Medical Institute, USA
    Hum Mol Genet 15:2098-105. 2006
    ..This motif contains the core element of binding sites from the Ets family of transcription factors. Thus, one or several factors from this family may play a key role in the regulation of endothelial gene expression...
  41. ncbi request reprint Lethal perinatal thrombosis in mice resulting from the interaction of tissue factor pathway inhibitor deficiency and factor V Leiden
    Daniel T Eitzman
    Division of Cardiology, University of Michigan Medical Center, Ann Arbor, Mich 48109 0644, USA
    Circulation 105:2139-42. 2002
    ..Variation in the expression of tissue factor pathway inhibitor (TFPI) has also been proposed as a risk factor for venous thrombosis and has been shown to enhance the prothrombotic effect of FVL in vitro...
  42. pmc What a polyclonal antibody sees in von Willebrand factor
    Fen Lai Tan
    Department of Internal Medicine, Life Science Institute, Howard Hughes Medical Institute, University of Michigan School of Medicine, Ann Arbor, MI 48109, USA
    Thromb Res 121:519-26. 2008
    ..Von Willebrand factor (VWF) plays a critical role in hemostasis by carrying factor VIII (FVIII) and binding to specific ligands on the surface of blood platelets and within the blood vessel wall...
  43. ncbi request reprint von Willebrand disease in the RIIIS/J mouse is caused by a defect outside of the von Willebrand factor gene
    W C Nichols
    Howard Hughes Medical Institute, Ann Arbor, MI
    Blood 83:3225-31. 1994
    ..These observations may provide new insights into the molecular basis and variable expressivity of human vWD...
  44. pmc Analysis of the relationship of von Willebrand disease (vWD) and hereditary hemorrhagic telangiectasia and identification of a potential type IIA vWD mutation (IIe865 to Thr)
    M C Iannuzzi
    Department of Internal Medicine, Howard Hughes Medical Institute, Ann Arbor, MI
    Am J Hum Genet 48:757-63. 1991
    ..This substitution is located immediately adjacent to two previously identified type IIA vWD mutations...
  45. ncbi request reprint Comparative mapping of distal murine chromosome 11 and human 17q21.3 in a region containing a modifying locus for murine plasma von Willebrand factor level
    K L Mohlke
    Department of Human Genetics, University of Michigan Medical School, Ann Arbor, Michigan, 48109, USA
    Genomics 54:19-30. 1998
    ..These data may also aid in the localization of other disease loci mapped to this region, including the gene for tricho-dento-osseous syndrome and a murine locus for susceptibility to ozone-induced acute lung injury...
  46. doi request reprint Modifier genes for disorders of thrombosis and hemostasis
    R J Westrick
    Department of Human Genetics, University of Michigan, Ann Arbor, MI 48109, USA
    J Thromb Haemost 7:132-5. 2009
    ....
  47. ncbi request reprint Familial multiple coagulation factor deficiencies: new biologic insight from rare genetic bleeding disorders
    B Zhang
    Department of Internal Medicine and Human Genetics, University of Michigan, Ann Arbor, MI 48109 0650, USA
    J Thromb Haemost 2:1564-72. 2004
    ..The multiple coagulation factor deficiencies provide a notable example of important basic biological insight gained through the study of rare human diseases...
  48. ncbi request reprint Rescue of fatal neonatal hemorrhage in factor V deficient mice by low level transgene expression
    T L Yang
    Department of Human Genetics, University of Michigan, Ann Arbor, USA
    Thromb Haemost 83:70-7. 2000
    ....
  49. ncbi request reprint The structure and function of murine factor V and its inactivation by protein C
    T L Yang
    Department of Human Genetics, University of Michigan Medical School, Ann Arbor, MI 48109 0650, USA
    Blood 91:4593-9. 1998
    ..Thus, the structure and function of FV and its interaction with APC are highly conserved across mammalian species...
  50. ncbi request reprint Getting at the variable expressivity of von Willebrand disease
    G Levy
    Program in Cellular and Molecular Biology, University of Michigan, Ann Arbor, USA
    Thromb Haemost 86:144-8. 2001
    ..This review will focus on the current understanding of the genetic causes for variation in VWF level, and will highlight future directions for getting at the variable expressivity of von Willebrand disease...
  51. ncbi request reprint Mutations in a member of the ADAMTS gene family cause thrombotic thrombocytopenic purpura
    G G Levy
    Howard Hughes Medical Institute, Departments of Internal Medicine and Human Genetics, and Cellular and Molecular Biology Program, University of Michigan Medical Center, Ann Arbor, Michigan 48109, USA
    Nature 413:488-94. 2001
    ..We show that deficiency of ADAMTS13 is the molecular mechanism responsible for TTP, and suggest that physiologic proteolysis of VWF and/or other ADAMTS13 substrates is required for normal vascular homeostasis...
  52. pmc Genetic regulation of plasma von Willebrand factor levels: quantitative trait loci analysis in a mouse model
    H L Lemmerhirt
    Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA
    J Thromb Haemost 5:329-35. 2007
    ..We have previously mapped two genes contributing to the regulation of plasma VWF levels in mice (Mvwf1 on chromosome 11 and Mvwf2 on chromosome 6)...
  53. ncbi request reprint LMAN1 is a molecular chaperone for the secretion of coagulation factor VIII
    M A Cunningham
    Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor, MI 48109 0650, USA
    J Thromb Haemost 1:2360-7. 2003
    ..These results are interpreted based on the recent determination of the crystal structure of the carbohydrate recognition domain of LMAN1...
  54. ncbi request reprint Characterization of Leu777Pro and Ile865Thr type IIA von Willebrand disease mutations
    S E Lyons
    Program in Cellular and Molecular Biology, Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arbor
    Blood 83:1551-7. 1994
    ..An increase in the proportion of high molecular weight multimers observed in type IIA vWD patient plasma, after renal transplantation from a normal donor, suggests that the kidney endothelium may be a major source of plasma vWF...

Research Grants7

  1. CKIS AND CONTROL OF VASCULAR SMOOTH MUSCLE CELL CYCLE
    David Ginsburg; Fiscal Year: 2001
    ..An understanding of these mechanisms should lend insight into the pathophysiology of vascular diseases, and determine whether enhancement of p21 and p27 expression in arteries may limit excessive vsmc proliferation in these diseases. ..
  2. 2002 Gordon Research Conference on Hemostasis
    David Ginsburg; Fiscal Year: 2002
    ..The extensive interactions and discussion that will occur at this conference will help identify new areas and directions for future research...
  3. Expression of Myomesin and SLIM1 in Heart Failure
    Fen Lai Tan; Fiscal Year: 2004
    ..abstract_text> ..
  4. MOLECULAR GENETIC STUDY OF VONWILLEBRAND FACTOR
    David Ginsburg; Fiscal Year: 2007
    ..The results of these studies should offer new insight into the biology of endothelial cell function and VWF biosynthesis and may also lead to improved diagnosis and therapy for VWD and thrombophilia. ..