G J Nabel

Summary

Affiliation: University of Michigan
Country: USA

Publications

  1. pmc Development of optimized vectors for gene therapy
    G J Nabel
    Howard Hughes Medical Institute, Department of Internal Medicine and Biological Chemistry, University of Michigan, 1150 West Medical Center Drive, 4520 MSRB I, Ann Arbor, MI 48109 0650, USA
    Proc Natl Acad Sci U S A 96:324-6. 1999
  2. pmc Role of the p21 cyclin-dependent kinase inhibitor in limiting intimal cell proliferation in response to arterial injury
    Z Y Yang
    Department of Internal Medicine, University of Michigan, Ann Arbor 48109, USA
    Proc Natl Acad Sci U S A 93:7905-10. 1996
  3. ncbi request reprint Regulation of the proinflammatory effects of Fas ligand (CD95L)
    J J Chen
    Howard Hughes Medical Institute, University of Michigan Medical Center, Departments of Internal Medicine and Biological Chemistry, 1150 West Medical Center Drive, 4520 Medical Science Research Building I, Ann Arbor, MI 48109 0650, USA
    Science 282:1714-7. 1998
  4. ncbi request reprint Distinct cellular interactions of secreted and transmembrane Ebola virus glycoproteins
    Z Yang
    Howard Hughes Medical Institute and Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA
    Science 279:1034-7. 1998
  5. ncbi request reprint Development of molecular genetic interventions for HIV infection
    C Woffendin
    University of Michigan Medical Center, Ann Arbor, Michigan, USA
    Curr Protoc Hum Genet . 2001
  6. pmc Gene transfer of Fas ligand induces tumor regression in vivo
    H Arai
    Howard Hughes Medical Institute, University of Michigan Medical Center, 1150 West Medical Center Drive, 4520 MSRB I, Ann Arbor, MI 48109 0650, USA
    Proc Natl Acad Sci U S A 94:13862-7. 1997

Collaborators

Detail Information

Publications6

  1. pmc Development of optimized vectors for gene therapy
    G J Nabel
    Howard Hughes Medical Institute, Department of Internal Medicine and Biological Chemistry, University of Michigan, 1150 West Medical Center Drive, 4520 MSRB I, Ann Arbor, MI 48109 0650, USA
    Proc Natl Acad Sci U S A 96:324-6. 1999
  2. pmc Role of the p21 cyclin-dependent kinase inhibitor in limiting intimal cell proliferation in response to arterial injury
    Z Y Yang
    Department of Internal Medicine, University of Michigan, Ann Arbor 48109, USA
    Proc Natl Acad Sci U S A 93:7905-10. 1996
    ....
  3. ncbi request reprint Regulation of the proinflammatory effects of Fas ligand (CD95L)
    J J Chen
    Howard Hughes Medical Institute, University of Michigan Medical Center, Departments of Internal Medicine and Biological Chemistry, 1150 West Medical Center Drive, 4520 Medical Science Research Building I, Ann Arbor, MI 48109 0650, USA
    Science 282:1714-7. 1998
    ..Providing TGF-beta to subcutaneous sites protected against tumor rejection. Thus, these cytokines together generate a microenvironment that promotes immunologic tolerance, which may aid in the amelioration of allograft rejection...
  4. ncbi request reprint Distinct cellular interactions of secreted and transmembrane Ebola virus glycoproteins
    Z Yang
    Howard Hughes Medical Institute and Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA
    Science 279:1034-7. 1998
    ....
  5. ncbi request reprint Development of molecular genetic interventions for HIV infection
    C Woffendin
    University of Michigan Medical Center, Ann Arbor, Michigan, USA
    Curr Protoc Hum Genet . 2001
    ..To monitor the effectiveness of gene transfer, genomic DNA is prepared from the patient's cells. Detection of vector DNA by PCR analysis of the patient's genomic DNA following gene transfer is also described in detail...
  6. pmc Gene transfer of Fas ligand induces tumor regression in vivo
    H Arai
    Howard Hughes Medical Institute, University of Michigan Medical Center, 1150 West Medical Center Drive, 4520 MSRB I, Ann Arbor, MI 48109 0650, USA
    Proc Natl Acad Sci U S A 94:13862-7. 1997
    ..These findings suggest that gene transfer of FasL generates apoptotic responses and induces potent inflammatory reactions that can be used to induce the regression of malignancies...