Y Minegishi

Summary

Affiliation: St. Jude Children's Research Hospital
Country: USA

Publications

  1. ncbi Mutations in the human lambda5/14.1 gene result in B cell deficiency and agammaglobulinemia
    Y Minegishi
    Department of Immunology, St Jude Children s Research Hospital, Memphis, Tennesse 38105, USA
    J Exp Med 187:71-7. 1998
  2. ncbi Mutations in Igalpha (CD79a) result in a complete block in B-cell development
    Y Minegishi
    Departments of Immunology, Hematology Oncology, and Pathology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    J Clin Invest 104:1115-21. 1999
  3. ncbi Defects in early B-cell development: comparing the consequences of abnormalities in pre-BCR signaling in the human and the mouse
    M E Conley
    Department of Immunology, St Jude Children s Research Hospital, Memphis, TN 38101 0318, USA
    Immunol Rev 178:75-90. 2000
  4. ncbi An essential role for BLNK in human B cell development
    Y Minegishi
    Department of Immunology, Department of Hematology Oncology, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Science 286:1954-7. 1999
  5. ncbi Analysis of SWAP-70 as a candidate gene for non-X-linked hyper IgM syndrome and common variable immunodeficiency
    L Rapalus
    Department of Immunology, St Jude Children s Research Hospital, Memphis, Tennessee, 38105, USA
    Clin Immunol 101:270-5. 2001
  6. ncbi Negative selection at the pre-BCR checkpoint elicited by human mu heavy chains with unusual CDR3 regions
    Y Minegishi
    Department of Immunology, St. Jude Children's Research Hospital, University of Tennessee College of Medicine, Memphis, TN 38105, USA
    Immunity 14:631-41. 2001
  7. ncbi Variations in the human phospholipase Cgamma2 gene in patients with B-cell defects of unknown etiology
    D Wang
    Department of Biochemistry, St Jude Children s Research Hospital, 332 N Lauderdale, Memphis, TN 38105, USA
    Immunogenetics 53:550-6. 2001
  8. ncbi Mutations in btk in patients with presumed X-linked agammaglobulinemia
    M E Conley
    Department of Pediatrics, University of Tennessee College of Medicine, Memphis, TN, USA
    Am J Hum Genet 62:1034-43. 1998
  9. ncbi Mutations in activation-induced cytidine deaminase in patients with hyper IgM syndrome
    Y Minegishi
    Department of Immunology, St Jude Children s Research Hospital, Memphis, Tennessee 38101 0318, USA
    Clin Immunol 97:203-10. 2000

Detail Information

Publications9

  1. ncbi Mutations in the human lambda5/14.1 gene result in B cell deficiency and agammaglobulinemia
    Y Minegishi
    Department of Immunology, St Jude Children s Research Hospital, Memphis, Tennesse 38105, USA
    J Exp Med 187:71-7. 1998
    ..1. These findings indicate that expression of the functional lambda5/14.1 is critical for B cell development in the human...
  2. ncbi Mutations in Igalpha (CD79a) result in a complete block in B-cell development
    Y Minegishi
    Departments of Immunology, Hematology Oncology, and Pathology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    J Clin Invest 104:1115-21. 1999
    ..Furthermore, they suggest that Igalpha does not play a critical role in B-cell development until it is expressed, along with mu heavy chain, as part of the pre-BCR...
  3. ncbi Defects in early B-cell development: comparing the consequences of abnormalities in pre-BCR signaling in the human and the mouse
    M E Conley
    Department of Immunology, St Jude Children s Research Hospital, Memphis, TN 38101 0318, USA
    Immunol Rev 178:75-90. 2000
    ..These findings suggest that requirements for signaling through the pre-BCR are more stringent in the human compared to the mouse. Possible explanations for this observation are discussed...
  4. ncbi An essential role for BLNK in human B cell development
    Y Minegishi
    Department of Immunology, Department of Hematology Oncology, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Science 286:1954-7. 1999
    ..The immune system and overall growth and development were otherwise normal in this patient, suggesting that BLNK function is highly specific...
  5. ncbi Analysis of SWAP-70 as a candidate gene for non-X-linked hyper IgM syndrome and common variable immunodeficiency
    L Rapalus
    Department of Immunology, St Jude Children s Research Hospital, Memphis, Tennessee, 38105, USA
    Clin Immunol 101:270-5. 2001
    ..However, none of the alterations appeared to be associated with disease in the patients screened...
  6. ncbi Negative selection at the pre-BCR checkpoint elicited by human mu heavy chains with unusual CDR3 regions
    Y Minegishi
    Department of Immunology, St. Jude Children's Research Hospital, University of Tennessee College of Medicine, Memphis, TN 38105, USA
    Immunity 14:631-41. 2001
    ..These results suggest that some mu heavy chains elicit negative selection at the pro-B cell to pre-B cell transition...
  7. ncbi Variations in the human phospholipase Cgamma2 gene in patients with B-cell defects of unknown etiology
    D Wang
    Department of Biochemistry, St Jude Children s Research Hospital, 332 N Lauderdale, Memphis, TN 38105, USA
    Immunogenetics 53:550-6. 2001
    ..Although 24 polymorphic variants of this gene were found in 35 patients, we did not identify any alterations that were likely to be the cause of disease...
  8. ncbi Mutations in btk in patients with presumed X-linked agammaglobulinemia
    M E Conley
    Department of Pediatrics, University of Tennessee College of Medicine, Memphis, TN, USA
    Am J Hum Genet 62:1034-43. 1998
    ..These studies indicate that 90%-95% of males with presumed XLA have mutations in Btk. The other patients are likely to have defects in other genes...
  9. ncbi Mutations in activation-induced cytidine deaminase in patients with hyper IgM syndrome
    Y Minegishi
    Department of Immunology, St Jude Children s Research Hospital, Memphis, Tennessee 38101 0318, USA
    Clin Immunol 97:203-10. 2000
    ..Lymphoid hyperplasia was seen in patients with hyper IgM syndrome and normal AID as well as the patients with hyper IgM syndrome and defects in AID...