Overexpression of src family gene for tyrosine-kinase p59(fyn) in CD4-CD8- T cells of mice with a lymphoproliferative disorder

T. Katagiri, K. Urakawa, Y. Yamanashi, Kentaro Senba, T. Takahashi, K. Toyoshima, T. Yamamoto, K. Kano

Research output: Contribution to journalArticle

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Abstract

Overexpression of a src family gene, lck, has been associated with differentiation of the murine thymic lymphoma line LSTRA. Recent findings by several groups strongly suggest a functional role for the gene product p56(lck) protein-tyrosine kinase (PTK) in the activation of normal T cells. A single recessive gene, lpr or gld, induces a lymphoproliferative disorder concomitant with autoimmune disease in mice. In this study, a 10-fold elevated activity of PTK encoded by fyn, another src family gene, was demonstrated in CD4-CD8- T cells in mutant mice. The increased PTK activity was consistent with overexpression of fyn mRNA. The elevated fyn mRNA expression appeared to be a characteristic of CD4-CD8- T cells, since it was not observed in normal T cells at any stage of differentiation. The fact that fyn mRNA expression was markedly induced in normal T cells by mitogenic stimulation with anti-T3ε antiserum supports the possibility that p59(fyn) PTK is a signal-generating molecule in T cells. Thus, our findings provide insight into the physiological role for a src gene family kinase in T-cell development and contribute to a better understanding of the molecular mechanisms of disease-inducing recessive genes.

Original languageEnglish
Pages (from-to)10064-10068
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume86
Issue number24
DOIs
Publication statusPublished - 1989
Externally publishedYes

Fingerprint

src Genes
Lymphoproliferative Disorders
src-Family Kinases
T-Lymphocytes
Recessive Genes
Protein-Tyrosine Kinases
Messenger RNA
Proto-Oncogene Proteins c-fyn
Lymphocyte Specific Protein Tyrosine Kinase p56(lck)
Autoimmune Diseases
Immune Sera
Lymphoma

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

Overexpression of src family gene for tyrosine-kinase p59(fyn) in CD4-CD8- T cells of mice with a lymphoproliferative disorder. / Katagiri, T.; Urakawa, K.; Yamanashi, Y.; Senba, Kentaro; Takahashi, T.; Toyoshima, K.; Yamamoto, T.; Kano, K.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 86, No. 24, 1989, p. 10064-10068.

Research output: Contribution to journalArticle

Katagiri, T. ; Urakawa, K. ; Yamanashi, Y. ; Senba, Kentaro ; Takahashi, T. ; Toyoshima, K. ; Yamamoto, T. ; Kano, K. / Overexpression of src family gene for tyrosine-kinase p59(fyn) in CD4-CD8- T cells of mice with a lymphoproliferative disorder. In: Proceedings of the National Academy of Sciences of the United States of America. 1989 ; Vol. 86, No. 24. pp. 10064-10068.
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abstract = "Overexpression of a src family gene, lck, has been associated with differentiation of the murine thymic lymphoma line LSTRA. Recent findings by several groups strongly suggest a functional role for the gene product p56(lck) protein-tyrosine kinase (PTK) in the activation of normal T cells. A single recessive gene, lpr or gld, induces a lymphoproliferative disorder concomitant with autoimmune disease in mice. In this study, a 10-fold elevated activity of PTK encoded by fyn, another src family gene, was demonstrated in CD4-CD8- T cells in mutant mice. The increased PTK activity was consistent with overexpression of fyn mRNA. The elevated fyn mRNA expression appeared to be a characteristic of CD4-CD8- T cells, since it was not observed in normal T cells at any stage of differentiation. The fact that fyn mRNA expression was markedly induced in normal T cells by mitogenic stimulation with anti-T3ε antiserum supports the possibility that p59(fyn) PTK is a signal-generating molecule in T cells. Thus, our findings provide insight into the physiological role for a src gene family kinase in T-cell development and contribute to a better understanding of the molecular mechanisms of disease-inducing recessive genes.",
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