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pubmed-article:8077655pubmed:abstractTextIg receptor (IgR) on the surface of B cells mediates the Ag-specific stimulatory signal for B cell proliferation and differentiation. In immature B cells, the stimulatory signal causes an inhibitory effect which is believed to be a key phenomenon in B cell tolerance or B cell anergy. Here, we studied the molecular mechanism of the inhibitory response of the IgR-mediated signal transduction that results in the programmed cell death of immature B cells. To analyze the downstream molecules of the IgR-mediated signal transduction, we prepared a mAb against a 160-kDa membrane protein (p160) that can coprecipitate the kinase molecule(s) acting on serine, threonine, and tyrosine residues. Anti-IgR stimulation induces the increase of the kinase activity coprecipitated with the p160 protein in mature B cell BAL17 and normal adult spleen B cells. This result suggest that the p160-associated kinase activity is one of the downstream events of the IgR-mediated signal transduction cascade. Interestingly, immature B cell lymphoma WEHI-231 and the neonatal spleen B cells showed the adverse reaction of the p160-associated kinase which results in the transient loss of the kinase activity. Moreover, the transient decrease of the p160-associated kinase was caused by the tyrosine phosphatase activity induced by the stimulation of IgR in WEHI-231. The results suggest that this molecular difference in the downstream events of the IgR-mediated signal transduction between immature B cells and mature B cells already begins at the transmembrane level in the IgR-mediated signal transduction pathway.lld:pubmed
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pubmed-article:8077655pubmed:pagination2381-93lld:pubmed
pubmed-article:8077655pubmed:dateRevised2009-11-19lld:pubmed
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pubmed-article:8077655pubmed:year1994lld:pubmed
pubmed-article:8077655pubmed:articleTitleB cell Ag receptor mediates different types of signals in the protein kinase activity between immature B cell and mature B cell.lld:pubmed
pubmed-article:8077655pubmed:affiliationDepartment of Immunology, School of Life Science, Faculty of Medicine, Tottori University, Yonago, Japan.lld:pubmed
pubmed-article:8077655pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:8077655pubmed:publicationTypeComparative Studylld:pubmed
pubmed-article:8077655pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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