pubmed-article:1847161 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1847161 | lifeskim:mentions | umls-concept:C0021289 | lld:lifeskim |
pubmed-article:1847161 | lifeskim:mentions | umls-concept:C0001675 | lld:lifeskim |
pubmed-article:1847161 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:1847161 | lifeskim:mentions | umls-concept:C0205252 | lld:lifeskim |
pubmed-article:1847161 | lifeskim:mentions | umls-concept:C0037993 | lld:lifeskim |
pubmed-article:1847161 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
pubmed-article:1847161 | lifeskim:mentions | umls-concept:C2752508 | lld:lifeskim |
pubmed-article:1847161 | lifeskim:mentions | umls-concept:C2754998 | lld:lifeskim |
pubmed-article:1847161 | lifeskim:mentions | umls-concept:C1167322 | lld:lifeskim |
pubmed-article:1847161 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
pubmed-article:1847161 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:1847161 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:1847161 | lifeskim:mentions | umls-concept:C1705241 | lld:lifeskim |
pubmed-article:1847161 | lifeskim:mentions | umls-concept:C1705242 | lld:lifeskim |
pubmed-article:1847161 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
pubmed-article:1847161 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:1847161 | pubmed:dateCreated | 1991-3-19 | lld:pubmed |
pubmed-article:1847161 | pubmed:abstractText | During the course of B lymphocyte development, newly emerging surface Ig+ B cells pass through a stage when Ag-Ag receptor interactions lead not to immune responsiveness but to a state of functional tolerance. We have explored the molecular basis of antigenic nonresponsiveness and tolerance susceptibility using tolerance-susceptible surface Ig+ splenic B lymphocytes from neonatal mice and anti-mu chain antibodies as a polyclonal ligand. In this population of cells, surface IgM is uncoupled from the inositol phospholipid (PI)-hydrolysis pathway at a point proximal to the receptor; anti-mu antibodies did not stimulate inositol phosphate generation despite the fact that PI-hydrolysis was observed after treatment with A1F4, implicating the existence of a functional G protein and phospholipase C. Further evidence for a difference early in the signal transduction pathway stems from the finding that anti-mu stimulation does not induce the expression of two immediate/early PKC-linked genes egr-1 and c-fos. This appears to be the primary signaling difference between the mature and immature B cells from the neonatal mouse splenic population, as these cells undergo a G0-G1 cell cycle phase transition when surface IgM is bypassed using phorbol diester and calcium ionophore. Interestingly, despite undetectable levels of PI-hydrolysis, we observed equivalent receptor-mediated changes in intracellular calcium when comparing the immature and mature populations. These results indicate incomplete coupling of surface IgM to the signal transduction machinery operative in mature, immunocompetent B cells and suggests a molecular mechanism accounting for the differential processing of surface IgM signals into activation vs tolerogenic responses observed in these two stages of B cell development. | lld:pubmed |
pubmed-article:1847161 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1847161 | pubmed:language | eng | lld:pubmed |
pubmed-article:1847161 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1847161 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:1847161 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:1847161 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1847161 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1847161 | pubmed:month | Mar | lld:pubmed |
pubmed-article:1847161 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:1847161 | pubmed:author | pubmed-author:BayW WWW | lld:pubmed |
pubmed-article:1847161 | pubmed:author | pubmed-author:GlennWW | lld:pubmed |
pubmed-article:1847161 | pubmed:author | pubmed-author:SukhatmeV PVP | lld:pubmed |
pubmed-article:1847161 | pubmed:author | pubmed-author:MonroeJ GJG | lld:pubmed |
pubmed-article:1847161 | pubmed:author | pubmed-author:YellenA JAJ | lld:pubmed |
pubmed-article:1847161 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1847161 | pubmed:day | 1 | lld:pubmed |
pubmed-article:1847161 | pubmed:volume | 146 | lld:pubmed |
pubmed-article:1847161 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1847161 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1847161 | pubmed:pagination | 1446-54 | lld:pubmed |
pubmed-article:1847161 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:1847161 | pubmed:year | 1991 | lld:pubmed |
pubmed-article:1847161 | pubmed:articleTitle | Signaling through surface IgM in tolerance-susceptible immature murine B lymphocytes. Developmentally regulated differences in transmembrane signaling in splenic B cells from adult and neonatal mice. | lld:pubmed |
pubmed-article:1847161 | pubmed:affiliation | Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104. | lld:pubmed |
pubmed-article:1847161 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1847161 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:1847161 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:1847161 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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