1.3E2, a variant of the B lymphoma 70Z/3, defective in activation of NF-?B and OTF-2
- 1 January 1990
- journal article
- research article
- Published by Springer Nature in Immunogenetics
- Vol. 31 (2) , 73-78
- https://doi.org/10.1007/bf00661216
Abstract
The mouse B-cell cell lymphoma 70Z/3 is a convenient model system in which to study the regulation of immunoglobulin synthesis. Three transcriptional activators of kappa (κ) light chain synthesis have been identified for these cells: bacterial lipopolysaccharide (LPS), interferon-γ (IFN), and interleukin-1 (IL-1). The response of the κ gene in 70Z/3 cells to LPS is mediated by increases in two transcription factors: NF-κB and OTF-2. In contrast, IFN has no effect on either of these factors in 70Z/3 cells. We have isolated by immunoselection an LPS− IFN+ variant of 70Z/3 called 1.3E2. We show here that LPS treatment of these cells causes no increase in nuclear localization of either NF-κB or OTF-2. Although they have normal levels of cytoplasmic NF-κB, it cannot be activated by LPS or by phorbol 12-myristate 13-acetate (PMA) treatment of the cells. These experiments expand the genetic dissection of the molecular pathways of activation of κ transcription in 70Z/3 cells.Keywords
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