Faculty Opinions recommendation of Development of immunoglobulin lambda-chain-positive B cells, but not editing of immunoglobulin kappa-chain, depends on NF-kappaB signals.

2009 ◽  
Author(s):  
Diane Jelinek ◽  
Stephen Mihalcik
Keyword(s):  
B Cells ◽  
Immunoglobulin Kappa ◽  
Kappa Chain ◽  
Nf Kappab ◽  
Immunoglobulin Lambda

scholarly journals Silencing of the expression of the immunoglobulin kappa gene in non-B cells

1991 ◽  
Vol 11 (3) ◽  
pp. 1431-1437
Author(s):  
J W Pierce ◽  
A M Gifford ◽  
D Baltimore
Keyword(s):  
T Cells ◽  
B Cells ◽  
Cell Types ◽  
Chain Gene ◽  
Nf Kappa B ◽  
Activated T Cells ◽  
Independent Manner ◽  
Immunoglobulin Kappa ◽  
Kappa Chain ◽  
B Lineage

Although the activating factor NF-kappa B can be present in the nucleus of many cell types, transcription and rearrangement of the immunoglobulin kappa chain gene is restricted to cells of the B lineage. Part of this specificity is determined by sequences within the major intron of the kappa gene that specifically silence gene expression in non-B cells (T cells and HeLa cells). These sequences are found in a 232-bp fragment located 5' of the NF-kappa B binding sequence of the enhancer. When this fragment is added back upstream of an active NF-kappa B site, it specifically decreases the expression of a linked gene by more than 10-fold in activated T cells but it has no effect on expression in B cells. The kappa silencer region acts in an orientation- and distance-independent manner and appears to be composed of multiple negative elements. The kappa silencer may act to restrict transcription and rearrangement of the C kappa locus to cells of the B lineage.

scholarly journals Silencing of the expression of the immunoglobulin kappa gene in non-B cells.

1991 ◽  
Vol 11 (3) ◽  
pp. 1431-1437 ◽  
Author(s):  
J W Pierce ◽  
A M Gifford ◽  
D Baltimore
Keyword(s):  
T Cells ◽  
B Cells ◽  
Cell Types ◽  
Chain Gene ◽  
Nf Kappa B ◽  
Activated T Cells ◽  
Independent Manner ◽  
Immunoglobulin Kappa ◽  
Kappa Chain ◽  
B Lineage

Although the activating factor NF-kappa B can be present in the nucleus of many cell types, transcription and rearrangement of the immunoglobulin kappa chain gene is restricted to cells of the B lineage. Part of this specificity is determined by sequences within the major intron of the kappa gene that specifically silence gene expression in non-B cells (T cells and HeLa cells). These sequences are found in a 232-bp fragment located 5' of the NF-kappa B binding sequence of the enhancer. When this fragment is added back upstream of an active NF-kappa B site, it specifically decreases the expression of a linked gene by more than 10-fold in activated T cells but it has no effect on expression in B cells. The kappa silencer region acts in an orientation- and distance-independent manner and appears to be composed of multiple negative elements. The kappa silencer may act to restrict transcription and rearrangement of the C kappa locus to cells of the B lineage.

scholarly journals The active immunoglobulin kappa chain gene is packaged by non-ubiquitin-conjugated nucleosomes.

1986 ◽  
Vol 83 (11) ◽  
pp. 3738-3742 ◽  
Author(s):  
S. Y. Huang ◽  
M. B. Barnard ◽  
M. Xu ◽  
S. Matsui ◽  
S. M. Rose ◽  
...  
Keyword(s):  
Chain Gene ◽  
Immunoglobulin Kappa ◽  
Kappa Chain

scholarly journals Sequences related to immunoglobulin kappa chain messenger RNA in T cells.

1976 ◽  
Vol 73 (7) ◽  
pp. 2467-2471 ◽  
Author(s):  
U. Storb ◽  
L. Hager ◽  
D. Putnam ◽  
L. Buck ◽  
F. Farin ◽  
...  
Keyword(s):  
T Cells ◽  
Messenger Rna ◽  
Immunoglobulin Kappa ◽  
Kappa Chain

scholarly journals E2A and IRF-4/Pip Promote Chromatin Modification and Transcription of the Immunoglobulin κ Locus in Pre-B Cells

2006 ◽  
Vol 26 (3) ◽  
pp. 810-821 ◽  
Author(s):  
Adam S. Lazorchak ◽  
Mark S. Schlissel ◽  
Yuan Zhuang
Keyword(s):  
B Cells ◽  
B Cell ◽  
Germ Line ◽  
Gene Dosage ◽  
Gene Activation ◽  
Chromatin Modification ◽  
Cell Stage ◽  
Immunoglobulin Kappa ◽  
Intronic Enhancer ◽  
Specific Manner

ABSTRACT The immunoglobulin kappa light chain (Igκ) locus is regulated in a lineage- and stage-specific manner during B-cell development. The highly restricted timing of V to J gene recombination at the pre-B-cell stage is under the control of two enhancers, the intronic enhancer (κEi) and the 3′ enhancer (κE3′), flanking the constant exon. E2A transcription factors have been indicated to be directly involved in the regulation of Igκ locus activation. In this study, we utilize E2A-deficient pre-B cells to directly investigate the mechanism of E2A-mediated Igκ activation. We demonstrate that Igκ germ line transcription is severely impaired and recombination is blocked in the absence of E2A. Reconstitution of E2A −/− pre-B cells with inducible human E2A (E47R) is sufficient to promote chromatin modification of Igκ and rescue Igκ germ line transcription and Jκ gene recombinase accessibility. Furthermore, we show that increased E2A recruitment to κEi and κE3′ correlates with activation of Igκ in pre-B cells and that recruitment of E2A to κE3′ is in part dependent on the transcription factor IRF-4. Inhibition of IRF-4 expression in pre-B cells leads to a significant reduction of Igκ germ line transcription and enhancer acetylation. In the absence of E2A, increased IRF-4 expression is not sufficient to promote Igκ enhancer chromatin modification or transcription, suggesting that the sequential involvement of IRF-4 and E2A is necessary for the activation of the Igκ locus. Finally, we provide genetic evidence in the mouse that E2A gene dosage can influence the development of pre-B cells during the phase of Igκ gene activation.

scholarly journals Lipopolysaccharide-unresponsive mutant pre-B-cell lines blocked in NF-kappa B activation.

1990 ◽  
Vol 10 (1) ◽  
pp. 422-425 ◽  
Author(s):  
M Briskin ◽  
M Damore ◽  
R Law ◽  
G Lee ◽  
P W Kincade ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Cell Lines ◽  
Chain Gene ◽  
Nf Kappa B ◽  
Light Chain Gene ◽  
Immunoglobulin Kappa ◽  
Variant Cell ◽  
Late Step ◽  
Mutant Lines

NF-kappa B activation is a crucial late step in the induction of immunoglobulin kappa light-chain gene expression in pre-B cells by lipopolysaccharide (LPS). We have analyzed NF-kappa B activation in three independent mutant lines of 70Z/3 pre-B cells which are unresponsive to LPS. All three variant cell lines failed to activate NF-kappa B when induced with LPS or the phorbol ester 12-O-tetradecanoylphorbol 13-acetate. However, all three cell lines contained functional NF-kappa B, as revealed by detergent treatment of cytoplasmic extracts. Moreover, cycloheximide induced limited activation of NF-kappa B comparable to that in wild-type 70Z/3 pre-B cells in two of the three variant lines. These results indicate that the mutations blocking kappa gene induction in these variant 70Z/3 pre-B-cell lines affect NF-kappa B activation.

scholarly journals Inhibition of c-myc expression induces apoptosis of WEHI 231 murine B cells.

1996 ◽  
Vol 16 (9) ◽  
pp. 5015-5025 ◽  
Author(s):  
M Wu ◽  
M Arsura ◽  
R E Bellas ◽  
M J FitzGerald ◽  
H Lee ◽  
...  
Keyword(s):  
B Cells ◽  
Specific Inhibitor ◽  
Related Factor ◽  
B Cell Tolerance ◽  
B Lymphoma Cells ◽  
Wehi 231 ◽  
Enhanced Expression ◽  
Myc Gene ◽  
Nf Kappab ◽  
Induced Apoptosis

Treatment of WEHI 231 immature B-lymphoma cells with an antibody against their surface immunoglobulin (anti-Ig) induces apoptosis and has been studied extensively as a model of B-cell tolerance. Anti-Ig treatment of exponentially growing WEHI 231 cells results in an early transient increase in c-myc expression that is followed by a decline to below basal levels; this decrease in c-myc expression immediately precedes the induction of cell death. Here we have modulated NF-kappaB/Rel factor activity, which regulates the rate of c-myc gene transcription, to determine whether the increase or decrease in c-Myc-levels mediates apoptosis in WEHI 231 cells. Addition of the serine/threonine protease inhibitor N-tosyl-L-phenylalanine chloromethyl ketone (TPCK), which blocks the normally rapid turnover of the specific inhibitor of NF-kappaB/Rel IkappaBalpha in these cells, caused a drop in Rel-related factor binding. TPCK treatment resulted in decreased c-myc expression, preventing the usual increase seen following anti-Ig treatment. Whereas inhibition of the induction of c-myc expression mediated by anti-Ig failed to block apoptosis, reduction of c-myc expression in exponentially growing WEHI 231 cells induced apoptosis even in the absence of anti-Ig treatment. In WEHI 231 clones ectopically expressing c-Myc, apoptosis induced by treatment with TPCK or anti-Ig was significantly diminished and cells continued to proliferate. Furthermore, apoptosis of WEHI 231 cells ensued following enhanced expression of Mad1, which has been found to reduce functional c-Myc levels. These results indicate that the decline in c-myc expression resulting from the drop in NF-kappaB/Rel binding leads to activation of apoptosis of WEHI 231 B cells.

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