Two distinct mechanisms contribute to the constitutive activation of RelB in lymphoid cells.

Lernbecher, T; Kistler, Barbara; Wirth, Thomas

doi:10.1002/j.1460-2075.1994.tb06723.x

Cited by 88 publications

(78 citation statements)

References 66 publications

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“…Previous studies stated that, while IkB-a or IkB-b mostly controlled the activity of NF-kB-p50/p65 complexes and IkB-e associated preferentially with cRel and p65, p100 regulated the activity of RelBcontaining complexes (Dobrzanski et al, 1994(Dobrzanski et al, , 1995Lernbecher et al, 1994). However, the present report demonstrates that p100, when highly expressed in adenocarcinoma cells, also sequestered most of p65 complexes in the cytoplasm.…”

Section: Discussioncontrasting

confidence: 56%

Regulation of NF-κB activity by IκB-related proteins in adenocarcinoma cells

et al. 1999

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Section: Discussioncontrasting

confidence: 56%

Regulation of NF-κB activity by IκB-related proteins in adenocarcinoma cells

et al. 1999

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“…It was indeed demonstrated that p100 can form cytoplasmic complexes with p65, p50 and RelB (Mercurio et al, 1993;Scheinman et al, 1993;Kanno et al, 1994;Dejardin et al, 1995). Previous reports indicated that RelB complexes poorly interact with IkB-a, p105 or Bcl-3 and are preferentially inhibited by p100 in B lymphocytes (Lernbecher et al, 1994;Dobrzanski et al, 1994Dobrzanski et al, , 1995. Our data con®rm that, in breast cancer cells, RelB-containing complexes are not inhibited by IkB-a but by p100, indicating a preferential interaction between RelB and the IkB-like molecule p100.…”

Section: Discussionmentioning

confidence: 93%

Regulation of major histocompatibility complex class I expression by NF-κB-related proteins in breast cancer cells

et al. 1998

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Downregulation of MHC Class I antigens has been observed in many cancers and usually results from a decreased gene transcription. A reporter CAT gene dependent on the MHC Class I kB site or on a longer promoter is transactivated by NF-kB complexes containing p65 or RelB. p100 as well as IkB-a are potent inhibitors of this transcription and p100 sequesters RelB and p65 complexes in the cytoplasm of breast cancer cells. However, although p100 is highly expressed in a number of breast cancer cell lines, MHC Class I antigen expression was observed on all the cell lines we analysed and could be further induced by stimulation with the cytokines IFN-g or TNF-a. Stable transfection of a unresponsive mutated IkB-a Ser 32-36 expression vector showed that TNF-a induced MHC Cl I expression in an NF-kB-dependent way while IFN-g did it independently of any NF-kB activation.

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“…Several mechanisms contribute to constitutive nuclear NF-KB expression. An increased turnover of IKBa (Miyamoto et al, 1994a), a selective change in the susceptibility in lymphoid tissue of RelB to inhibition by IKBa (Lernbecher et al, 1994), and differential affinities of various NF-KB/Rel dimers for IKBa (Dobrzanski et al, 1994) have all been demonstrated. Since a large proportion of the constitutive activity in these cells is accounted for by p50-containing species, the requirements for NFKB1 synthesis may be different than those in other cell types.…”

Section: Discussionmentioning

confidence: 99%

The nfkb1 promoter is controlled by proteins of the Ets family.

Lambert

Ludford-Menting

Deacon

et al. 1997

MBoC

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The gene encoding NFKB1 is autoregulated, responding to NF-KB/Rel activation through NF-KB binding sites in its promoter, which also contains putative sites for Ets proteins. One of the Ets sites, which we refer to as EBS4, is located next to an NF-KB/Rel binding site, kB3, which is absolutely required for activity of the promoter in Jurkat T cells in response to activation by phorbol 12-myristate 13-acetate (PMA), PMA/ionomycin, or the Tax protein from human T cell leukemia virus type I. We show that EBS4 is required for the full response of the nfkbl promoter to PMA or PMA/ionomycin in Jurkat cells. EBS4 is bound by Ets-1, Elf-1, and other species. Overexpression of Ets-1 augments the response to PMA/ionomycin and this is reduced by mutation of EBS4. Elf-1 has less effect in conjunction with PMA/ionomycin, but by itself activates the promoter 12-fold. This activation is only partly affected by mutation of EBS4, and a mutant promoter that binds Ets-1, but not Elf-1, at the EBS4 site responds to PMA/ionomycin as efficiently as the wild-type. Ets proteins may be responsible for fine-tuning the activity of the nfkbl gene in a cell-type-specific manner.

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Two distinct mechanisms contribute to the constitutive activation of RelB in lymphoid cells.

Abstract: The KB-motif is an important regulatory element both for constitutive lymphoid-specific as well as ubiquitous inducible transcriptional activity. We

Cited by 88 publications

References 66 publications

Regulation of NF-κB activity by IκB-related proteins in adenocarcinoma cells

Regulation of NF-κB activity by IκB-related proteins in adenocarcinoma cells

Regulation of major histocompatibility complex class I expression by NF-κB-related proteins in breast cancer cells

The nfkb1 promoter is controlled by proteins of the Ets family.

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