ArticleNucleic acids research1994
An AP1 binding site upstream of the kappa immunoglobulin intron enhancer binds inducible factors and contributes to expression.
Article in Nucleic acids research, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- JNK/AP1 Pathway Regulates MYC Expression and BCR Signaling through Ig Enhancers in Burkitt Lymphoma Cells.Journal of Cancer · 2020Article
- Elongation factor 1 alpha1 and genes associated with Usher syndromes are downstream targets of GBX2.PloS one · 2012Article
- LMP1-augmented kappa intron enhancer activity contributes to upregulation expression of Ig kappa light chain via NF-kappaB and AP-1 pathways in nasopharyngeal carcinoma cells.Molecular cancer · 2009Article
- Activation of c-Jun N-terminal kinase (JNK) signalling in experimentally induced gastric lesions in rats.Clinical and experimental immunology · 2006Article
- SP600125, an anthrapyrazolone inhibitor of Jun N-terminal kinase.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- The effect of high dose endotoxin on CYP3A2 expression in the rat.Pharmaceutical research · 1998Article
- Net-b, a Ras-insensitive factor that forms ternary complexes with serum response factor on the serum response element of the fos promoter.Molecular and cellular biology · 1997Article
- Coordinate transcription and V(D)J recombination of the kappa immunoglobulin light-chain locus: NF-kappaB-dependent and -independent pathways of activation.Molecular and cellular biology · 1997Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Expression of the kappa immunoglobulin light chain gene requires developmental- and tissue-specific regulation by trans-acting factors which interact with two distinct enhancer elements. A new protein-DNA interaction has been identified upstream of the intron enhancer, within the matrix-associated region of the J-C intron. The binding activity is greatly inducible in pre-B cells by bacterial lipopolysaccharide and interleukin-1 but specific complexes are found at all stages of B cell development tested. The footprinted binding site is homologous to the consensus AP1 motif. The protein components of this complex are specifically competed by an AP1 consensus motif and were shown by supershift to include c-Jun and c-Fos, suggesting that this binding site is an AP1 motif and that the Jun and Fos families of transcription factors play a role in the regulation of the kappa light chain gene. Mutation of the AP1 motif in the context of the intron enhancer was shown to decrease enhancer-mediated activation of the promoter in both pre-B cells induced with LPS and constitutive expression in mature B cells.
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