ArticleMolecular and cellular biology1998
Exploring functional redundancy in the immunoglobulin mu heavy-chain gene enhancer.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- Targeting of somatic hypermutation by immunoglobulin enhancer and enhancer-like sequences.PLoS biology · 2014Article
- The zebrafish IgH locus contains multiple transcriptional regulatory regions.Developmental and comparative immunology · 2011Article
- Memories of lost enhancers.Genes & development · 2010Article
- A likelihood-based index of protein protein binding affinities with application to influenza HA escape from antibodies.Molecular biology and evolution · 2007Article
- Evolution of transcriptional enhancers in the immunoglobulin heavy-chain gene: functional characteristics of the zebrafish Emu3' enhancer.Immunogenetics · 2005Article
- Activation of c-myc promoter P1 by immunoglobulin kappa gene enhancers in Burkitt lymphoma: functional characterization of the intron enhancer motifs kappaB, E box 1 and E box 2, and of the 3' enhancer motif PU.Nucleic acids research · 2000Article
- Definition of a T-cell receptor beta gene core enhancer of V(D)J recombination by transgenic mapping.Molecular and cellular biology · 2000Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Immunoglobulin (Ig) mu heavy-chain gene enhancer activity is mediated by multiple DNA binding proteins. Mutations of several protein binding sites in the enhancer do not affect enhancer activity significantly. This feature, termed redundancy, is thought to be due to functional compensation of the mutated sites by other elements within the enhancer. In this study, we identified the elements that make the basic helix-loop-helix (bHLH) protein binding sites, muE2 and muE3, redundant. The major compensatory element is a binding site for interferon regulatory factors (IRFs) and not one of several other bHLH protein binding sites. These studies also provide the first evidence for a role of IRF proteins in Ig heavy-chain gene expression. In addition, we reconstituted the activity of a monomeric mu enhancer in nonlymphoid cells and defined the domains of the ETS gene required for function.
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Registered trials
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