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.
journal_name
Mol Cell Bioljournal_title
Molecular and cellular biologyauthors
Dang W,Nikolajczyk BS,Sen Rdoi
10.1128/mcb.18.11.6870subject
Has Abstractpub_date
1998-11-01 00:00:00pages
6870-8issue
11eissn
0270-7306issn
1098-5549journal_volume
18pub_type
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