ArticleMolecular and cellular biology1992
Two conserved essential motifs of the murine immunoglobulin lambda enhancers bind B-cell-specific factors.
Article in Molecular and cellular biology, 1992. 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, 25 citations in OpenAlex.
- Targeting of somatic hypermutation by immunoglobulin enhancer and enhancer-like sequences.PLoS biology · 2014Article
- Transcription-coupled eviction of histones H2A/H2B governs V(D)J recombination.The EMBO journal · 2013Article
- Distinct roles for E12 and E47 in B cell specification and the sequential rearrangement of immunoglobulin light chain loci.The Journal of experimental medicine · 2009Article
- Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers.The EMBO journal · 1999Article
- Molecular cloning of LSIRF, a lymphoid-specific member of the interferon regulatory factor family that binds the interferon-stimulated response element (ISRE).Nucleic acids research · 1995Article
- The chicken immunoglobulin lambda light chain gene is transcriptionally controlled by a modularly organized enhancer and an octamer-dependent silencer.Nucleic acids research · 1995Article
- Crossing the SJL lambda locus into kappa-knockout mice reveals a dysfunction of the lambda 1-containing immunoglobulin receptor in B cell differentiation.The EMBO journal · 1994Article
- E2A expression, nuclear localization, and in vivo formation of DNA- and non-DNA-binding species during B-cell development.Molecular and cellular biology · 1993Article
- PU.1 is a component of a multiprotein complex which binds an essential site in the murine immunoglobulin lambda 2-4 enhancer.Molecular and cellular biology · 1993Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Two highly homologous enhancers associated with the two murine immunoglobulin lambda constant-region clusters were recently identified. In order to better understand the molecular basis for the developmental stage- and cell-type-restricted expression of lambda genes, we have undertaken an analysis of the putative regulatory domains of these enhancers. By using a combination of DNase I footprinting, electrophoretic mobility shift assay, and site-specific mutations, four candidate protein binding sites have been identified at analogous positions in both enhancers. A mutation of any of these sites decreases enhancer activity. Two of the sites, lambda A and lambda B, are essential for enhancer function, and both of these sites appear to bind both B-cell-specific and general factors. Nevertheless, isolated lambda A and lambda B sites show no evidence of inherent transactivating potential, alone or together, even when present in up to three copies. We suggest that the generation of transactivating signals from these enhancers may require the complex interaction of multiple B-cell-specific and nonspecific DNA-binding factors.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.