ArticlePloS one2014
Ikaros and RAG-2-mediated antisense transcription are responsible for lymphocyte-specific inactivation of NWC promoter.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed.
- CRISPR-Cas9 engineering of the RAG2 locus via complete coding sequence replacement for therapeutic applications.Nature communications · 2023Article
- Variation in genes implicated in B-cell development and antibody production affects susceptibility to pemphigus.Immunology · 2021Article
- The Interplay Between Chromatin Architecture and Lineage-Specific Transcription Factors and the Regulation ofFrontiers in immunology · 2021Review
- Article
- Search for the Function of NWC, Third Gene Within RAG Locus: Generation and Characterization of NWC-Deficient Mice.Archivum immunologiae et therapiae experimentalis · 2016Article
Corrections and comments
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Authors and funding
7 authors.
Funding
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Abstract
Recombination activating gene-2 (RAG-2) and NWC are strongly evolutionarily conserved overlapping genes which are convergently transcribed. In non-lymphoid cells the NWC promoter is active whereas in lymphocytes it is inactive due to the DNA methylation. Analysing the mechanism responsible for lymphocyte-specific methylation and inactivation of NWC promoter we found that Ikaros, a lymphocyte-specific transcription factor, acts as a repressor of NWC promoter--thus identifying a new Ikaros target--but is insufficient for inducing its methylation which depends on the antisense transcription driven by RAG-2 promoter. Possible implications of these observations for understanding evolutionary mechanisms leading to lymphocyte specific expression of RAG genes are discussed.
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