Document Detail

Concerted action of Helios and Ikaros controls the expression of the inositol 5-phosphatase SHIP.
MedLine Citation:
PMID:  20602434     Owner:  NLM     Status:  MEDLINE    
Ikaros family transcription factors have a key role in lymphoid development, and their aberrant function contributes to a multitude of lymphoid malignancies. Ikaros and Helios bind to similar DNA sequences, and Helios associates with Ikaros-containing chromatin remodeling complexes. Previously, we have shown that loss of Ikaros leads to diminished BCR-signaling strength. In this study, we describe a Helios-deficient chicken DT40 B-cell line with a BCR signaling phenotype that is the opposite to that of Ikaros-deficient cells. In contrast to Ikaros-deficient cells, Helios(-/-) B cells exhibit increased calcium release to the cytoplasm after BCR crosslinking, but diminished BCR-induced phosphorylation of signaling molecules. The inositol 5-phosphatase SHIP, an important regulator in several signaling pathways, is differentially expressed in Ikaros- and Helios-deficient cells. In the absence of Ikaros, SHIP is upregulated, whereas Helios deficiency leads to the downregulation of SHIP expression. We also show with ChIP that Ikaros binds to the promoter of the INPP5D gene-encoding SHIP. Considering the critical role of SHIP in the BCR signaling pathway, our findings provide insight into the mechanism of how both Helios and Ikaros are involved in the regulation of BCR signaling.
Jukka Alinikula; Pekka Kohonen; Kalle-Pekka Nera; Olli Lassila
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European journal of immunology     Volume:  40     ISSN:  1521-4141     ISO Abbreviation:  Eur. J. Immunol.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-09-02     Completed Date:  2010-11-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  1273201     Medline TA:  Eur J Immunol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  2599-607     Citation Subset:  IM    
Turku Graduate School of Biomedical Sciences, University of Turku, Turku, Finland.
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MeSH Terms
B-Lymphocytes / immunology,  metabolism*,  pathology
Calcium Signaling / genetics,  immunology
Cell Line
Gene Expression Regulation
Gene Knockout Techniques
Ikaros Transcription Factor / genetics,  immunology,  metabolism*
Phosphoric Monoester Hydrolases / genetics,  immunology,  metabolism*
Promoter Regions, Genetic
Protein Binding
Receptors, Antigen, B-Cell / immunology
Signal Transduction / genetics,  immunology
Reg. No./Substance:
0/Receptors, Antigen, B-Cell; 148971-36-2/Ikaros Transcription Factor; EC 3.1.3.-/Phosphoric Monoester Hydrolases; EC,4,5-trisphosphate 5-phosphatase

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