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Article ; Online: Correction: Ikaros antagonizes DNA binding by STAT5 in pre-B cells.

Heizmann, Beate / Le Gras, Stéphanie / Simand, Célestine / Marchal, Patricia / Chan, Susan / Kastner, Philippe

PloS one

2021 Volume 16, Issue 1, Page(s) e0246570

Abstract: This corrects the article DOI: 10.1371/journal.pone.0242211.]. ...

Abstract	[This corrects the article DOI: 10.1371/journal.pone.0242211.].
Language	English
Publishing date	2021-01-29
Publishing country	United States
Document type	Published Erratum
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0246570
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Article ; Online: Kidins220 and Aiolos promote thymic iNKT cell development by reducing TCR signals.

Herr, Laurenz A / Fiala, Gina J / Sagar / Schaffer, Anna-Maria / Hummel, Jonas F / Zintchenko, Marina / Raute, Katrin / Velasco Cárdenas, Rubí M-H / Heizmann, Beate / Ebert, Karolina / Fehrenbach, Kerstin / Janowska, Iga / Chan, Susan / Tanriver, Yakup / Minguet, Susana / Schamel, Wolfgang W

Science advances

2024 Volume 10, Issue 11, Page(s) eadj2802

Abstract: Development of T cells is controlled by the signal strength of the TCR. The scaffold protein kinase D-interacting substrate of 220 kilodalton (Kidins220) binds to the TCR; however, its role in T cell development was unknown. Here, we show that T cell- ... ...

Abstract	Development of T cells is controlled by the signal strength of the TCR. The scaffold protein kinase D-interacting substrate of 220 kilodalton (Kidins220) binds to the TCR; however, its role in T cell development was unknown. Here, we show that T cell-specific Kidins220 knockout (T-KO) mice have strongly reduced invariant natural killer T (iNKT) cell numbers and modest decreases in conventional T cells. Enhanced apoptosis due to increased TCR signaling in T-KO iNKT thymocytes of developmental stages 2 and 3 shows that Kidins220 down-regulates TCR signaling at these stages. scRNA-seq indicated that the transcription factor Aiolos is down-regulated in Kidins220-deficient iNKT cells. Analysis of an Aiolos KO demonstrated that Aiolos is a downstream effector of Kidins220 during iNKT cell development. In the periphery, T-KO iNKT cells show reduced TCR signaling upon stimulation with α-galactosylceramide, suggesting that Kidins220 promotes TCR signaling in peripheral iNKT cells. Thus, Kidins220 reduces or promotes signaling dependent on the iNKT cell developmental stage.
MeSH term(s)	Animals ; Mice ; Cell Differentiation ; Gene Expression Regulation ; Mice, Inbred C57BL ; Mice, Knockout ; Natural Killer T-Cells/metabolism ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; Membrane Proteins/metabolism ; Ikaros Transcription Factor/metabolism ; Thymus Gland/cytology ; Thymus Gland/metabolism
Chemical Substances	Receptors, Antigen, T-Cell ; Kidins220 protein, mouse ; Ikzf3 protein, mouse ; Membrane Proteins ; Ikaros Transcription Factor (148971-36-2)
Language	English
Publishing date	2024-03-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.adj2802
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Article ; Online: Ikaros antagonizes DNA binding by STAT5 in pre-B cells.

Heizmann, Beate / Le Gras, Stéphanie / Simand, Célestine / Marchal, Patricia / Chan, Susan / Kastner, Philippe

PloS one

2020 Volume 15, Issue 11, Page(s) e0242211

Abstract: The IKZF1 gene, which encodes the Ikaros transcription factor, is frequently deleted or mutated in patients with B-cell precursor acute lymphoblastic leukemias that express oncogenes, like BCR-ABL, which activate the JAK-STAT5 pathway. Ikaros ... ...

Abstract	The IKZF1 gene, which encodes the Ikaros transcription factor, is frequently deleted or mutated in patients with B-cell precursor acute lymphoblastic leukemias that express oncogenes, like BCR-ABL, which activate the JAK-STAT5 pathway. Ikaros functionally antagonizes the transcriptional programs downstream of IL-7/STAT5 during B cell development, as well as STAT5 activity in leukemic cells. However, the mechanisms by which Ikaros interferes with STAT5 function is unknown. We studied the genomic distribution of Ikaros and STAT5 on chromatin in a murine pre-B cell line, and found that both proteins colocalize on >60% of STAT5 target regions. Strikingly, Ikaros activity leads to widespread loss of STAT5 binding at most of its genomic targets within two hours of Ikaros induction, suggesting a direct mechanism. Ikaros did not alter the level of total or phosphorylated STAT5 proteins, nor did it associate with STAT5. Using sequences from the Cish, Socs2 and Bcl6 genes that Ikaros and STAT5 target, we show that both proteins bind overlapping sequences at GGAA motifs. Our results demonstrate that Ikaros antagonizes STAT5 DNA binding, in part by competing for common target sequences. Our study has implications for understanding the functions of Ikaros and STAT5 in B cell development and transformation.
MeSH term(s)	Animals ; Base Sequence ; Cell Line ; Chromatin/metabolism ; DNA/chemistry ; DNA/metabolism ; Ikaros Transcription Factor/deficiency ; Ikaros Transcription Factor/genetics ; Ikaros Transcription Factor/metabolism ; Interleukin-17/pharmacology ; Mice ; Mice, Knockout ; Phosphorylation ; Precursor Cells, B-Lymphoid/cytology ; Precursor Cells, B-Lymphoid/metabolism ; Protein Binding ; STAT5 Transcription Factor/genetics ; STAT5 Transcription Factor/metabolism ; Suppressor of Cytokine Signaling Proteins/chemistry ; Suppressor of Cytokine Signaling Proteins/metabolism ; Up-Regulation/drug effects
Chemical Substances	Chromatin ; Interleukin-17 ; STAT5 Transcription Factor ; Socs2 protein, mouse ; Suppressor of Cytokine Signaling Proteins ; Zfpn1a1 protein, mouse ; cytokine inducible SH2-containing protein ; Ikaros Transcription Factor (148971-36-2) ; DNA (9007-49-2)
Language	English
Publishing date	2020-11-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0242211
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Article ; Online: The Ikaros family in lymphocyte development.

Heizmann, Beate / Kastner, Philippe / Chan, Susan

Current opinion in immunology

2017 Volume 51, Page(s) 14–23

Abstract: The IKZF family of transcription factors are essential regulators of lymphopoiesis. Ikaros, Helios, Aiolos and Eos function as transcriptional repressors and activators during T and B cell differentiation and in mature cell function, depending on the ... ...

Abstract	The IKZF family of transcription factors are essential regulators of lymphopoiesis. Ikaros, Helios, Aiolos and Eos function as transcriptional repressors and activators during T and B cell differentiation and in mature cell function, depending on the stage of development and/or cell type. Their potential mechanisms of action are varied. Ikaros family proteins partner with multiple complexes, including NuRD, PRC2 and transcription elongation factors, to modulate gene expression and the chromatin state. In humans, mutations in the IKZF genes are associated with B cell deficiency, leukemias and autoimmunity. In this review, we focus on the function of Ikaros family proteins in early T and B lymphocyte development, and discuss the molecular and physiological activities of this family.
MeSH term(s)	Animals ; Cell Differentiation/genetics ; Cell Lineage ; Gene Expression Regulation ; Humans ; Ikaros Transcription Factor/genetics ; Ikaros Transcription Factor/metabolism ; Lymphocyte Subsets/cytology ; Lymphocyte Subsets/immunology ; Lymphocyte Subsets/metabolism ; Lymphocytes/cytology ; Lymphocytes/immunology ; Lymphocytes/metabolism ; Lymphopoiesis/genetics ; Mice ; Multigene Family ; Signal Transduction
Chemical Substances	Ikaros Transcription Factor (148971-36-2)
Language	English
Publishing date	2017-12-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2017.11.005
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Zs.A 2773: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Ikaros deficiency is associated with aggressive BCR-ABL1 B-cell precursor acute lymphoblastic leukemia independent of the lineage and developmental origin.

Simand, Célestine / Keime, Céline / Cayé, Aurélie / Arfeuille, Chloé / Passet, Marie / Kim, Rathana / Cavé, Hélène / Clappier, Emmanuelle / Kastner, Philippe / Chan, Susan / Heizmann, Beate

Haematologica

2022 Volume 107, Issue 1, Page(s) 316–320

MeSH term(s)	Fusion Proteins, bcr-abl/genetics ; Humans ; Ikaros Transcription Factor/genetics ; Ikaros Transcription Factor/metabolism ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma
Chemical Substances	IKZF1 protein, human ; Ikaros Transcription Factor (148971-36-2) ; Fusion Proteins, bcr-abl (EC 2.7.10.2)
Language	English
Publishing date	2022-01-01
Publishing country	Italy
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2021.279125
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Article: Ikaros limits follicular B cell activation by regulating B cell receptor signaling pathways

Heizmann, Beate / MacLean Sellars / Alejandra Macias-Garcia / Susan Chan / Philippe Kastner

Biochemical and biophysical research communications. 2016 Feb. 12, v. 470

2016

Abstract: The Ikaros transcription factor is essential for early B cell development, but its effect on mature B cells is debated. We show that Ikaros is required to limit the response of naive splenic B cells to B cell receptor signals. Ikaros deficient follicular ...

Abstract	The Ikaros transcription factor is essential for early B cell development, but its effect on mature B cells is debated. We show that Ikaros is required to limit the response of naive splenic B cells to B cell receptor signals. Ikaros deficient follicular B cells grow larger and enter cell cycle faster after anti-IgM stimulation. Unstimulated mutant B cells show deregulation of positive and negative regulators of signal transduction at the mRNA level, and constitutive phosphorylation of ERK, p38, SYK, BTK, AKT and LYN. Stimulation results in enhanced and prolonged ERK and p38 phosphorylation, followed by hyper-proliferation. Pharmacological inhibition of ERK and p38 abrogates the increased proliferative response of Ikaros deficient cells. These results suggest that Ikaros functions as a negative regulator of follicular B cell activation.
Keywords	cell cycle ; gene expression ; messenger RNA ; mitogen-activated protein kinase ; mutants ; phosphorylation ; signal transduction ; transcription factors ; MAPK ; B cell signaling ; Transcription factor ; B cell receptor ; Transcriptional program ; Activation ; Ikaros
Language	English
Dates of publication	2016-0212
Size	p. 714-720.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2016.01.060
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Article ; Online: Ikaros is absolutely required for pre-B cell differentiation by attenuating IL-7 signals.

Heizmann, Beate / Kastner, Philippe / Chan, Susan

The Journal of experimental medicine

2013 Volume 210, Issue 13, Page(s) 2823–2832

Abstract: Pre-B cell receptor (pre-BCR) signaling and migration from IL-7-rich environments cooperate to drive pre-B cell differentiation via transcriptional programs that remain unclear. We show that the Ikaros transcription factor is required for the ... ...

Abstract	Pre-B cell receptor (pre-BCR) signaling and migration from IL-7-rich environments cooperate to drive pre-B cell differentiation via transcriptional programs that remain unclear. We show that the Ikaros transcription factor is required for the differentiation of large pre-B to small pre-B cells. Mice deleted for Ikaros in pro/pre-B cells show a complete block of differentiation at the fraction C' stage, and Ikaros-null pre-B cells cannot differentiate upon withdrawal of IL-7 in vitro. Restoration of Ikaros function rescues pre-B cell differentiation in vitro and in vivo and depends on DNA binding. Ikaros is required for the down-regulation of the pre-BCR, Igκ germline transcription, and Ig L chain recombination. Furthermore, Ikaros antagonizes the IL-7-dependent regulation of >3,000 genes, many of which are up- or down-regulated between fractions C' and D. Affected genes include those important for survival, metabolism, B cell signaling, and function, as well as transcriptional regulators like Ebf1, Pax5, and the Foxo1 family. Our data thus identify Ikaros as a central regulator of IL-7 signaling and pre-B cell development.
MeSH term(s)	Animals ; B-Lymphocytes/cytology ; Cell Differentiation ; Cell Separation ; Down-Regulation ; Flow Cytometry ; Ikaros Transcription Factor/metabolism ; Immunoglobulin kappa-Chains/genetics ; Immunoglobulin lambda-Chains/genetics ; Interleukin-7/metabolism ; Leukemia/genetics ; Leukemia/metabolism ; Mice ; Mice, Knockout ; Mutation ; Phenotype ; Recombination, Genetic ; Retroviridae/genetics ; Signal Transduction ; Transcription, Genetic ; Transcriptome ; VDJ Recombinases/metabolism
Chemical Substances	Immunoglobulin kappa-Chains ; Immunoglobulin lambda-Chains ; Interleukin-7 ; Zfpn1a1 protein, mouse ; Ikaros Transcription Factor (148971-36-2) ; VDJ Recombinases (EC 2.7.7.-)
Language	English
Publishing date	2013-12-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20131735
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Article ; Online: Ikaros limits follicular B cell activation by regulating B cell receptor signaling pathways.

Heizmann, Beate / Sellars, MacLean / Macias-Garcia, Alejandra / Chan, Susan / Kastner, Philippe

Biochemical and biophysical research communications

2016 Volume 470, Issue 3, Page(s) 714–720

Abstract	The Ikaros transcription factor is essential for early B cell development, but its effect on mature B cells is debated. We show that Ikaros is required to limit the response of naive splenic B cells to B cell receptor signals. Ikaros deficient follicular B cells grow larger and enter cell cycle faster after anti-IgM stimulation. Unstimulated mutant B cells show deregulation of positive and negative regulators of signal transduction at the mRNA level, and constitutive phosphorylation of ERK, p38, SYK, BTK, AKT and LYN. Stimulation results in enhanced and prolonged ERK and p38 phosphorylation, followed by hyper-proliferation. Pharmacological inhibition of ERK and p38 abrogates the increased proliferative response of Ikaros deficient cells. These results suggest that Ikaros functions as a negative regulator of follicular B cell activation.
MeSH term(s)	Animals ; B-Lymphocytes ; Cell Proliferation/physiology ; Cells, Cultured ; Gene Expression Regulation/physiology ; Ikaros Transcription Factor/metabolism ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, B-Cell/metabolism ; Signal Transduction/physiology ; Spleen/cytology
Chemical Substances	Receptors, Antigen, B-Cell ; Zfpn1a1 protein, mouse ; Ikaros Transcription Factor (148971-36-2)
Language	English
Publishing date	2016-02-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2016.01.060
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Article: Syk is a dual-specificity kinase that self-regulates the signal output from the B-cell antigen receptor

Heizmann, Beate / Reth, Michael / Infantino, Simona

Proceedings of the National Academy of Sciences of the United States of America. 2010 Oct. 26, v. 107, no. 43

2010

Abstract: Upon B-cell activation, the signaling subunits Ig-α and Ig-β of the B-cell antigen receptor become phosphorylated not only on tyrosines but also on serine residues. Using a specific antibody, we show that serine 197 (S197) in the cytoplasmic tail of Ig-α ...

Abstract	Upon B-cell activation, the signaling subunits Ig-α and Ig-β of the B-cell antigen receptor become phosphorylated not only on tyrosines but also on serine residues. Using a specific antibody, we show that serine 197 (S197) in the cytoplasmic tail of Ig-α is phosphorylated upon B-cell antigen receptor activation, and that this modification inhibits the signal output of the B-cell antigen receptor. Surprisingly, we found that the well-known protein tyrosine kinase Syk (spleen tyrosine kinase) phosphorylates S197 on Ig-α, thus not only activating but also inhibiting signaling from the B-cell antigen receptor. This finding identifies Syk as a dual-specificity kinase and establishes a previously unexplored paradigm for the self-regulation of biological signaling processes.
Keywords	B-lymphocytes ; antibodies ; antigens ; dual-specificity kinase ; non-specific protein-tyrosine kinase ; serine
Language	English
Dates of publication	2010-1026
Size	p. 18563-18568.
Publishing place	National Academy of Sciences
Document type	Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1009048107
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Article ; Online: Syk is a dual-specificity kinase that self-regulates the signal output from the B-cell antigen receptor.

Heizmann, Beate / Reth, Michael / Infantino, Simona

Proceedings of the National Academy of Sciences of the United States of America

2010 Volume 107, Issue 43, Page(s) 18563–18568

Abstract	Upon B-cell activation, the signaling subunits Ig-α and Ig-β of the B-cell antigen receptor become phosphorylated not only on tyrosines but also on serine residues. Using a specific antibody, we show that serine 197 (S197) in the cytoplasmic tail of Ig-α is phosphorylated upon B-cell antigen receptor activation, and that this modification inhibits the signal output of the B-cell antigen receptor. Surprisingly, we found that the well-known protein tyrosine kinase Syk (spleen tyrosine kinase) phosphorylates S197 on Ig-α, thus not only activating but also inhibiting signaling from the B-cell antigen receptor. This finding identifies Syk as a dual-specificity kinase and establishes a previously unexplored paradigm for the self-regulation of biological signaling processes.
MeSH term(s)	Amino Acid Sequence ; Animals ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; CD79 Antigens/chemistry ; CD79 Antigens/genetics ; CD79 Antigens/metabolism ; Cell Line ; Drosophila ; Intracellular Signaling Peptides and Proteins/chemistry ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Mice, Transgenic ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Protein-Tyrosine Kinases/chemistry ; Protein-Tyrosine Kinases/genetics ; Protein-Tyrosine Kinases/metabolism ; Receptors, Antigen, B-Cell/chemistry ; Receptors, Antigen, B-Cell/genetics ; Receptors, Antigen, B-Cell/metabolism ; Recombinant Proteins/chemistry ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; Serine/chemistry ; Signal Transduction ; Structural Homology, Protein ; Syk Kinase
Chemical Substances	CD79 Antigens ; Cd79a protein, mouse ; Intracellular Signaling Peptides and Proteins ; Receptors, Antigen, B-Cell ; Recombinant Proteins ; Serine (452VLY9402) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Syk Kinase (EC 2.7.10.2) ; Syk protein, mouse (EC 2.7.10.2)
Language	English
Publishing date	2010-10-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1009048107
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