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Conventional Light Chains Inhibit the Autonomous Signaling Capacity of the B Cell Receptor

Immunity (Cambridge, Mass.), 2007-03, Vol.26 (3), p.323-333

2007

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Deregulated Syk inhibits differentiation and induces growth factor-independent proliferation of pre-B cells

The Journal of experimental medicine, 2006-12, Vol.203 (13), p.2829-2840

2006

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AID‐expressing epithelium is protected from oncogenic transformation by an NKG2D surveillance pathway

EMBO molecular medicine, 2015-10, Vol.7 (10), p.1327-1336

2015

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Chronic lymphocytic leukaemia is driven by antigen-independent cell-autonomous signalling

Nature (London), 2012-09, Vol.489 (7415), p.309-312

2012

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The BTG2-PRMT1 module limits pre-B cell expansion by regulating the CDK4-Cyclin-D3 complex

Nature immunology, 2017-08, Vol.18 (8), p.911-920

2017

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Responsiveness of B cells is regulated by the hinge region of IgD

Nature immunology, 2015-05, Vol.16 (5), p.534-543

2015

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FoxO1 induces Ikaros splicing to promote immunoglobulin gene recombination

The Journal of experimental medicine, 2012-02, Vol.209 (2), p.395-406

2012

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N-linked glycosylation selectively regulates autonomous precursor BCR function

Nature immunology, 2010-08, Vol.11 (8), p.759-765

2010

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Amplification of B Cell Antigen Receptor Signaling by a Syk/ITAM Positive Feedback Loop

Molecular cell, 2002-11, Vol.10 (5), p.1057-1069

2002

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The Role of the BCR Class Expressed by Eμ-TCL1tg Mice and Human CLL

Blood, 2012-11, Vol.120 (21), p.182-182

2012

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Erratum: Responsiveness of B cells is regulated by the hinge region of IgD

Nature immunology, 2015-07, Vol.16 (7), p.785-785

2015

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AID ‐expressing epithelium is protected from oncogenic transformation by an NKG 2D surveillance pathway

EMBO molecular medicine, 2015-10, Vol.7 (10), p.1327-1336

2015

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AID-expressing epithelium is protected from oncogenic transformation by an NKG2D surveillance pathway

EMBO molecular medicine, 2015-10, Vol.7 (10), p.1327

2015

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B cell antigen receptor assembly and Syk activation in the S2 cell reconstitution system

Immunology letters, 2004-03, Vol.92 (1), p.67-73

2004

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Identification of a pre-BCR lacking surrogate light chain

The Journal of experimental medicine, 2003-12, Vol.198 (11), p.1699-1706

2003

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Deregulated Syk inhibits differentiation and induces growth factor–independent proliferation of pre–B cells

The Journal of cell biology, 2006-12, Vol.175 (6), p.i14-i14

2006

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Frequent Loss of the SLP-65 Adapter Protein in Childhood Acute B-Precursor Lymphoblastic Leukemia (ALL) with TEL/AML1 Rearrangement

Blood, 2005-11, Vol.106 (11), p.741-741

2005

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The Expression of the Adaptor Protein SLP-65 Is Freqently Lost in Childhood B-Lineage Acute Lymphoblastic Leukemia (ALL)

Blood, 2004-11, Vol.104 (11), p.1118-1118

2004

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Conventional Light Chains Inhibit the Autonomous Signaling Capacity of the B Cell Receptor

Deregulated Syk inhibits differentiation and induces growth factor-independent proliferation of pre-B cells

AID‐expressing epithelium is protected from oncogenic transformation by an NKG2D surveillance pathway

Chronic lymphocytic leukaemia is driven by antigen-independent cell-autonomous signalling

The BTG2-PRMT1 module limits pre-B cell expansion by regulating the CDK4-Cyclin-D3 complex

Responsiveness of B cells is regulated by the hinge region of IgD

FoxO1 induces Ikaros splicing to promote immunoglobulin gene recombination

N-linked glycosylation selectively regulates autonomous precursor BCR function

Amplification of B Cell Antigen Receptor Signaling by a Syk/ITAM Positive Feedback Loop

The Role of the BCR Class Expressed by Eμ-TCL1tg Mice and Human CLL

Erratum: Responsiveness of B cells is regulated by the hinge region of IgD

AID ‐expressing epithelium is protected from oncogenic transformation by an NKG 2D surveillance pathway

AID-expressing epithelium is protected from oncogenic transformation by an NKG2D surveillance pathway

B cell antigen receptor assembly and Syk activation in the S2 cell reconstitution system

Identification of a pre-BCR lacking surrogate light chain

Deregulated Syk inhibits differentiation and induces growth factor–independent proliferation of pre–B cells

Frequent Loss of the SLP-65 Adapter Protein in Childhood Acute B-Precursor Lymphoblastic Leukemia (ALL) with TEL/AML1 Rearrangement

The Expression of the Adaptor Protein SLP-65 Is Freqently Lost in Childhood B-Lineage Acute Lymphoblastic Leukemia (ALL)

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