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Book ; Online ; Thesis: MALT1 phosphorylation controls activation of T lymphocytes

Gehring, Torben [Verfasser] / Krappmann, Daniel [Akademischer Betreuer]

2019

Author's details	Torben Gehring ; Betreuer: Daniel Krappmann
Keywords	Biowissenschaften, Biologie ; Life Science, Biology
Subject code	sg570
Language	English
Publisher	Universitätsbibliothek der Ludwig-Maximilians-Universität
Publishing place	München
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article: BCL10 - Bridging CARDs to Immune Activation.

Gehring, Torben / Seeholzer, Thomas / Krappmann, Daniel

Frontiers in immunology

2018 Volume 9, Page(s) 1539

Abstract: Since the B-cell lymphoma/leukemia 10 (BCL10) protein was first described in 1999, numerous studies have elucidated its key functions in channeling adaptive and innate immune signaling downstream of CARMA/caspase-recruitment domain (CARD) scaffold ... ...

Abstract	Since the B-cell lymphoma/leukemia 10 (BCL10) protein was first described in 1999, numerous studies have elucidated its key functions in channeling adaptive and innate immune signaling downstream of CARMA/caspase-recruitment domain (CARD) scaffold proteins. While T and B cell antigen receptor (TCR/BCR) signaling induces the recruitment of BCL10 bound to mucosa-associated lymphoid tissue (MALT)1 to the lymphocyte-specific CARMA1/CARD11-BCL10-MALT1 (CBM-1) signalosome, alternative CBM complexes utilize different CARMA/CARD scaffolds in distinct innate or inflammatory pathways. BCL10 constitutes the smallest subunit in all CBM signalosomes, containing a 233 amino acid coding for N-terminal CARD as well as a C-terminal Ser/Thr-rich region. BCL10 forms filaments, thereby aggregating into higher-order clusters that mediate and amplify stimulation-induced signals, ultimately leading to MALT1 protease activation and canonical NF-κB and JNK signaling. BCL10 additionally undergoes extensive post-translational regulation involving phosphorylation, ubiquitination, MALT1-catalyzed cleavage, and degradation. Through these feedback and feed-forward events, BCL10 integrates positive and negative regulatory processes that govern the function as well as the dynamic assembly, disassembly, and destruction of CBM complexes. Thus, BCL10 is a critical regulator for activation as well as termination of immune cell signaling, revealing that its role extends far beyond that of a mere linking factor in CBM complexes.
Language	English
Publishing date	2018
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2018.01539
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Article ; Online: Phosphorylation of serine-893 in CARD11 suppresses the formation and activity of the CARD11-BCL10-MALT1 complex in T and B cells.

Kutzner, Kerstin / Woods, Simone / Karayel, Ozge / Gehring, Torben / Yin, Hongli / Flatley, Andrew / Graß, Carina / Wimberger, Nicole / Tofaute, Marie J / Seeholzer, Thomas / Feederle, Regina / Mann, Matthias / Krappmann, Daniel

Science signaling

2022 Volume 15, Issue 723, Page(s) eabk3083

Abstract: CARD11 acts as a gatekeeper for adaptive immune responses after T cell or B cell antigen receptor (TCR/BCR) ligation on lymphocytes. PKCθ/β-catalyzed phosphorylation of CARD11 promotes the assembly of the CARD11-BCL10-MALT1 (CBM) complex and lymphocyte ... ...

Abstract	CARD11 acts as a gatekeeper for adaptive immune responses after T cell or B cell antigen receptor (TCR/BCR) ligation on lymphocytes. PKCθ/β-catalyzed phosphorylation of CARD11 promotes the assembly of the CARD11-BCL10-MALT1 (CBM) complex and lymphocyte activation. Here, we demonstrated that PKCθ/β-dependent CARD11 phosphorylation also suppressed CARD11 functions in T or B cells. Through mass spectrometry-based proteomics analysis, we identified multiple constitutive and inducible CARD11 phosphorylation sites in T cells. We demonstrated that a single TCR- or BCR-inducible phosphorylation on Ser
MeSH term(s)	B-Cell CLL-Lymphoma 10 Protein/genetics ; B-Cell CLL-Lymphoma 10 Protein/metabolism ; B-Lymphocytes/metabolism ; CARD Signaling Adaptor Proteins/genetics ; CARD Signaling Adaptor Proteins/metabolism ; Guanylate Cyclase/genetics ; Guanylate Cyclase/metabolism ; Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein/genetics ; Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein/metabolism ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Phosphorylation ; Serine
Chemical Substances	B-Cell CLL-Lymphoma 10 Protein ; CARD Signaling Adaptor Proteins ; NF-kappa B ; Serine (452VLY9402) ; Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein (EC 3.4.22.-) ; Guanylate Cyclase (EC 4.6.1.2)
Language	English
Publishing date	2022-03-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2417226-1
ISSN	1937-9145 ; 1945-0877
ISSN (online)	1937-9145
ISSN	1945-0877
DOI	10.1126/scisignal.abk3083
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Article: A20 and ABIN-1 cooperate in balancing CBM complex-triggered NF-κB signaling in activated T cells

Yin, Hongli / Karayel, Ozge / Chao, Ying-Yin / Seeholzer, Thomas / Hamp, Isabel / Plettenburg, Oliver / Gehring, Torben / Zielinski, Christina / Mann, Matthias / Krappmann, Daniel

Cellular and molecular life sciences. 2022 Feb., v. 79, no. 2

2022

Abstract: T cell activation initiates protective adaptive immunity, but counterbalancing mechanisms are critical to prevent overshooting responses and to maintain immune homeostasis. The CARD11-BCL10-MALT1 (CBM) complex bridges T cell receptor engagement to NF-κB ... ...

Abstract	T cell activation initiates protective adaptive immunity, but counterbalancing mechanisms are critical to prevent overshooting responses and to maintain immune homeostasis. The CARD11-BCL10-MALT1 (CBM) complex bridges T cell receptor engagement to NF-κB signaling and MALT1 protease activation. Here, we show that ABIN-1 is modulating the suppressive function of A20 in T cells. Using quantitative mass spectrometry, we identified ABIN-1 as an interactor of the CBM signalosome in activated T cells. A20 and ABIN-1 counteract inducible activation of human primary CD4 and Jurkat T cells. While A20 overexpression is able to silence CBM complex-triggered NF-κB and MALT1 protease activation independent of ABIN-1, the negative regulatory function of ABIN-1 depends on A20. The suppressive function of A20 in T cells relies on ubiquitin binding through the C-terminal zinc finger (ZnF)4/7 motifs, but does not involve the deubiquitinating activity of the OTU domain. Our mechanistic studies reveal that the A20/ABIN-1 module is recruited to the CBM complex via A20 ZnF4/7 and that proteasomal degradation of A20 and ABIN-1 releases the CBM complex from the negative impact of both regulators. Ubiquitin binding to A20 ZnF4/7 promotes destructive K48-polyubiquitination to itself and to ABIN-1. Further, after prolonged T cell stimulation, ABIN-1 antagonizes MALT1-catalyzed cleavage of re-synthesized A20 and thereby diminishes sustained CBM complex signaling. Taken together, interdependent post-translational mechanisms are tightly controlling expression and activity of the A20/ABIN-1 silencing module and the cooperative action of both negative regulators is critical to balance CBM complex signaling and T cell activation.
Keywords	T-lymphocytes ; adaptive immunity ; homeostasis ; humans ; mass spectrometry ; proteinases ; signalosome ; ubiquitin ; zinc finger motif
Language	English
Dates of publication	2022-02
Size	p. 112.
Publishing place	Springer International Publishing
Document type	Article
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-022-04154-z
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: A20 and ABIN-1 cooperate in balancing CBM complex-triggered NF-κB signaling in activated T cells.

Yin, Hongli / Karayel, Ozge / Chao, Ying-Yin / Seeholzer, Thomas / Hamp, Isabel / Plettenburg, Oliver / Gehring, Torben / Zielinski, Christina / Mann, Matthias / Krappmann, Daniel

Cellular and molecular life sciences : CMLS

2022 Volume 79, Issue 2, Page(s) 112

Abstract	T cell activation initiates protective adaptive immunity, but counterbalancing mechanisms are critical to prevent overshooting responses and to maintain immune homeostasis. The CARD11-BCL10-MALT1 (CBM) complex bridges T cell receptor engagement to NF-κB signaling and MALT1 protease activation. Here, we show that ABIN-1 is modulating the suppressive function of A20 in T cells. Using quantitative mass spectrometry, we identified ABIN-1 as an interactor of the CBM signalosome in activated T cells. A20 and ABIN-1 counteract inducible activation of human primary CD4 and Jurkat T cells. While A20 overexpression is able to silence CBM complex-triggered NF-κB and MALT1 protease activation independent of ABIN-1, the negative regulatory function of ABIN-1 depends on A20. The suppressive function of A20 in T cells relies on ubiquitin binding through the C-terminal zinc finger (ZnF)4/7 motifs, but does not involve the deubiquitinating activity of the OTU domain. Our mechanistic studies reveal that the A20/ABIN-1 module is recruited to the CBM complex via A20 ZnF4/7 and that proteasomal degradation of A20 and ABIN-1 releases the CBM complex from the negative impact of both regulators. Ubiquitin binding to A20 ZnF4/7 promotes destructive K48-polyubiquitination to itself and to ABIN-1. Further, after prolonged T cell stimulation, ABIN-1 antagonizes MALT1-catalyzed cleavage of re-synthesized A20 and thereby diminishes sustained CBM complex signaling. Taken together, interdependent post-translational mechanisms are tightly controlling expression and activity of the A20/ABIN-1 silencing module and the cooperative action of both negative regulators is critical to balance CBM complex signaling and T cell activation.
MeSH term(s)	B-Cell CLL-Lymphoma 10 Protein/metabolism ; CARD Signaling Adaptor Proteins/metabolism ; Cells, Cultured ; DNA-Binding Proteins/physiology ; Guanylate Cyclase/metabolism ; HEK293 Cells ; Humans ; Jurkat Cells ; Lymphocyte Activation/genetics ; Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein/metabolism ; Multiprotein Complexes/metabolism ; NF-kappa B/metabolism ; Protein Binding ; RNA Interference/immunology ; Signal Transduction/physiology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Tumor Necrosis Factor alpha-Induced Protein 3/physiology
Chemical Substances	B-Cell CLL-Lymphoma 10 Protein ; BCL10 protein, human ; CARD Signaling Adaptor Proteins ; DNA-Binding Proteins ; Multiprotein Complexes ; NF-kappa B ; TNIP1 protein, human ; TNFAIP3 protein, human (EC 3.4.19.12) ; Tumor Necrosis Factor alpha-Induced Protein 3 (EC 3.4.19.12) ; MALT1 protein, human (EC 3.4.22.-) ; Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein (EC 3.4.22.-) ; CARD11 protein, human (EC 4.6.1.2) ; Guanylate Cyclase (EC 4.6.1.2)
Language	English
Publishing date	2022-01-31
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-022-04154-z
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Article ; Online: Human immune disorder associated with homozygous hypomorphic mutation affecting MALT1B splice variant.

Kutukculer, Necil / Seeholzer, Thomas / O'Neill, Thomas J / Graß, Carina / Aykut, Ayca / Karaca, Neslihan Edeer / Durmaz, Asude / Cogulu, Ozgur / Aksu, Guzide / Gehring, Torben / Gewies, Andreas / Krappmann, Daniel

The Journal of allergy and clinical immunology

2020 Volume 147, Issue 2, Page(s) 775–778.e8

MeSH term(s)	Adolescent ; Consanguinity ; Female ; Humans ; Immune System Diseases/genetics ; Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein/genetics ; Mutation, Missense ; Pedigree ; Protein Isoforms
Chemical Substances	Protein Isoforms ; MALT1 protein, human (EC 3.4.22.-) ; Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein (EC 3.4.22.-)
Keywords	covid19
Language	English
Publishing date	2020-08-25
Publishing country	United States
Document type	Case Reports ; Letter
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2020.07.034
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Article ; Online: BCL10-CARD11 Fusion Mimics an Active CARD11 Seed That Triggers Constitutive BCL10 Oligomerization and Lymphocyte Activation.

Seeholzer, Thomas / Kurz, Susanne / Schlauderer, Florian / Woods, Simone / Gehring, Torben / Widmann, Simon / Lammens, Katja / Krappmann, Daniel

Frontiers in immunology

2018 Volume 9, Page(s) 2695

Abstract: Assembly of the CARD11/CARMA1-BCL10-MALT1 (CBM) signaling complex upon T or B cell antigen receptor (TCR or BCR) engagement drives lymphocyte activation. Recruitment of pre-assembled BCL10-MALT1 complexes to CARD11 fosters activation of the MALT1 ... ...

Abstract	Assembly of the CARD11/CARMA1-BCL10-MALT1 (CBM) signaling complex upon T or B cell antigen receptor (TCR or BCR) engagement drives lymphocyte activation. Recruitment of pre-assembled BCL10-MALT1 complexes to CARD11 fosters activation of the MALT1 protease and canonical NF-
MeSH term(s)	B-Cell CLL-Lymphoma 10 Protein/genetics ; B-Cell CLL-Lymphoma 10 Protein/immunology ; CARD Signaling Adaptor Proteins/genetics ; CARD Signaling Adaptor Proteins/immunology ; Guanylate Cyclase/genetics ; Guanylate Cyclase/immunology ; HEK293 Cells ; Humans ; Jurkat Cells ; Lymphocyte Activation ; Protein Multimerization/genetics ; Protein Multimerization/immunology ; Recombinant Fusion Proteins/genetics ; Recombinant Fusion Proteins/immunology ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology
Chemical Substances	B-Cell CLL-Lymphoma 10 Protein ; BCL10 protein, human ; CARD Signaling Adaptor Proteins ; Recombinant Fusion Proteins ; CARD11 protein, human (EC 4.6.1.2) ; Guanylate Cyclase (EC 4.6.1.2)
Language	English
Publishing date	2018-11-20
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2018.02695
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Article ; Online: Molecular architecture and regulation of BCL10-MALT1 filaments

Florian Schlauderer / Thomas Seeholzer / Ambroise Desfosses / Torben Gehring / Mike Strauss / Karl-Peter Hopfner / Irina Gutsche / Daniel Krappmann / Katja Lammens

Nature Communications, Vol 9, Iss 1, Pp 1-

2018 Volume 12

Abstract: The BCL10-MALT1 complex is a central signaling hub in lymphocytes and linked to various human immune pathologies. Here the authors present the cryo-EM structure of the BCL10-MALT1 filament core and verify the identified BCL10/MALT1 interface with ... ...

Abstract	The BCL10-MALT1 complex is a central signaling hub in lymphocytes and linked to various human immune pathologies. Here the authors present the cryo-EM structure of the BCL10-MALT1 filament core and verify the identified BCL10/MALT1 interface with mutagenesis studies.
Keywords	Science ; Q
Language	English
Publishing date	2018-10-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Molecular architecture and regulation of BCL10-MALT1 filaments

Florian Schlauderer / Thomas Seeholzer / Ambroise Desfosses / Torben Gehring / Mike Strauss / Karl-Peter Hopfner / Irina Gutsche / Daniel Krappmann / Katja Lammens

Nature Communications, Vol 9, Iss 1, Pp 1-

2018 Volume 12

Abstract	The BCL10-MALT1 complex is a central signaling hub in lymphocytes and linked to various human immune pathologies. Here the authors present the cryo-EM structure of the BCL10-MALT1 filament core and verify the identified BCL10/MALT1 interface with mutagenesis studies.
Keywords	Science ; Q
Language	English
Publishing date	2018-10-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Pathological RANK signaling in B cells drives autoimmunity and chronic lymphocytic leukemia.

Alankus, Begüm / Ecker, Veronika / Vahl, Nathalie / Braun, Martina / Weichert, Wilko / Macher-Göppinger, Stephan / Gehring, Torben / Neumayer, Tanja / Zenz, Thorsten / Buchner, Maike / Ruland, Jürgen

The Journal of experimental medicine

2020 Volume 218, Issue 2

Abstract: Clinical evidence suggests alterations in receptor activator of NF-κB (RANK) signaling are key contributors to B cell autoimmunity and malignancy, but the pathophysiological consequences of aberrant B cell-intrinsic RANK signaling remain unknown. We ... ...

Abstract	Clinical evidence suggests alterations in receptor activator of NF-κB (RANK) signaling are key contributors to B cell autoimmunity and malignancy, but the pathophysiological consequences of aberrant B cell-intrinsic RANK signaling remain unknown. We generated mice that express a human lymphoma-derived, hyperactive RANKK240E variant in B lymphocytes in vivo. Forced RANK signaling disrupted B cell tolerance and induced a fully penetrant systemic lupus erythematosus-like disease in addition to the development of chronic lymphocytic leukemia (CLL). Importantly, RANKK240E transgenic CLL cells as well as CLL cells of independent murine and of human origin depend on microenvironmental RANK ligand (RANKL) for tumor cell survival. Consequently, inhibition of the RANKL-RANK axis with anti-RANKL antibodies killed murine and human CLL cells in vitro and in vivo. These results establish pathological B cell-intrinsic RANK signaling as a potential driver of autoimmunity and B cell malignancy, and they suggest the exploitation of clinically available anti-RANKL compounds for CLL treatment.
MeSH term(s)	Animals ; Autoimmunity/immunology ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; Cell Line, Tumor ; Cell Survival/immunology ; Female ; HEK293 Cells ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/immunology ; Leukemia, Lymphocytic, Chronic, B-Cell/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; NF-kappa B/metabolism ; Receptor Activator of Nuclear Factor-kappa B/metabolism ; Signal Transduction/immunology
Chemical Substances	NF-kappa B ; Receptor Activator of Nuclear Factor-kappa B ; TNFRSF11A protein, human
Language	English
Publishing date	2020-11-06
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.20200517
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