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Book ; Thesis: Rolle der Raf Kinasen und des LIM-Domänen Proteins FHL2 während der Zelldifferenzierung

Wixler, Viktor

2003

Author's details	vorgelegt von Viktor Wixler
Language	German
Size	4 Bl. : Ill., graph. Darst.
Publishing country	Germany
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Erlangen-Nürnberg, Univ., Diss., 2003
Note	Enth. Zs-Aufsätze als Anfang
HBZ-ID	HT014006592
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: The role of FHL2 in wound healing and inflammation.

Wixler, Viktor

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2019 Volume 33, Issue 7, Page(s) 7799–7809

Abstract: The 4-and-a-half LIM domain protein 2 (FHL2) is a multifunctional adaptor protein that can interact with cell surface receptors, cytosolic adaptor and structural proteins, kinases, and nuclear transcription factors. It is involved in numerous functional ... ...

Abstract	The 4-and-a-half LIM domain protein 2 (FHL2) is a multifunctional adaptor protein that can interact with cell surface receptors, cytosolic adaptor and structural proteins, kinases, and nuclear transcription factors. It is involved in numerous functional activities, including the epithelial-mesenchymal transition, cell proliferation, apoptosis, adhesion, migration, structural stability, and gene expression. Despite this, FHL2-knockout (KO) mice are viable and fertile with no obvious abnormalities, rather suggesting a high capacity for fine-tuning adjustment and functional redundancy of FHL2. Indeed, challenging FHL2-KO cells or mice provided numerous evidences for the great functional significance of FHL2. In recent years, several reviews have been published describing the high capacity of FHL2 to bind diverse proteins as well as the versatile functions of FHL2, emphasizing in particular its role in cardiovascular diseases and carcinogenesis. Here, we view the function of FHL2 from a different perspective. We summarize the published data demonstrating the impact of FHL2 on wound healing and inflammation. FHL2 seems to be involved in numerous steps of these extremely complex and multidirectional but tightly regulated tissue remodeling processes, supporting tissue repair and coordinating inflammation. Deficiency of FHL2 not only slows down ongoing wound healing but also often turns it into a chronic condition.-Wixler, V. The role of FHL2 in wound healing and inflammation.
MeSH term(s)	Animals ; Chemotaxis, Leukocyte/physiology ; Cytokines/physiology ; Epithelial-Mesenchymal Transition/physiology ; Inflammation/immunology ; Inflammation/physiopathology ; LIM-Homeodomain Proteins/biosynthesis ; LIM-Homeodomain Proteins/deficiency ; LIM-Homeodomain Proteins/genetics ; LIM-Homeodomain Proteins/physiology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Muscle Proteins/biosynthesis ; Muscle Proteins/deficiency ; Muscle Proteins/genetics ; Muscle Proteins/physiology ; Myofibroblasts/physiology ; Regeneration/physiology ; Signal Transduction/physiology ; Transcription Factors/biosynthesis ; Transcription Factors/deficiency ; Transcription Factors/genetics ; Transcription Factors/physiology ; Transcription, Genetic/physiology ; Up-Regulation ; Wound Healing/physiology
Chemical Substances	Cytokines ; Fhl2 protein, mouse ; LIM-Homeodomain Proteins ; Muscle Proteins ; Transcription Factors
Language	English
Publishing date	2019-04-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.201802765RR
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Article ; Online: Small Spleen Peptides (SSPs) Shape Dendritic Cell Differentiation through Modulation of Extracellular ATP Synthesis Profile.

Wixler, Viktor / Leite Dantas, Rafael / Varga, Georg / Boergeling, Yvonne / Ludwig, Stephan

Biomolecules

2024 Volume 14, Issue 4

Abstract: Restoring peripheral immune tolerance is crucial for addressing autoimmune diseases. An ancient mechanism in maintaining the balance between inflammation and tolerance is the ratio of extracellular ATP (exATP) and adenosine. Our previous research ... ...

Abstract	Restoring peripheral immune tolerance is crucial for addressing autoimmune diseases. An ancient mechanism in maintaining the balance between inflammation and tolerance is the ratio of extracellular ATP (exATP) and adenosine. Our previous research demonstrated the effectiveness of small spleen peptides (SSPs) in inhibiting psoriatic arthritis progression, even in the presence of the pro-inflammatory cytokine TNFα, by transforming dendritic cells (DCs) into tolerogenic cells and fostering regulatory Foxp3
MeSH term(s)	Dendritic Cells/metabolism ; Dendritic Cells/drug effects ; Dendritic Cells/immunology ; Adenosine Triphosphate/metabolism ; Adenosine Triphosphate/pharmacology ; Animals ; Cell Differentiation/drug effects ; Spleen/cytology ; Spleen/metabolism ; Spleen/drug effects ; Spleen/immunology ; Mice ; Thymosin/pharmacology ; Thymosin/metabolism ; Peptides/pharmacology ; Arthritis, Psoriatic/drug therapy ; Arthritis, Psoriatic/metabolism ; Arthritis, Psoriatic/immunology ; Humans ; Mice, Inbred C57BL ; Immune Tolerance/drug effects
Chemical Substances	Adenosine Triphosphate (8L70Q75FXE) ; Thymosin (61512-21-8) ; Peptides ; thymosin beta(4) (549LM7U24W)
Language	English
Publishing date	2024-04-11
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom14040469
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Article: Replication-incompetent influenza A viruses armed with IFN-γ effectively mediate immune modulation and tumor destruction in mice harboring lung cancer.

Meissner, Ramona / Wixler, Viktor / Wulfert, Franziska Paulina / Jacob, Jasmin Carina / Hale, Benjamin G / Robeck, Thomas / Masemann, Dörthe / Boergeling, Yvonne / Ludwig, Stephan

Molecular therapy oncolytics

2023 Volume 31, Page(s) 100741

Abstract: Low pathogenic influenza A viruses (IAVs) have shown promising oncolytic potential in lung cancer-bearing mice. However, as replication-competent pathogens, they may cause side effects in immunocompromised cancer patients. To circumvent this problem, we ... ...

Abstract	Low pathogenic influenza A viruses (IAVs) have shown promising oncolytic potential in lung cancer-bearing mice. However, as replication-competent pathogens, they may cause side effects in immunocompromised cancer patients. To circumvent this problem, we genetically engineered nonreplicating IAVs lacking the hemagglutinin (HA) gene (ΔHA IAVs), but reconstituted the viral envelope with recombinant HA proteins to allow a single infection cycle. To optimize the therapeutic potential and improve immunomodulatory properties, these replication-incompetent IAVs were complemented with a murine interferon-gamma (mIFN-γ) gene. After intratracheal administration to transgenic mice that develop non-small cell lung cancer (NSCLC), the ΔHA IAVs induced potent tumor destruction. However, ΔHA IAVs armed with mIFN-γ exhibited an even stronger and more sustained effect, achieving 85% tumor reduction at day 12 postinfection. In addition, ΔHA-mIFN-γ viruses were proven to be efficient in recruiting and activating natural killer cells and macrophages from the periphery and in inducing cytotoxic T lymphocytes. Most important, both viruses, and particularly IFN-γ-encoding viruses, activated tumor-associated alveolar macrophages toward a proinflammatory M1-like phenotype. Therefore, replication-incompetent ΔHA-mIFN-γ-IAVs are safe and efficient oncolytic viruses that additionally exhibit immune cell activating properties and thus represent a promising innovative therapeutic option in the fight against NSCLC.
Language	English
Publishing date	2023-10-31
Publishing country	United States
Document type	Journal Article
ISSN	2372-7705
ISSN	2372-7705
DOI	10.1016/j.omto.2023.100741
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Article ; Online: Inflammatory Cytokines Stabilize SOXC Transcription Factors to Mediate the Transformation of Fibroblast-Like Synoviocytes in Arthritic Disease.

Bhattaram, Pallavi / Muschler, George / Wixler, Viktor / Lefebvre, Véronique

Arthritis & rheumatology (Hoboken, N.J.)

2018 Volume 70, Issue 3, Page(s) 371–382

Abstract: Objective: Fibroblast-like synoviocytes (FLS) produce key synovial fluid and tissue components to ensure joint integrity under healthy conditions, whereas they become cancer-like and aggressively contribute to joint degeneration in inflammatory ... ...

Abstract	Objective: Fibroblast-like synoviocytes (FLS) produce key synovial fluid and tissue components to ensure joint integrity under healthy conditions, whereas they become cancer-like and aggressively contribute to joint degeneration in inflammatory arthritis. The aim of this study was to determine whether the SOXC transcription factors SOX4 and SOX11, whose functions are critical in joint development and many cancer types, contribute to FLS activities under normal and inflammatory conditions. Methods: We inactivated the SOXC genes in FLS from adult mice and studied the effect on joint homeostasis and tumor necrosis factor (TNF)-induced arthritis. We used primary cells and synovial biopsy specimens from arthritis patients to analyze the interactions between inflammatory signals and SOXC proteins. Results: Postnatal inactivation of the SOXC genes had no major effect on joint integrity in otherwise healthy mice. However, it hampered synovial hyperplasia and joint degeneration in transgenic mice expressing human TNF. These effects were explained by the ability of SOX4/11 to amplify the pathogenic impact of TNF on FLS by increasing their survival and migration. SOXC RNA levels were not changed by TNF and other proinflammatory cytokines, but SOXC proteins were strongly stabilized and able to potentiate the TNF-induced up-regulation of genes involved in FLS transformation. Substantiating the relevance of these findings in human disease, SOXC protein levels, but not RNA levels, were significantly higher in inflamed synovium than in noninflamed synovium from arthritis patients. Conclusion: SOXC proteins are targets and pivotal mediators of proinflammatory cytokines during FLS transformation in arthritic diseases. Targeting of these proteins could thus improve current strategies to treat arthritic diseases and possibly other inflammatory diseases.
MeSH term(s)	Animals ; Arthritis/metabolism ; Cell Transformation, Neoplastic/metabolism ; Cells, Cultured ; Cytokines/metabolism ; Humans ; In Situ Hybridization ; Mice ; Real-Time Polymerase Chain Reaction ; SOXC Transcription Factors/metabolism ; Synovial Membrane/metabolism ; Synoviocytes/metabolism ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Cytokines ; SOXC Transcription Factors ; TNF protein, human ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2018-02-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2756371-6
ISSN	2326-5205 ; 2326-5191
ISSN (online)	2326-5205
ISSN	2326-5191
DOI	10.1002/art.40386
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Article: PD-1 IC Inhibition Synergistically Improves Influenza A Virus-Mediated Oncolysis of Metastatic Pulmonary Melanoma.

Sitnik, Siarhei / Masemann, Dörthe / Leite Dantas, Rafael / Wixler, Viktor / Ludwig, Stephan

Molecular therapy oncolytics

2020 Volume 17, Page(s) 190–204

Abstract: Recently, we showed that infection of primary lung tumor-bearing mice with oncolytic influenza A viruses (IAVs) led to strong virus-induced tumor cell lysis but also to restoration of immune competence of innate immune cells. Murine B16-F10 melanoma ... ...

Abstract	Recently, we showed that infection of primary lung tumor-bearing mice with oncolytic influenza A viruses (IAVs) led to strong virus-induced tumor cell lysis but also to restoration of immune competence of innate immune cells. Murine B16-F10 melanoma cells are known for their high lung tropism and progressive growth. As these cells are also highly permissive for IAVs, we analyzed their oncolytic and immunomodulatory efficiency against pulmonary B16-F10 lung metastases
Language	English
Publishing date	2020-04-08
Publishing country	United States
Document type	Journal Article
ISSN	2372-7705
ISSN	2372-7705
DOI	10.1016/j.omto.2020.03.023
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Article ; Online: Influenza A virus NS1 protein-induced JNK activation and apoptosis are not functionally linked.

Nacken, Wolfgang / Wixler, Viktor / Ehrhardt, Christina / Ludwig, Stephan

Cellular microbiology

2017 Volume 19, Issue 7

Abstract: Expression of the influenza A virus (IAV) nonstructural protein (NS1) results in the activation of c-Jun N-terminal kinase (JNK). Both NS1 and JNK are involved in apoptosis induction. To investigate their interrelationship, we stably expressed a ... ...

Abstract	Expression of the influenza A virus (IAV) nonstructural protein (NS1) results in the activation of c-Jun N-terminal kinase (JNK). Both NS1 and JNK are involved in apoptosis induction. To investigate their interrelationship, we stably expressed a tamoxifen inducible NS1 oestrogen receptor fusion-protein (NS1ERT) in mammalian cells. Upon tamoxifen stimulation, NS1ERT-expressing cells partially rescued the attenuated replication of NS1-deficient IAVs and also inhibited interferon up-regulation, confirming the functional competence of NS1ERT. Tamoxifen-induced NS1ERT created a cytopathic phenotype and led to the activation of JNK and apoptosis. Induction of NS1F103SERT mutant failed to activate JNK, but induced apoptosis, whereas the induction of NS1M106IERT led to JNK phosphorylation, but not apoptosis, indicating that JNK activation and apoptosis induction are not functionally linked. Further mutational analysis highlighted that apoptosis induction is a function of the C-terminal effector domain of NS1. Finally, IAVs encoding mutant NS1 revealed a modulating effect of NS1 on apoptosis induction in a genuine infection. With respect to apoptogenicity, an NS1 mutant virus that results in a super activation of JNK behaves similarly to the JNK nonactivating virus expressing NS1F103S, thus confirming that NS1-mediated JNK activation and apoptosis induction are also functionally independent from each other in vivo.
Language	English
Publishing date	2017-07
Publishing country	England
Document type	Journal Article
ZDB-ID	1468320-9
ISSN	1462-5822 ; 1462-5814
ISSN (online)	1462-5822
ISSN	1462-5814
DOI	10.1111/cmi.12721
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Article ; Online: Synergistic anti-tumor efficacy of oncolytic influenza viruses and B7-H3 immune- checkpoint inhibitors against IC-resistant lung cancers.

Masemann, Dörthe / Meissner, Ramona / Schied, Tanja / Lichty, Brian D / Rapp, Ulf R / Wixler, Viktor / Ludwig, Stephan

Oncoimmunology

2021 Volume 10, Issue 1, Page(s) 1885778

Abstract: Non-small cell lung cancers (NSCLCs) establish a highly immunosuppressive tumor microenvironment supporting cancer growth. To interfere with cancer-mediated immunosuppression, selective immune-checkpoint inhibitors (ICIs) have been approved as a standard- ...

Abstract	Non-small cell lung cancers (NSCLCs) establish a highly immunosuppressive tumor microenvironment supporting cancer growth. To interfere with cancer-mediated immunosuppression, selective immune-checkpoint inhibitors (ICIs) have been approved as a standard-of-care treatment for NSCLCs. However, the majority of patients poorly respond to ICI-based immunotherapies. Oncolytic viruses are amongst the many promising immunomodulatory treatments tested as standalone therapy or in combination with ICIs to improve therapeutic outcome. Previously, we demonstrated the oncolytic and immunomodulatory efficacy of low-pathogenic influenza Aviruses (IAVs) against NSCLCs in immunocompetent transgenic mice with alung-specific overexpression of active Raf kinase (Raf-BxB). IAV infection not only resulted in significant primary virus-induced oncolysis, but also caused afunctional reversion of tumor-associated macrophages (TAMs) comprising additional anti-cancer activity. Here we show that NSCLCs as well as TAMs and cytotoxic immune cells overexpress IC molecules of the PD-L2/PD-1 and B7-H3 signaling axes. Thus, we aimed to combine oncolytic IAV-infection with ICIs to exploit the benefits of both anti-cancer approaches. Strikingly, IAV infection combined with the novel B7-H3 ICI led to increased levels of M1-polarized alveolar macrophages and increased lung infiltration by cytotoxic Tlymphocytes, which finally resulted in significantly improved oncolysis of about 80% of existing tumors. In contrast, application of clinically approved α-PD-1 IC antibodies alone or in combination with oncolytic IAV did not provide additional oncolytic or immunomodulatory efficacy. Thus, individualized therapy with synergistically acting oncolytic IAV and B7-H3 ICI might be an innovative future approach to target NSCLCs that are resistant to approved ICIs in patients.
MeSH term(s)	Animals ; Humans ; Immune Checkpoint Inhibitors ; Influenza, Human ; Lung ; Lung Neoplasms/therapy ; Mice ; Oncolytic Viruses/genetics ; Orthomyxoviridae ; Tumor Microenvironment
Chemical Substances	Immune Checkpoint Inhibitors
Language	English
Publishing date	2021-02-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2645309-5
ISSN	2162-402X ; 2162-4011
ISSN (online)	2162-402X
ISSN	2162-4011
DOI	10.1080/2162402X.2021.1885778
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Article ; Online: Phosphorylation of JIP4 at S730 Presents Antiviral Properties against Influenza A Virus Infection.

Del Sarto, Juliana / Gerlt, Vanessa / Friedrich, Marcel Edgar / Anhlan, Darisuren / Wixler, Viktor / Teixeira, Mauro Martins / Boergeling, Yvonne / Ludwig, Stephan

Journal of virology

2021 Volume 95, Issue 20, Page(s) e0067221

Abstract: Influenza A virus (IAV) is the causative agent of flu disease that results in annual epidemics and occasional pandemics. IAV alters several signaling pathways of the cellular host response in order to promote its replication. Therefore, some of these ... ...

Abstract	Influenza A virus (IAV) is the causative agent of flu disease that results in annual epidemics and occasional pandemics. IAV alters several signaling pathways of the cellular host response in order to promote its replication. Therefore, some of these pathways can serve as targets for novel antiviral agents. Here, we show that c-Jun NH
MeSH term(s)	A549 Cells ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Chlorocebus aethiops ; Dogs ; Host-Pathogen Interactions/genetics ; Humans ; Immune Evasion/genetics ; Immunity, Innate/genetics ; Influenza A virus/metabolism ; Influenza A virus/physiology ; Influenza, Human/virology ; Interferons/genetics ; Madin Darby Canine Kidney Cells ; Phosphorylation ; Signal Transduction/genetics ; Vero Cells ; Virus Replication/genetics ; p38 Mitogen-Activated Protein Kinases/genetics ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; SPAG9 protein, human ; Interferons (9008-11-1) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2021-07-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.00672-21
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Article ; Online: Phosphorylation of Influenza A Virus NS1 at Serine 205 Mediates Its Viral Polymerase-Enhancing Function.

Patil, Amol / Anhlan, Darisuren / Ferrando, Verónica / Mecate-Zambrano, Angeles / Mellmann, Alexander / Wixler, Viktor / Boergeling, Yvonne / Ludwig, Stephan

Journal of virology

2021 Volume 95, Issue 6

Abstract: Influenza A virus (IAV) nonstructural protein 1 (NS1) is a protein with multiple functions that are regulated by phosphorylation. Phosphoproteomic screening of H1N1 virus-infected cells revealed that NS1 was phosphorylated at serine 205 in intermediate ... ...

Abstract	Influenza A virus (IAV) nonstructural protein 1 (NS1) is a protein with multiple functions that are regulated by phosphorylation. Phosphoproteomic screening of H1N1 virus-infected cells revealed that NS1 was phosphorylated at serine 205 in intermediate stages of the viral life cycle. Interestingly, S205 is one of six amino acid changes in NS1 of post-pandemic H1N1 viruses currently circulating in humans compared to the original swine-origin 2009 pandemic (H1N1pdm09) virus, suggesting a role in host adaptation. To identify NS1 functions regulated by S205 phosphorylation, we generated recombinant PR8 H1N1 NS1 mutants with S205G (nonphosphorylatable) or S205N (H1N1pdm09 signature), as well as H1N1pdm09 viruses harboring the reverse mutation NS1 N205S or N205D (phosphomimetic). Replication of PR8 NS1 mutants was attenuated relative to wild-type (WT) virus replication in a porcine cell line. However, PR8 NS1 S205N showed remarkably higher attenuation than PR8 NS1 S205G in a human cell line, highlighting a potential host-independent advantage of phosphorylatable S205, while an asparagine at this position led to a potential host-specific attenuation. Interestingly, PR8 NS1 S205G did not show polymerase activity-enhancing functions, in contrast to the WT, which can be attributed to diminished interaction with cellular restriction factor DDX21. Analysis of the respective kinase mediating S205 phosphorylation indicated an involvement of casein kinase 2 (CK2). CK2 inhibition significantly reduced the replication of WT viruses and decreased NS1-DDX21 interaction, as observed for NS1 S205G. In summary, NS1 S205 is required for efficient NS1-DDX21 binding, resulting in enhanced viral polymerase activity, which is likely to be regulated by transient phosphorylation.
MeSH term(s)	Adaptation, Physiological/genetics ; Animals ; Casein Kinase II/metabolism ; Cell Line ; DEAD-box RNA Helicases/metabolism ; Host-Pathogen Interactions ; Humans ; Influenza A Virus, H1N1 Subtype/genetics ; Influenza A Virus, H1N1 Subtype/metabolism ; Influenza A Virus, H1N1 Subtype/physiology ; Influenza A virus/genetics ; Influenza A virus/metabolism ; Influenza A virus/physiology ; Mutation ; Phosphorylation ; Protein Binding ; RNA-Dependent RNA Polymerase/metabolism ; Serine/metabolism ; Swine ; Viral Nonstructural Proteins/genetics ; Viral Nonstructural Proteins/metabolism ; Virus Replication
Chemical Substances	INS1 protein, influenza virus ; Viral Nonstructural Proteins ; Serine (452VLY9402) ; Casein Kinase II (EC 2.7.11.1) ; RNA-Dependent RNA Polymerase (EC 2.7.7.48) ; DDX21 protein, human (EC 3.6.1.-) ; DEAD-box RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2021-02-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.02369-20
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