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Book: UEBER DIE HAEUFIGKEIT UND DEN THERAPEUTISCHEN EFFEKT DER BEI ENTZUENDLICHEN GELENK- UND WIRBELSAEULENERKRANKUNGEN DURCHGEFUEHRTEN HERDSANIERUNGEN

Zenz, Rainer

1977

Size	42 S.
Document type	Book
Note	MAINZ, UNIV., FACHBEREICH 05-10 - MEDIZIN, DISS., 1977
HBZ-ID	HT002590846
Database	Catalogue ZB MED Medicine, Health

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Article: Jun signalling in the epidermis: From developmental defects to psoriasis and skin tumors.

Zenz, Rainer / Wagner, Erwin F

The international journal of biochemistry & cell biology

2006 Volume 38, Issue 7, Page(s) 1043–1049

Abstract: The Jun proteins Jun, JunB and JunD are core members of activator protein-1 (AP-1), a dimeric transcription factor complex consisting of homo- and heterodimers of the Jun, Fos, activating transcription factor (ATF) and musculoaponeurotic fibrosarcoma ( ... ...

Abstract	The Jun proteins Jun, JunB and JunD are core members of activator protein-1 (AP-1), a dimeric transcription factor complex consisting of homo- and heterodimers of the Jun, Fos, activating transcription factor (ATF) and musculoaponeurotic fibrosarcoma (Maf) families. Growth factors, hormones and a variety of environmental stresses activate mitogen activated protein kinase (MAPK) cascades that enhance Jun/AP-1 activity, e.g. through phosphorylation thereby regulating cell proliferation, differentiation, transformation and/or apoptosis. Embryonic lethality of various AP-1 knock-outs, e.g. for Jun, JunB, Fra-1 and Fra-2 largely prevented functional studies in vivo. Therefore, conditional knock-out strategies, in particular for the epidermis, have become an important model to study the regulation and function of AP-1 subunits in physiological and pathological processes in vivo. Jun is regarded as a positive regulator of keratinocyte proliferation/differentiation during development and in skin cancer through its direct transcriptional effect on epidermal growth factor receptor (EGFR) expression. In contrast, JunB can antagonize proliferation of keratinocytes and hematopoietic stem cells. Furthermore, it has been demonstrated in patient's samples and an inducible mouse model that down-regulation of JunB/AP-1 in keratinocytes is one initiating event in the aetiology of psoriasis which is characterized by increased cell proliferation and deregulated cytokine expression.
MeSH term(s)	Activating Transcription Factors/metabolism ; Animals ; DNA-Binding Proteins/metabolism ; Developmental Biology ; Epidermis/metabolism ; Humans ; Keratinocytes/metabolism ; MAP Kinase Kinase 1/metabolism ; Mice ; Proto-Oncogene Proteins c-fos/metabolism ; Proto-Oncogene Proteins c-jun/metabolism ; Psoriasis/physiopathology ; Signal Transduction/physiology ; Skin Neoplasms/physiopathology ; Transcription Factor AP-1/metabolism ; Transcription Factors/metabolism
Chemical Substances	Activating Transcription Factors ; DNA-Binding Proteins ; Proto-Oncogene Proteins c-fos ; Proto-Oncogene Proteins c-jun ; Transcription Factor AP-1 ; Transcription Factors ; MAP Kinase Kinase 1 (EC 2.7.12.2)
Language	English
Publishing date	2006
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2005.11.011
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Article ; Online: STAT3 promotes melanoma metastasis by CEBP-induced repression of the MITF pathway.

Swoboda, Alexander / Soukup, Robert / Eckel, Oliver / Kinslechner, Katharina / Wingelhofer, Bettina / Schörghofer, David / Sternberg, Christina / Pham, Ha T T / Vallianou, Maria / Horvath, Jaqueline / Stoiber, Dagmar / Kenner, Lukas / Larue, Lionel / Poli, Valeria / Beermann, Friedrich / Yokota, Takashi / Kubicek, Stefan / Krausgruber, Thomas / Rendeiro, André F /

Bock, Christoph / Zenz, Rainer / Kovacic, Boris / Aberger, Fritz / Hengstschläger, Markus / Petzelbauer, Peter / Mikula, Mario / Moriggl, Richard

Oncogene

2020 Volume 40, Issue 6, Page(s) 1091–1105

Abstract: Metastatic melanoma is hallmarked by its ability of phenotype switching to more slowly proliferating, but highly invasive cells. Here, we tested the impact of signal transducer and activator of transcription 3 (STAT3) on melanoma progression in ... ...

Abstract	Metastatic melanoma is hallmarked by its ability of phenotype switching to more slowly proliferating, but highly invasive cells. Here, we tested the impact of signal transducer and activator of transcription 3 (STAT3) on melanoma progression in association with melanocyte inducing transcription factor (MITF) expression levels. We established a mouse melanoma model for deleting Stat3 in melanocytes with specific expression of human hyperactive NRAS
MeSH term(s)	Animals ; CCAAT-Enhancer-Binding Protein-beta/genetics ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Disease Models, Animal ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Melanocytes/drug effects ; Melanoma/genetics ; Melanoma/pathology ; Mice ; Microphthalmia-Associated Transcription Factor/genetics ; Neoplasm Metastasis ; STAT3 Transcription Factor/genetics ; Signal Transduction/drug effects
Chemical Substances	CCAAT-Enhancer-Binding Protein-beta ; Cebpb protein, mouse ; Microphthalmia-Associated Transcription Factor ; Mitf protein, mouse ; STAT3 Transcription Factor ; Stat3 protein, mouse
Language	English
Publishing date	2020-12-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-020-01584-6
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Article: PhiC31-mediated cassette exchange into a bacterial artificial chromosome.

Blaas, Leander / Musteanu, Monica / Zenz, Rainer / Eferl, Robert / Casanova, Emilio

BioTechniques

2007 Volume 43, Issue 5, Page(s) 659–60, 662, 664

Abstract: The use of bacterial artificial chromosomes (BACs) modified via homologous recombination in Escherichia coli has become a powerful tool in the transgenic field. Homologous recombination allows the manipulation of BACs in very different ways. However this ...

Abstract	The use of bacterial artificial chromosomes (BACs) modified via homologous recombination in Escherichia coli has become a powerful tool in the transgenic field. Homologous recombination allows the manipulation of BACs in very different ways. However this process can be cumbersome and problematic when using large targeting constructs containing several repeated elements. In order to address this problem, we have established a phiC31 integrase-mediated cassette exchange into a BAC. As an example of this technique, we have exchanged a cassette previously recombined into a BAC containing the Rosa 26 locus, by a 16.5-kb incoming construct containing several repeated elements. The combination of homologous recombination in E. coli and cassette exchange should expand the tools for manipulating BACs, thus facilitating the generation of constructs with higher complexity.
MeSH term(s)	Bacteriophages/enzymology ; Chromosomes, Artificial, Bacterial/genetics ; Integrases/metabolism ; Mutagenesis, Insertional/methods
Chemical Substances	Integrases (EC 2.7.7.-)
Language	English
Publishing date	2007-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	48453-2
ISSN	1940-9818 ; 0736-6205
ISSN (online)	1940-9818
ISSN	0736-6205
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Article: Simultaneous generation of fra-2 conditional and fra-2 knock-out mice.

Eferl, Robert / Zenz, Rainer / Theussl, Hans-Christian / Wagner, Erwin F

Genesis (New York, N.Y. : 2000)

2007 Volume 45, Issue 7, Page(s) 447–451

Abstract: Loss of function mouse models comprise knock-out mice, where a gene is deleted in the germline, and conditional knock-out mice with somatic deletion of a floxed allele in defined tissues. Both types of mice are used for comprehensive studies of gene ... ...

Abstract	Loss of function mouse models comprise knock-out mice, where a gene is deleted in the germline, and conditional knock-out mice with somatic deletion of a floxed allele in defined tissues. Both types of mice are used for comprehensive studies of gene functions in vivo. Here, we describe a simple method for simultaneous generation of mice with conditional or knock-out alleles for the transcription factor fra-2 (Fos-related antigen 2) using a single embryonic stem (ES) cell clone. ES cells with a floxed fra-2 allele were transiently transfected with a Cre-recombinase expression plasmid and plated at low density. Most of the resulting ES cell colonies consisted of a mixture of cells that have either retained or lost the conditional allele. We demonstrate that these mixed ES cell clones can be directly used for generation of chimeras that give rise to offspring with conditional or knock-out alleles simultaneously. This strategy shortens the time and reduces the number of germline transmission events to generate genetically modified mice.
MeSH term(s)	Animals ; Fos-Related Antigen-2/deficiency ; Fos-Related Antigen-2/genetics ; Genes, Lethal ; Mice ; Mice, Knockout
Chemical Substances	Fos-Related Antigen-2 ; Fosl2 protein, mouse
Language	English
Publishing date	2007-07
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2004544-X
ISSN	1526-968X ; 1526-954X
ISSN (online)	1526-968X
ISSN	1526-954X
DOI	10.1002/dvg.20311
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Article ; Online: Differentiation-induced skin cancer suppression by FOS, p53, and TACE/ADAM17.

Guinea-Viniegra, Juan / Zenz, Rainer / Scheuch, Harald / Jiménez, María / Bakiri, Latifa / Petzelbauer, Peter / Wagner, Erwin F

The Journal of clinical investigation

2012 Volume 122, Issue 8, Page(s) 2898–2910

Abstract: Squamous cell carcinomas (SCCs) are heterogeneous and aggressive skin tumors for which innovative, targeted therapies are needed. Here, we identify a p53/TACE pathway that is negatively regulated by FOS and show that the FOS/p53/TACE axis suppresses SCC ... ...

Abstract	Squamous cell carcinomas (SCCs) are heterogeneous and aggressive skin tumors for which innovative, targeted therapies are needed. Here, we identify a p53/TACE pathway that is negatively regulated by FOS and show that the FOS/p53/TACE axis suppresses SCC by inducing differentiation. We found that epidermal Fos deletion in mouse tumor models or pharmacological FOS/AP-1 inhibition in human SCC cell lines induced p53 expression. Epidermal cell differentiation and skin tumor suppression were caused by a p53-dependent transcriptional activation of the metalloprotease TACE/ADAM17 (TNF-α-converting enzyme), a previously unknown p53 target gene that was required for NOTCH1 activation. Although half of cutaneous human SCCs display p53-inactivating mutations, restoring p53/TACE activity in mouse and human skin SCCs induced tumor cell differentiation independently of the p53 status. We propose FOS/AP-1 inhibition or p53/TACE reactivating strategies as differentiation-inducing therapies for SCCs.
MeSH term(s)	ADAM Proteins/genetics ; ADAM Proteins/metabolism ; ADAM17 Protein ; Animals ; Base Sequence ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/pathology ; Carcinoma, Squamous Cell/therapy ; Cell Differentiation ; Cell Line, Tumor ; DNA Primers/genetics ; Gene Expression ; Humans ; Keratinocytes/metabolism ; Keratinocytes/pathology ; Mice ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Proto-Oncogene Proteins c-fos/antagonists & inhibitors ; Proto-Oncogene Proteins c-fos/deficiency ; Proto-Oncogene Proteins c-fos/genetics ; Proto-Oncogene Proteins c-fos/metabolism ; Signal Transduction ; Skin Neoplasms/genetics ; Skin Neoplasms/metabolism ; Skin Neoplasms/pathology ; Skin Neoplasms/therapy ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	DNA Primers ; Proto-Oncogene Proteins c-fos ; Tumor Suppressor Protein p53 ; ADAM Proteins (EC 3.4.24.-) ; ADAM17 Protein (EC 3.4.24.86) ; ADAM17 protein, human (EC 3.4.24.86) ; Adam17 protein, mouse (EC 3.4.24.86)
Language	English
Publishing date	2012-07-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI63103
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Article ; Online: EGFR has a tumour-promoting role in liver macrophages during hepatocellular carcinoma formation.

Lanaya, Hanane / Natarajan, Anuradha / Komposch, Karin / Li, Liang / Amberg, Nicole / Chen, Lei / Wculek, Stefanie K / Hammer, Martina / Zenz, Rainer / Peck-Radosavljevic, Markus / Sieghart, Wolfgang / Trauner, Michael / Wang, Hongyang / Sibilia, Maria

Nature cell biology

2014 Volume 16, Issue 10, Page(s) 972–977

Abstract: Hepatocellular carcinoma (HCC) is a frequent cancer with limited treatment options and poor prognosis. Tumorigenesis has been linked with macrophage-mediated chronic inflammation and diverse signalling pathways, including the epidermal growth factor ... ...

Abstract	Hepatocellular carcinoma (HCC) is a frequent cancer with limited treatment options and poor prognosis. Tumorigenesis has been linked with macrophage-mediated chronic inflammation and diverse signalling pathways, including the epidermal growth factor receptor (EGFR) pathway. The precise role of EGFR in HCC is unknown, and EGFR inhibitors have shown disappointing clinical results. Here we discover that EGFR is expressed in liver macrophages in both human HCC and in a mouse HCC model. Mice lacking EGFR in macrophages show impaired hepatocarcinogenesis, whereas mice lacking EGFR in hepatocytes unexpectedly develop more HCC owing to increased hepatocyte damage and compensatory proliferation. Mechanistically, following interleukin-1 stimulation, EGFR is required in liver macrophages to transcriptionally induce interleukin-6, which triggers hepatocyte proliferation and HCC. Importantly, the presence of EGFR-positive liver macrophages in HCC patients is associated with poor survival. This study demonstrates a tumour-promoting mechanism for EGFR in non-tumour cells, which could lead to more effective precision medicine strategies.
MeSH term(s)	Animals ; Blotting, Western ; Carcinoma, Hepatocellular/chemically induced ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Cells, Cultured ; Diethylnitrosamine ; ErbB Receptors/genetics ; ErbB Receptors/metabolism ; Hepatocytes/metabolism ; Humans ; Immunohistochemistry ; Interleukin-1beta/pharmacology ; Kupffer Cells/drug effects ; Kupffer Cells/metabolism ; Liver/metabolism ; Liver/pathology ; Liver Neoplasms/chemically induced ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Macrophages/metabolism ; Male ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Knockout ; Mice, Transgenic ; Phosphorylation/drug effects
Chemical Substances	Interleukin-1beta ; Diethylnitrosamine (3IQ78TTX1A) ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2014-08-31
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/ncb3031
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Book ; Thesis: Über die Häufigkeit und den therapeutischen Effekt der bei entzündlichen Gelenk- und Wirbelsäulenerkrankungen durchgeführten Herdsanierungen

Zenz, Rainer

1977

Author's details	Rainer Zenz
Language	German
Size	42 S
Document type	Book ; Thesis
Thesis / German Habilitation thesis	@Mainz, Univ., Fachbereich 05-10 - Medizin, Diss. : 1977
Database	Former special subject collection: coastal and deep sea fishing

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Article ; Online: TNFalpha shedding and epidermal inflammation are controlled by Jun proteins.

Guinea-Viniegra, Juan / Zenz, Rainer / Scheuch, Harald / Hnisz, Denes / Holcmann, Martin / Bakiri, Latifa / Schonthaler, Helia B / Sibilia, Maria / Wagner, Erwin F

Genes & development

2009 Volume 23, Issue 22, Page(s) 2663–2674

Abstract: Inducible epidermal deletion of JunB and c-Jun in adult mice causes a psoriasis-like inflammatory skin disease. Increased levels of the proinflammatory cytokine TNFalpha play a major role in this phenotype. Here we define the underlying molecular ... ...

Abstract	Inducible epidermal deletion of JunB and c-Jun in adult mice causes a psoriasis-like inflammatory skin disease. Increased levels of the proinflammatory cytokine TNFalpha play a major role in this phenotype. Here we define the underlying molecular mechanism using genetic mouse models. We show that Jun proteins control TNFalpha shedding in the epidermis by direct transcriptional activation of tissue inhibitor of metalloproteinase-3 (TIMP-3), an inhibitor of the TNFalpha-converting enzyme (TACE). TIMP-3 is down-regulated and TACE activity is specifically increased, leading to massive, cell-autonomous TNFalpha shedding upon loss of both JunB and c-Jun. Consequently, a prominent TNFalpha-dependent cytokine cascade is initiated in the epidermis, inducing severe skin inflammation and perinatal death of newborns from exhaustion of energy reservoirs such as glycogen and lipids. Importantly, this metabolic "cachectic" phenotype can be genetically rescued in a TNFR1-deficient background or by epidermis-specific re-expression of TIMP-3. These findings reveal that Jun proteins are essential physiological regulators of TNFalpha shedding by controlling the TIMP-3/TACE pathway. This novel mechanism describing how Jun proteins control skin inflammation offers potential targets for the treatment of skin pathologies associated with increased TNFalpha levels.
MeSH term(s)	Animals ; Cachexia/genetics ; Cachexia/mortality ; Cells, Cultured ; Cytokines/metabolism ; Epidermis/metabolism ; Epidermis/pathology ; Gene Expression Regulation ; Inflammation/physiopathology ; Keratinocytes/metabolism ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Knockout ; Phenotype ; Promoter Regions, Genetic/genetics ; Proto-Oncogene Proteins c-jun/deficiency ; Proto-Oncogene Proteins c-jun/genetics ; Proto-Oncogene Proteins c-jun/metabolism ; Skin Diseases/physiopathology ; Tissue Inhibitor of Metalloproteinase-3/metabolism ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Cytokines ; Proto-Oncogene Proteins c-jun ; Tissue Inhibitor of Metalloproteinase-3 ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2009-11-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.543109
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Article ; Online: Development of pulmonary fibrosis through a pathway involving the transcription factor Fra-2/AP-1.

Eferl, Robert / Hasselblatt, Peter / Rath, Martina / Popper, Helmut / Zenz, Rainer / Komnenovic, Vukoslav / Idarraga, Maria-Helena / Kenner, Lukas / Wagner, Erwin F

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

2008 Volume 105, Issue 30, Page(s) 10525–10530

Abstract: Studies using genetically modified mice have revealed fundamental functions of the transcription factor Fos/AP-1 in bone biology, inflammation, and cancer. However, the biological role of the Fos-related protein Fra-2 is not well defined in vivo. Here we ...

Abstract	Studies using genetically modified mice have revealed fundamental functions of the transcription factor Fos/AP-1 in bone biology, inflammation, and cancer. However, the biological role of the Fos-related protein Fra-2 is not well defined in vivo. Here we report an unexpected profibrogenic function of Fra-2 in transgenic mice, in which ectopic expression of Fra-2 in various organs resulted in generalized fibrosis with predominant manifestation in the lung. The pulmonary phenotype was characterized by vascular remodeling and obliteration of pulmonary arteries, which coincided with expression of osteopontin, an AP-1 target gene involved in vascular remodeling and fibrogenesis. These alterations were followed by inflammation; release of profibrogenic factors, such as IL-4, insulin-like growth factor 1, and CXCL5; progressive fibrosis; and premature mortality. Genetic experiments and bone marrow reconstitutions suggested that fibrosis developed independently of B and T cells and was not mediated by autoimmunity despite the marked inflammation observed in transgenic lungs. Importantly, strong expression of Fra-2 was also observed in human samples of idiopathic and autoimmune-mediated pulmonary fibrosis. These findings indicate that Fra-2 expression is sufficient to cause pulmonary fibrosis in mice, possibly by linking vascular remodeling and fibrogenesis, and suggest that Fra-2 has to be considered a contributing pathogenic factor of pulmonary fibrosis in humans.
MeSH term(s)	Animals ; Chemokine CXCL5/metabolism ; Female ; Fibrosis ; Fos-Related Antigen-2/biosynthesis ; Humans ; Inflammation ; Insulin-Like Growth Factor I/metabolism ; Interleukin-4/metabolism ; Lung/pathology ; Mice ; Mice, Transgenic ; Neoplasms/immunology ; Neoplasms/pathology ; Pulmonary Fibrosis/genetics ; Pulmonary Fibrosis/pathology ; Transcription Factor AP-1/metabolism
Chemical Substances	CXCL5 protein, human ; Chemokine CXCL5 ; Fos-Related Antigen-2 ; Transcription Factor AP-1 ; Interleukin-4 (207137-56-2) ; Insulin-Like Growth Factor I (67763-96-6)
Language	English
Publishing date	2008-07-18
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.0801414105
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