Inactivation of tankyrases reduces experimental fibrosis by inhibiting canonical Wnt signalling
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- Extent
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Online-Ressource
- Language
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Englisch
- Bibliographic citation
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In: Annals of the Rheumatic Diseases 72.9 (2013): S. 1575-1580.
- Keyword
-
-
Krebs
Onkologie
- Event
-
Veröffentlichung
- (where)
-
Erlangen
- (who)
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Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU)
- (when)
-
2013
- Creator
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Distler, Alfiya
Deloch, Lisa
Huang, Jingang
Dees, Clara
Lin, Neng-Yu
Palumbo-Zerr, Katrin
Beyer, Christian
Weidemann, Alexander
Distler, Oliver
Schett, Georg
Distler, Jörg H. W.
- URN
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urn:nbn:de:bvb:29-opus4-78569
- Rights
-
Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
14.08.2025, 10:48 AM CEST
Data provider
This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Distler, Alfiya
- Deloch, Lisa
- Huang, Jingang
- Dees, Clara
- Lin, Neng-Yu
- Palumbo-Zerr, Katrin
- Beyer, Christian
- Weidemann, Alexander
- Distler, Oliver
- Schett, Georg
- Distler, Jörg H. W.
- Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU)
Time of origin
- 2013
Other Objects (12)
Inactivation of evenness interrupted (EVI) reduces experimental fibrosis by combined inhibition of canonical and non-canonical Wnt signalling
Inhibition of glycogen synthase kinase 3β induces dermal fibrosis by activation of the canonical Wnt pathway
Combined inhibition of morphogen pathways demonstrates additive antifibrotic effects and improved tolerability
Notch signalling regulates fibroblast activation and collagen release in systemic sclerosis
The Wnt antagonists DKK1 and SFRP1 are downregulated by promoter hypermethylation in systemic sclerosis
Nintedanib inhibits fibroblast activation and ameliorates fibrosis in preclinical models of systemic sclerosis
Type 2 innate lymphoid cell counts are increased in patients with systemic sclerosis and correlate with the extent of fibrosis
Inactivation of autophagy ameliorates glucocorticoid-induced and ovariectomy-induced bone loss
Inhibition of casein kinase II reduces TGFβ induced fibroblast activation and ameliorates experimental fibrosis
Activating transcription factor 3 regulates canonical TGFβ signalling in systemic sclerosis
Inactivation of fatty acid amide hydrolase exacerbates experimental fibrosis by enhanced endocannabinoid-mediated activation of CB1
Bewerbung des Christian Beyer um die Berufszulassung im medizinischen Bereich in Öhningen und der Reichenau.
Inactivation of evenness interrupted (EVI) reduces experimental fibrosis by combined inhibition of canonical and non-canonical Wnt signalling
Inhibition of glycogen synthase kinase 3β induces dermal fibrosis by activation of the canonical Wnt pathway
Combined inhibition of morphogen pathways demonstrates additive antifibrotic effects and improved tolerability
Notch signalling regulates fibroblast activation and collagen release in systemic sclerosis
The Wnt antagonists DKK1 and SFRP1 are downregulated by promoter hypermethylation in systemic sclerosis
Nintedanib inhibits fibroblast activation and ameliorates fibrosis in preclinical models of systemic sclerosis
Type 2 innate lymphoid cell counts are increased in patients with systemic sclerosis and correlate with the extent of fibrosis
Inactivation of autophagy ameliorates glucocorticoid-induced and ovariectomy-induced bone loss
Inhibition of casein kinase II reduces TGFβ induced fibroblast activation and ameliorates experimental fibrosis
Activating transcription factor 3 regulates canonical TGFβ signalling in systemic sclerosis
Inactivation of fatty acid amide hydrolase exacerbates experimental fibrosis by enhanced endocannabinoid-mediated activation of CB1
Bewerbung des Christian Beyer um die Berufszulassung im medizinischen Bereich in Öhningen und der Reichenau.
Inactivation of evenness interrupted (EVI) reduces experimental fibrosis by combined inhibition of canonical and non-canonical Wnt signalling
Inhibition of glycogen synthase kinase 3β induces dermal fibrosis by activation of the canonical Wnt pathway
Combined inhibition of morphogen pathways demonstrates additive antifibrotic effects and improved tolerability
Notch signalling regulates fibroblast activation and collagen release in systemic sclerosis
The Wnt antagonists DKK1 and SFRP1 are downregulated by promoter hypermethylation in systemic sclerosis
Nintedanib inhibits fibroblast activation and ameliorates fibrosis in preclinical models of systemic sclerosis
Type 2 innate lymphoid cell counts are increased in patients with systemic sclerosis and correlate with the extent of fibrosis
Inactivation of autophagy ameliorates glucocorticoid-induced and ovariectomy-induced bone loss
Inhibition of casein kinase II reduces TGFβ induced fibroblast activation and ameliorates experimental fibrosis
Activating transcription factor 3 regulates canonical TGFβ signalling in systemic sclerosis
Inactivation of fatty acid amide hydrolase exacerbates experimental fibrosis by enhanced endocannabinoid-mediated activation of CB1