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231223s2006 xx ||||| 00| ||eng c |
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|a pubmed24n1374.xml
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|a (DE-627)NLM162166281
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|a (NLM)16631408
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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1 |
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|a Cuzzocrea, Salvatore
|e verfasserin
|4 aut
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|a Glycogen synthase kinase-3beta inhibition attenuates the degree of arthritis caused by type II collagen in the mouse
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|c 2006
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|a Text
|b txt
|2 rdacontent
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|a ohne Hilfsmittel zu benutzen
|b n
|2 rdamedia
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|a Band
|b nc
|2 rdacarrier
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|a Date Completed 03.08.2006
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|a Date Revised 12.04.2024
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|a published: Print-Electronic
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|a RetractionIn: Clin Immunol. 2024 May;262:110198. - PMID 38555221
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|a Citation Status MEDLINE
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|a Recently, glycogen synthase kinase-3 (GSK-3) has being identified as an ubiquitous serine-threonine protein kinase that participates in a multitude of cellular processes and plays an important role in the pathophysiology of a number of diseases. The aim of this study was to investigate the effects of GSK-3beta inhibition on the degree of arthritis caused by type II collagen (CII) in the mouse (collagen-induced arthritis; CIA). Mice developed erosive hind paw arthritis when immunized with CII in an emulsion in complete Freund's adjuvant (CFA). The incidence of CIA was 100% by day 28 in the CII-challenged mice and the severity of CIA progressed over a 35-day period with radiographic evaluation revealing focal resorption of bone. The histopathology of CIA included erosion of the cartilage at the joint margins. Treatment of mice with the GSK-3beta inhibitor TDZD-8 (1 mg/kg/day i.p.) starting at the onset of arthritis (day 25) ameliorated the clinical signs at days 26-35 and improved histological status in the joint and paw. Immunohistochemical analysis for nitrotyrosine, poly(ADP-ribose) (PAR), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) revealed a positive staining in inflamed joints from mice subjected to CIA. The degree of staining for nitrotyrosine, PAR, iNOS, and COX-2 was significantly reduced in CII-challenged mice treated with the GSK-3beta inhibitor. Plasma levels of tumor necrosis factor (TNF)-alpha and the joint tissue levels of macrophage inflammatory protein (MIP)-1alpha and MIP-2 were also significantly reduced by GSK-3beta inhibition. These data demonstrate that GSK-3beta inhibition exerts an anti-inflammatory effect during chronic inflammation and is able to ameliorate the tissue damage associated with CIA
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Retracted Publication
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|a 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione
|2 NLM
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7 |
|a Chemokine CCL3
|2 NLM
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|a Chemokine CCL4
|2 NLM
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|a Chemokine CXCL2
|2 NLM
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|a Collagen Type II
|2 NLM
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|a Interleukin-6
|2 NLM
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|a Macrophage Inflammatory Proteins
|2 NLM
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|a Monokines
|2 NLM
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|a Protein Kinase Inhibitors
|2 NLM
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|a Thiadiazoles
|2 NLM
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7 |
|a Tumor Necrosis Factor-alpha
|2 NLM
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|a 3-nitrotyrosine
|2 NLM
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|a 3604-79-3
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|a Tyrosine
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|a 42HK56048U
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|a EC 1.14.13.39
|2 NLM
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|a Cyclooxygenase 2
|2 NLM
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|a EC 1.14.99.1
|2 NLM
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|a Poly(ADP-ribose) Polymerases
|2 NLM
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650 |
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|a EC 2.4.2.30
|2 NLM
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|a Glycogen Synthase Kinase 3 beta
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|a EC 2.7.11.1
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|a Gsk3b protein, mouse
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|a EC 2.7.11.1
|2 NLM
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|a Glycogen Synthase Kinase 3
|2 NLM
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|a EC 2.7.11.26
|2 NLM
|
700 |
1 |
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|a Mazzon, Emanuela
|e verfasserin
|4 aut
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700 |
1 |
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|a Di Paola, Rosanna
|e verfasserin
|4 aut
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700 |
1 |
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|a Muià, Carmelo
|e verfasserin
|4 aut
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700 |
1 |
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|a Crisafulli, Concetta
|e verfasserin
|4 aut
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700 |
1 |
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|a Dugo, Laura
|e verfasserin
|4 aut
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700 |
1 |
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|a Collin, Marika
|e verfasserin
|4 aut
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700 |
1 |
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|a Britti, Domenico
|e verfasserin
|4 aut
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700 |
1 |
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|a Caputi, Achille P
|e verfasserin
|4 aut
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700 |
1 |
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|a Thiemermann, Christoph
|e verfasserin
|4 aut
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773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 120(2006), 1 vom: 18. Juli, Seite 57-67
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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773 |
1 |
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|g volume:120
|g year:2006
|g number:1
|g day:18
|g month:07
|g pages:57-67
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|a GBV_ILN_350
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|a AR
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|d 120
|j 2006
|e 1
|b 18
|c 07
|h 57-67
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