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231223s2009 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2009.06.006
|2 doi
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|a pubmed24n0633.xml
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|a (DE-627)NLM189941146
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|a (NLM)19596610
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Tang, Bo
|e verfasserin
|4 aut
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|a T cell receptor signaling induced by an analog peptide of type II collagen requires activation of Syk
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|c 2009
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 08.10.2009
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|a Date Revised 20.10.2021
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|a published: Print
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|a Citation Status MEDLINE
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|a We have previously described an analog peptide of type II collagen (CII) that can suppress collagen-induced arthritis (CIA). This analog peptide represents CII(245-270), the immunodominant epitope of CII, but with substitutions at 260, 261, and 263 - CII(245-270) (A(260), B(261), and N(263)) (A9). To elucidate the mechanisms responsible for suppression, we used mice transgenic for a collagen-specific T cell receptor (TCR). When we found that APCs pulsed with A9 failed to induce T cell phosphorylation of TCR-zeta and ZAP-70, we explored alternative signaling pathways. We determined that A9 instead induced phosphorylation of spleen tyrosine kinase (Syk). The importance of Syk was confirmed by the use of chemical Syk inhibitors, which blocked both cytokine secretion and activation of GATA-3 mediated by peptide A9. In summary, T cells use an alternative pathway in response to A9 that involves Syk. This novel T cell pathway may represent an important means for altering T cell phenotypes
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|a Journal Article
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|a Research Support, N.I.H., Extramural
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|a Research Support, Non-U.S. Gov't
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|a Research Support, U.S. Gov't, Non-P.H.S.
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|a Collagen Type II
|2 NLM
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|a Cytokines
|2 NLM
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|a GATA3 Transcription Factor
|2 NLM
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|a Gata3 protein, mouse
|2 NLM
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|a Intracellular Signaling Peptides and Proteins
|2 NLM
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|a Oligopeptides
|2 NLM
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|a Receptors, Antigen, T-Cell
|2 NLM
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|a Stilbenes
|2 NLM
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|a Sulfonamides
|2 NLM
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|a 3,3',4,5'-tetrahydroxystilbene
|2 NLM
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|a 6KS3LS0D4F
|2 NLM
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|a Protein-Tyrosine Kinases
|2 NLM
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|a EC 2.7.10.1
|2 NLM
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|a Syk Kinase
|2 NLM
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|a EC 2.7.10.2
|2 NLM
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|a Syk protein, mouse
|2 NLM
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|a EC 2.7.10.2
|2 NLM
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|a Extracellular Signal-Regulated MAP Kinases
|2 NLM
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|a EC 2.7.11.24
|2 NLM
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|a JNK Mitogen-Activated Protein Kinases
|2 NLM
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|a EC 2.7.11.24
|2 NLM
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|a p38 Mitogen-Activated Protein Kinases
|2 NLM
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|a EC 2.7.11.24
|2 NLM
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|a Zhou, Jing
|e verfasserin
|4 aut
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|a Park, Jeoung-Eun
|e verfasserin
|4 aut
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|a Cullins, David
|e verfasserin
|4 aut
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|a Yi, Ae-Kyung
|e verfasserin
|4 aut
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|a Kang, Andrew H
|e verfasserin
|4 aut
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|a Stuart, John M
|e verfasserin
|4 aut
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|a Myers, Linda K
|e verfasserin
|4 aut
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 133(2009), 1 vom: 01. Okt., Seite 145-53
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:133
|g year:2009
|g number:1
|g day:01
|g month:10
|g pages:145-53
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|u http://dx.doi.org/10.1016/j.clim.2009.06.006
|3 Volltext
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|a GBV_USEFLAG_A
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|a SYSFLAG_A
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|a GBV_NLM
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|a GBV_ILN_11
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|a GBV_ILN_24
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|a GBV_ILN_350
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|a AR
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|d 133
|j 2009
|e 1
|b 01
|c 10
|h 145-53
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