Defective T cell differentiation in the absence of Jnk1
| dc.contributor.author | Dong, Chen | |
| dc.contributor.author | Yang, Derek D. | |
| dc.contributor.author | Wysk, Mark Allen | |
| dc.contributor.author | Whitmarsh, Alan J. | |
| dc.contributor.author | Davis, Roger J. | |
| dc.contributor.author | Flavell, Richard A. | |
| dc.date | 2022-08-11T08:08:57.000 | |
| dc.date.accessioned | 2022-08-23T16:13:34Z | |
| dc.date.available | 2022-08-23T16:13:34Z | |
| dc.date.issued | 1998-12-16 | |
| dc.date.submitted | 2008-09-04 | |
| dc.identifier.citation | <p>Science. 1998 Dec 11;282(5396):2092-5.</p> | |
| dc.identifier.issn | 0036-8075 (Print) | |
| dc.identifier.doi | 10.1126/science.282.5396.2092 | |
| dc.identifier.pmid | 9851932 | |
| dc.identifier.uri | http://hdl.handle.net/20.500.14038/33655 | |
| dc.description.abstract | The c-Jun NH2-terminal kinase (JNK) signaling pathway has been implicated in the immune response that is mediated by the activation and differentiation of CD4 helper T (TH) cells into TH1 and TH2 effector cells. JNK activity observed in wild-type activated TH cells was severely reduced in TH cells from Jnk1-/- mice. The Jnk1-/- T cells hyperproliferated, exhibited decreased activation-induced cell death, and preferentially differentiated to TH2 cells. The enhanced production of TH2 cytokines by Jnk1-/- cells was associated with increased nuclear accumulation of the transcription factor NFATc. Thus, the JNK1 signaling pathway plays a key role in T cell receptor-initiated TH cell proliferation, apoptosis, and differentiation. | |
| dc.language.iso | en_US | |
| dc.relation | <p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9851932&dopt=Abstract">Link to article in PubMed</a></p> | |
| dc.relation.url | https://doi.org/10.1126/science.282.5396.2092 | |
| dc.subject | Animals; Apoptosis; Calcium-Calmodulin-Dependent Protein Kinases; Cell Differentiation; Cell Division; DNA-Binding Proteins; Female; Gene Targeting; Hemocyanin; Interferon Type II; Interleukins; JNK Mitogen-Activated Protein Kinases; *Lymphocyte Activation; Male; Mice; Mice, Knockout; *Mitogen-Activated Protein Kinases; NFATC Transcription Factors; *Nuclear Proteins; Signal Transduction; T-Lymphocytes, Helper-Inducer; Th1 Cells; Th2 Cells; Transcription Factors | |
| dc.subject | Life Sciences | |
| dc.subject | Medicine and Health Sciences | |
| dc.title | Defective T cell differentiation in the absence of Jnk1 | |
| dc.type | Journal Article | |
| dc.source.journaltitle | Science (New York, N.Y.) | |
| dc.source.volume | 282 | |
| dc.source.issue | 5396 | |
| dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/gsbs_sp/321 | |
| dc.identifier.contextkey | 619033 | |
| html.description.abstract | <p>The c-Jun NH2-terminal kinase (JNK) signaling pathway has been implicated in the immune response that is mediated by the activation and differentiation of CD4 helper T (TH) cells into TH1 and TH2 effector cells. JNK activity observed in wild-type activated TH cells was severely reduced in TH cells from Jnk1-/- mice. The Jnk1-/- T cells hyperproliferated, exhibited decreased activation-induced cell death, and preferentially differentiated to TH2 cells. The enhanced production of TH2 cytokines by Jnk1-/- cells was associated with increased nuclear accumulation of the transcription factor NFATc. Thus, the JNK1 signaling pathway plays a key role in T cell receptor-initiated TH cell proliferation, apoptosis, and differentiation.</p> | |
| dc.identifier.submissionpath | gsbs_sp/321 | |
| dc.contributor.department | Howard Hughes Medical Institute, Program in Molecular Medicine | |
| dc.contributor.department | Graduate School of Biomedical Sciences | |
| dc.source.pages | 2092-5 |
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