Molecular cloning of multiple splicing variants of JIP-1 preferentially expressed in brain

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dc.contributor.authorIn Jung Kim-
dc.contributor.authorKo Woon Lee-
dc.contributor.authorByung Young Park-
dc.contributor.authorJa Kyeong Lee-
dc.contributor.authorJi Hyun Park-
dc.contributor.authorIn Young Choi-
dc.contributor.authorSoo Jung Eom-
dc.contributor.authorTong Shin Chang-
dc.contributor.authorMyung Jin Kim-
dc.contributor.authorYoung Il Yeom-
dc.contributor.authorSung Key Chang-
dc.contributor.authorYoung Don Lee-
dc.contributor.authorEui Ju Choi-
dc.contributor.authorPyung Lim Han-
dc.date.accessioned2017-04-19T08:56:02Z-
dc.date.available2017-04-19T08:56:02Z-
dc.date.issued1999-
dc.identifier.issn0022-3042-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/4703-
dc.description.abstractStress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) is activated by a variety of cellular or environmental stresses. Proper regulation of the SAPK/JNK pathway may be critical for cell survival or death under various conditions. In this study, we report the molecular cloning of novel isoforms of JIP-1, which harbor a putative phosphotyrosine interaction domain and a helix-loop-helix domain, as well as an SH3 homologous region in the C terminus. Northern analysis indicates that transcription variant jip-1 is expressed in brain and kidney and transcription variants jip-2 and jip-3 are specifically expressed in brain. In situ hybridization data showed that the hybridized jip messages were heavily concentrated in adult brain, and were particularly enriched in the cerebral cortex and hippocampus, the brain regions vulnerable to pathological states such as hypoxia-ischemia, epilepsy, and Alzheimer's disease. All the deduced protein products of the jip transcription variants appear to have a similar property in that they inhibit the SAPK/JNK stimulation when overexpressed. Inhibition of SAPK activation by overexpression of the novel isoform JIP-2a resulted in suppression of etoposide-induced cell death in a neuroglioma cell line, N18TG. These findings suggest that JIP may play an important role in regulation of the SAPK pathway that is involved in stress-induced cellular responses.-
dc.publisherWiley-
dc.titleMolecular cloning of multiple splicing variants of JIP-1 preferentially expressed in brain-
dc.title.alternativeMolecular cloning of multiple splicing variants of JIP-1 preferentially expressed in brain-
dc.typeArticle-
dc.citation.titleJournal of Neurochemistry-
dc.citation.number4-
dc.citation.endPage1343-
dc.citation.startPage1335-
dc.citation.volume72-
dc.contributor.affiliatedAuthorKo Woon Lee-
dc.contributor.affiliatedAuthorYoung Il Yeom-
dc.contributor.affiliatedAuthorPyung Lim Han-
dc.contributor.alternativeName김인정-
dc.contributor.alternativeName이고운-
dc.contributor.alternativeName박병영-
dc.contributor.alternativeName이자경-
dc.contributor.alternativeName박지현-
dc.contributor.alternativeName최인영-
dc.contributor.alternativeName음수중-
dc.contributor.alternativeName장동신-
dc.contributor.alternativeName김명진-
dc.contributor.alternativeName염영일-
dc.contributor.alternativeName장성계-
dc.contributor.alternativeName이영돈-
dc.contributor.alternativeName최의주-
dc.contributor.alternativeName한평림-
dc.identifier.bibliographicCitationJournal of Neurochemistry, vol. 72, no. 4, pp. 1335-1343-
dc.identifier.doi10.1046/j.1471-4159.1999.721335.x-
dc.subject.keywordSAPK/JNK-
dc.subject.keywordApoptosis-
dc.subject.keywordAnti-cell death function-
dc.subject.keywordBrain expression-
dc.subject.keywordJIP isoforms-
dc.subject.localSAPK/JNK-
dc.subject.localapoptosis-
dc.subject.localApoptosis-
dc.subject.localAnti-cell death function-
dc.subject.localbrain expression-
dc.subject.localBrain expression-
dc.subject.localJIP isoforms-
dc.description.journalClassY-
Appears in Collections:
Division of Biomedical Research > Personalized Genomic Medicine Research Center > 1. Journal Articles
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