Induction of Mac-2BP by nerve growth factor is regulated by the PI3K/Akt/NF-kappaB-dependent pathway in the HEK293 cell line

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dc.contributor.authorYuk-Pheel Park-
dc.contributor.authorSeung-Chul Choi-
dc.contributor.authorBo Yeon Kim-
dc.contributor.authorJong-Tae Kim-
dc.contributor.authorEun Young Song-
dc.contributor.authorS H Kang-
dc.contributor.authorD Y Yoon-
dc.contributor.authorS G Paik-
dc.contributor.authorK D Kim-
dc.contributor.authorJ W Kim-
dc.contributor.authorHee Gu Lee-
dc.date.accessioned2017-04-19T09:12:08Z-
dc.date.available2017-04-19T09:12:08Z-
dc.date.issued2008-
dc.identifier.issn12258687-
dc.identifier.uri10.5483/BMBRep.2008.41.11.784ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/8700-
dc.description.abstractMac-2BP is a ligand of the galectin family that has been suggested to affect tumor proliferation and metastasis formation. We assessed Mac-2BP expression at the transcriptional and translational levels to evaluate nerve growth factor (NGF)-induced Mac-2BP expression. A time kinetic analysis using reverse transcription-polymerase chain reaction showed that NGF-induced Mac-2BP transcript levels were 4-5 times higher than in controls. Mac-2BP enzyme-linked immunosorbent assay and immunofluorescence staining showed a 2-3-fold increase in intracellular and secreted Mac-2BP as a result of NGF stimulation. This increase was regulated by Akt activation and NF-κB binding. p65 and p50-NF-κB are major transcriptional factors in the Mac-2BP promoter region, and were shown to be regulated in accordance with the Akt activation states. Collectively, these results suggest that NGF induces Mac-2BP expression via the PI3K/Akt/NF-κB pathway.-
dc.publisherSouth Korea-
dc.titleInduction of Mac-2BP by nerve growth factor is regulated by the PI3K/Akt/NF-kappaB-dependent pathway in the HEK293 cell line-
dc.title.alternativeInduction of Mac-2BP by nerve growth factor is regulated by the PI3K/Akt/NF-kappaB-dependent pathway in the HEK293 cell line-
dc.typeArticle-
dc.citation.titleBMB Reports-
dc.citation.number11-
dc.citation.endPage789-
dc.citation.startPage784-
dc.citation.volume41-
dc.contributor.affiliatedAuthorJong-Tae Kim-
dc.contributor.affiliatedAuthorHee Gu Lee-
dc.contributor.alternativeName박육필-
dc.contributor.alternativeName최승철-
dc.contributor.alternativeName김보연-
dc.contributor.alternativeName김종태-
dc.contributor.alternativeName송은영-
dc.contributor.alternativeName강성호-
dc.contributor.alternativeName윤도영-
dc.contributor.alternativeName백상기-
dc.contributor.alternativeName김광동-
dc.contributor.alternativeName김종완-
dc.contributor.alternativeName이희구-
dc.identifier.bibliographicCitationBMB Reports, vol. 41, no. 11, pp. 784-789-
dc.identifier.doi10.5483/BMBRep.2008.41.11.784-
dc.subject.keywordAkt-
dc.subject.keywordMac-2 BP-
dc.subject.keywordNGF-
dc.subject.keywordPI3K-
dc.subject.keywordnerve growth factor-
dc.subject.keywordNF-kappa B-
dc.subject.keywordOncogene Protein v-맛-
dc.subject.localAkt-
dc.subject.localMac-2 BP-
dc.subject.localMac-2BP-
dc.subject.localNGF-
dc.subject.localPI3K-
dc.subject.localnerve growth factor-
dc.subject.localNF-kappa B-
dc.subject.localNF-kB-
dc.subject.localOncogene Protein v-맛-
dc.description.journalClassY-
Appears in Collections:
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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