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- Publisher Website: 10.1016/S0012-1606(02)90781-5
- Scopus: eid_2-s2.0-0036402460
- PMID: 12376107
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Article: SEK1/MKK4-mediated SAPK/JNK signaling participates in embryonic hepatoblast proliferation via a pathway different from NF-κB-induced anti-apoptosis
Title | SEK1/MKK4-mediated SAPK/JNK signaling participates in embryonic hepatoblast proliferation via a pathway different from NF-κB-induced anti-apoptosis |
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Authors | Watanabe, TomomiNakagawa, KentaroOhata, ShinyaKitagawa, DaijuNishitai, GenSeo, JungwonTanemura, ShuheiShimizu, NaoKishimoto, HiroyukiWada, TeijiAoki, JunkenArai, HiroyukiIwatsubo, TakeshiMochita, MiyukiWatanabe, ToshioSatake, MasanobuIto, YoshiakiMatsuyama, ToshifumiMak, Tak W.Penninger, Josef M.Nishina, HiroshiKatada, Toshiaki |
Keywords | NF-κB c-Jun SEK1 Hematopoiesis Hepatogenesis HGF |
Issue Date | 2002 |
Citation | Developmental Biology, 2002, v. 250, n. 2, p. 332-347 How to Cite? |
Abstract | Mice lacking the stress-signaling kinase SEK1 die from embryonic day 10.5 (E10.5) to E12.5. Although a defect in liver formation is accompanied with the embryonic lethality of sek1-1- mice, the mechanism of the liver defect has remained unknown. In the present study, we first produced a monoclonal antibody specifically recognizing murine hepatoblasts for the analysis of liver development and further investigated genetic interaction of sek1 with tumor necrosis factor-α receptor 1 gene (tnfr1) and protooncogene c-jun, which are also responsible for liver formation and cell apoptosis. The defective liver formation in sek1-1- embryos was not protected by additional tnfr1 mutation, which rescues the embryonic lethality of mice lacking NF-κB signaling components. There was a progressive increase in the hepatoblast cell numbers of wild-type embryos from E10.5 to E12.5. Instead, impaired hepatoblast proliferation was observed in sek1-1- rivers from E10.5, though fetal liver-specific gene expression was normal. The impaired phenotype in sek1-1- livers was more severe than in c-jun-1- embryos, and sek1-1- c-jun-1- embryos died more rapidly before E8.5. The hepatoblast proliferation required no hematopoiesis, since liver development was not impaired in AML1-1- mice that lack hematopoietic functions. Stimulation of stress-activated protein kinase/c-Jun N-terminal kinase by hepatocyte growth factor was attenuated in sek1-1- livers. Thus, SEK1 appears to play a crucial role in hepatoblast proliferation and survival in a manner apparently different from NF-κB or c-Jun. © 2002 Elsevier Science (USA). |
Persistent Identifier | http://hdl.handle.net/10722/291596 |
ISSN | 2021 Impact Factor: 3.148 2020 SCImago Journal Rankings: 1.770 |
DC Field | Value | Language |
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dc.contributor.author | Watanabe, Tomomi | - |
dc.contributor.author | Nakagawa, Kentaro | - |
dc.contributor.author | Ohata, Shinya | - |
dc.contributor.author | Kitagawa, Daiju | - |
dc.contributor.author | Nishitai, Gen | - |
dc.contributor.author | Seo, Jungwon | - |
dc.contributor.author | Tanemura, Shuhei | - |
dc.contributor.author | Shimizu, Nao | - |
dc.contributor.author | Kishimoto, Hiroyuki | - |
dc.contributor.author | Wada, Teiji | - |
dc.contributor.author | Aoki, Junken | - |
dc.contributor.author | Arai, Hiroyuki | - |
dc.contributor.author | Iwatsubo, Takeshi | - |
dc.contributor.author | Mochita, Miyuki | - |
dc.contributor.author | Watanabe, Toshio | - |
dc.contributor.author | Satake, Masanobu | - |
dc.contributor.author | Ito, Yoshiaki | - |
dc.contributor.author | Matsuyama, Toshifumi | - |
dc.contributor.author | Mak, Tak W. | - |
dc.contributor.author | Penninger, Josef M. | - |
dc.contributor.author | Nishina, Hiroshi | - |
dc.contributor.author | Katada, Toshiaki | - |
dc.date.accessioned | 2020-11-17T14:54:42Z | - |
dc.date.available | 2020-11-17T14:54:42Z | - |
dc.date.issued | 2002 | - |
dc.identifier.citation | Developmental Biology, 2002, v. 250, n. 2, p. 332-347 | - |
dc.identifier.issn | 0012-1606 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291596 | - |
dc.description.abstract | Mice lacking the stress-signaling kinase SEK1 die from embryonic day 10.5 (E10.5) to E12.5. Although a defect in liver formation is accompanied with the embryonic lethality of sek1-1- mice, the mechanism of the liver defect has remained unknown. In the present study, we first produced a monoclonal antibody specifically recognizing murine hepatoblasts for the analysis of liver development and further investigated genetic interaction of sek1 with tumor necrosis factor-α receptor 1 gene (tnfr1) and protooncogene c-jun, which are also responsible for liver formation and cell apoptosis. The defective liver formation in sek1-1- embryos was not protected by additional tnfr1 mutation, which rescues the embryonic lethality of mice lacking NF-κB signaling components. There was a progressive increase in the hepatoblast cell numbers of wild-type embryos from E10.5 to E12.5. Instead, impaired hepatoblast proliferation was observed in sek1-1- rivers from E10.5, though fetal liver-specific gene expression was normal. The impaired phenotype in sek1-1- livers was more severe than in c-jun-1- embryos, and sek1-1- c-jun-1- embryos died more rapidly before E8.5. The hepatoblast proliferation required no hematopoiesis, since liver development was not impaired in AML1-1- mice that lack hematopoietic functions. Stimulation of stress-activated protein kinase/c-Jun N-terminal kinase by hepatocyte growth factor was attenuated in sek1-1- livers. Thus, SEK1 appears to play a crucial role in hepatoblast proliferation and survival in a manner apparently different from NF-κB or c-Jun. © 2002 Elsevier Science (USA). | - |
dc.language | eng | - |
dc.relation.ispartof | Developmental Biology | - |
dc.subject | NF-κB | - |
dc.subject | c-Jun | - |
dc.subject | SEK1 | - |
dc.subject | Hematopoiesis | - |
dc.subject | Hepatogenesis | - |
dc.subject | HGF | - |
dc.title | SEK1/MKK4-mediated SAPK/JNK signaling participates in embryonic hepatoblast proliferation via a pathway different from NF-κB-induced anti-apoptosis | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1016/S0012-1606(02)90781-5 | - |
dc.identifier.pmid | 12376107 | - |
dc.identifier.scopus | eid_2-s2.0-0036402460 | - |
dc.identifier.volume | 250 | - |
dc.identifier.issue | 2 | - |
dc.identifier.spage | 332 | - |
dc.identifier.epage | 347 | - |
dc.identifier.issnl | 0012-1606 | - |