| Project/Area Number |
14560257
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Basic veterinary science/Basic zootechnical science
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| Research Institution | Kyorin University |
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Principal Investigator |
KANAI Masami Kyorin University, Medical School, Assistant Professor, 医学部, 助手 (70321883)
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| Co-Investigator(Kenkyū-buntansha) |
KAWAKAMI Hayato Kyorin University, Medical School, Professor, 医学部, 教授 (30146542)
HAYASHI Yoshihiro Kyorin University, Faculty of Agriculture, Professor, 大学院・農学生命科学研究科, 教授 (90092303)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2003: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2002: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Skeletal muscle development / kinase / GCK / Transgenic mouse / MAP4K |
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| Research Abstract |
Nck-interacting kinase (NIK)-related kinase (NRK) is a protein kinase that belongs to the germinal center kinase (GCK) family, and active the c-Jun N-terminal kinase (JNK) signaling pathway. In this study, we examined the effect of NRK on actin cytoskeletal organization in mouse muscle development. Overexpression of NRK in COS7 cells induced accumulation of polymerized actin at the perinuclear. Phosphorylation of cofilin, an actin-depolymerized factor, was increased in NRK-expressing HEK 293T cells. In addition, in vitro phosphorylation occurred at the serine residue of position 3 (Ser-3). Since the phosphorylation at Ser-3 inactives the actin-depolymerizing activitiy of cofilin, these results suggest that NRK induces actin polymerization through cofilin kinase, or through the activation of JNK. Thus, cofilin is likely to be a direct substrate o NRK. NRK is predominantly expressed in skeletal muscle during late stage of mouse embryogenesis. Thus, NRK may be involved in the regulation of actin cytoskeletal organization in skeletal muscle cells through cofilin phosphorylation. We have made the transgenic mouse that constracted Nrk or dominant negative Nrk (Nrk-K54 E) at the downstream of myogenin promoter, which overlapped the expression pattern with Nrk. Further studies are needed to clarify the involvement of NRK in the activity of cofilin and the regulation of actin assembly in skeletal muscle cells during mammalian embryogenesis.
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