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タイトル: | Impaired lymphocyte trafficking in mice deficient in the kinase activity of PKN1 |
著者: | Mashud, Rana Nomachi, Akira Hayakawa, Akihide Kubouchi, Koji Danno, Sally Hirata, Takako Matsuo, Kazuhiko Nakayama, Takashi Satoh, Ryosuke Sugiura, Reiko Abe, Manabu Sakimura, Kenji Wakana, Shigeharu Ohsaki, Hiroyuki Kamoshida, Shingo Mukai, Hideyuki |
著者名の別形: | 野町, 昭 |
キーワード: | Chemotaxis Phosphorylation |
発行日: | 9-Aug-2017 |
出版者: | Springer Nature |
誌名: | Scientific Reports |
巻: | 7 |
論文番号: | 7663 |
抄録: | Knock-in mice lacking PKN1 kinase activity were generated by introducing a T778A point mutation in the catalytic domain. PKN1[T778A] mutant mice developed to adulthood without apparent external abnormalities, but exhibited lower T and B lymphocyte counts in the peripheral blood than those of wild-type (WT) mice. T and B cell development proceeded in an apparently normal fashion in bone marrow and thymus of PKN1[T778A] mice, however, the number of T and B cell counts were significantly higher in the lymph nodes and spleen of mutant mice in those of WT mice. After transfusion into WT recipients, EGFP-labelled PKN1[T778A] donor lymphocytes were significantly less abundant in the peripheral circulation and more abundant in the spleen and lymph nodes of recipient mice compared with EGFP-labelled WT donor lymphocytes, likely reflecting lymphocyte sequestration in the spleen and lymph nodes in a cell-autonomous fashion. PKN1[T778A] lymphocytes showed significantly lower chemotaxis towards chemokines and sphingosine 1-phosphate (S1P) than WT cells in vitro. The biggest migration defect was observed in response to S1P, which is essential for lymphocyte egress from secondary lymphoid organs. These results reveal a novel role of PKN1 in lymphocyte migration and localization. |
著作権等: | © The Author(s) 2017. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. |
URI: | http://hdl.handle.net/2433/227928 |
DOI(出版社版): | 10.1038/s41598-017-07936-9 |
PubMed ID: | 28794483 |
出現コレクション: | 学術雑誌掲載論文等 |
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