کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1931146 1050542 2011 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
A cell-death-defying factor, anamorsin mediates cell growth through inactivation of PKC and p38MAPK
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
A cell-death-defying factor, anamorsin mediates cell growth through inactivation of PKC and p38MAPK
چکیده انگلیسی

Anamorsin (AM) plays crucial roles in hematopoiesis and embryogenesis. AM deficient (AM KO) mice die during late gestation; AM KO embryos are anemic and very small compared to wild type (WT) embryos. To determine which signaling pathways AM utilizes for these functions, we used murine embryonic fibroblast (MEF) cells generated from E-14.5 AM KO or WT embryos. Proliferation of AM KO MEF cells was markedly retarded, and PKCθ, PKCδ, and p38MAPK were more highly phosphorylated in AM KO MEF cells. Expression of cyclinD1, the target molecule of p38MAPK, was down-regulated in AM KO MEF cells. p38MAPK inhibitor as well as PKC inhibitor restored expression of cyclinD1 and cell growth in AM KO MEF cells. These data suggest that PKCθ, PKCδ, and p38MAPK activation lead to cell cycle retardation in AM KO MEF cells, and that AM may negatively regulate novel PKCs and p38MAPK in MEF cells.

Research highlights
► Anamorsin (AM) (also called CIAPIN-1) is a cell-death-defying factor.
► Biological mechanisms of AM functions have not been elucidated yet.
► PKCθ , PKCδ and p38MAPK were more phosphorylated in AM deficient MEF cells.
► AM may negatively regulates PKCs and p38MAPK in MEF cells.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 405, Issue 2, 11 February 2011, Pages 303–307
نویسندگان
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