Granulocyte colony stimulating factor (G-CSF) regulates survival, proliferation, differentiation, and activation of myeloid cells. It binds to a high affinity receptor (G-CSF-R) expressed on myeloid cells, for which the signal transduction mechanisms other than protein tyrosine kinase (PTK) activati
Granulocyte colony-stimulating factor promotes the translocation of protein kinase Cι in neutrophilic differentiation cells
✍ Scribed by Toshie Kanayasu-Toyoda; Takayoshi Suzuki; Tadashi Oshizawa; Eriko Uchida; Takao Hayakawa; Teruhide Yamaguchi
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 374 KB
- Volume
- 211
- Category
- Article
- ISSN
- 0021-9541
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✦ Synopsis
Abstract
Previously, we suggested that the phosphatidylinositol 3‐kinase (PI3K)‐p70 S6 kinase (p70 S6K) pathway plays an important role in granulocyte colony‐stimulating factor (G‐CSF)‐dependent enhancement of the neutrophilic differentiation and proliferation of HL‐60 cells. While atypical protein kinase C (PKC) has been reported to be a regulator of p70 S6K, abundant expression of PKCι was observed in myeloid and lymphoid cells. Therefore, we analyzed the participation of PKCι in G‐CSF‐dependent proliferation. The maximum stimulation of PKCι was observed from 15 to 30 min after the addition of G‐CSF. From 5 to 15 min into this lag time, PKCι was found to translocate from the nucleus to the membrane. At 30 min it re‐translocated to the cytosol. This dynamic translocation of PKCι was also observed in G‐CSF‐stimulated myeloperoxidase‐positive cells differentiated from cord blood cells. Small interfering RNA for PKCι inhibited G‐CSF‐induced proliferation and the promotion of neutrophilic differentiation of HL‐60 cells. These data indicate that the G‐CSF‐induced dynamic translocation and activation processes of PKCι are important to neutrophilic proliferation. J. Cell. Physiol. 211: 189–196, 2007. © 2006 Wiley‐Liss, Inc.
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