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Phorbol Ester‐induced G1 Arrest in BALB/MK‐2 Mouse Keratinocytes Is Mediated by δ and η Isoforms of Protein Kinase C

We investigated the possible negative regulation of the cell cycle by protein kinase C (PKC) isoforms in synchronously grown BALB/MK‐2 mouse keratinocytes, in which PKC isoforms were overexpressed by using the adenovirus vector Ax. Cells at the G1/S boundary of the cell cycle were the most sensitive...

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Detalles Bibliográficos
Autores principales: Ishino, Keiko, Ohba, Motoi, Kashiwagi, Mariko, Kawabe, Shoko, Chida, Kazuhiro, Kuroki, Toshio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 1998
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5921714/
https://www.ncbi.nlm.nih.gov/pubmed/9914781
http://dx.doi.org/10.1111/j.1349-7006.1998.tb00507.x
Descripción
Sumario:We investigated the possible negative regulation of the cell cycle by protein kinase C (PKC) isoforms in synchronously grown BALB/MK‐2 mouse keratinocytes, in which PKC isoforms were overexpressed by using the adenovirus vector Ax. Cells at the G1/S boundary of the cell cycle were the most sensitive to the inhibitory effect of 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA), a PKC agonist, resulting in G1 arrest. TPA‐induced inhibition of DNA synthesis was augmented by overexpression of the η and δ isoforms, but rescued by the dominant‐negative and antisense η isoforms. In contrast, the α and ζ isoforms showed no effect on DNA synthesis with or without TPA treatment. Immunoblotting indicated cell cycle‐dependent expression of the η isoform, being highest in cells at the G1/S boundary. The present study provides evidence that the η and δ isoforms of PKC are involved in negative regulation of cell cycle at the G1/S boundary in mouse keratinocytes.