Open AccessPhorbol Ester‐induced G1 Arrest in BALB/MK‐2 Mouse Keratinocytes Is Mediated by δ and η Isoforms of Protein Kinase C
Author(s) -
Ishino Keiko,
Ohba Motoi,
Kashiwagi Mariko,
Kawabe Shoko,
Chida Kazuhiro,
Kuroki Toshio
Publication year - 1998
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1998.tb00507.x
Subject(s) - gene isoform , protein kinase c , cell cycle , tetradecanoylphorbol acetate , microbiology and biotechnology , biology , cell culture , kinase , cell , biochemistry , gene , genetics
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.