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Cell cycle regulators in the keratinocyte (cyclin‐cdk)
Author(s) -
Inohara S.,
Kitano Y.,
Kitagawa K.
Publication year - 1995
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.1995.tb00215.x
Subject(s) - cyclin dependent kinase , cyclin d , cyclin a , cyclin e , microbiology and biotechnology , cyclin b , cyclin a2 , cell cycle , carcinogenesis , cancer research , cyclin , cyclin d1 , biology , cell growth , kinase , cyclin dependent kinase 2 , protein kinase a , cell , genetics , cancer
It has recently become clear that cyclin‐dependent kinase (cdk) complex regulates the cell cycle by phosphorylating Rb protein, a tumor suppressor protein. It is likely that this complex is a target of various growth factors and anti‐growth factors (UV TGF‐β etc.) in keratinocyte (KC). It has also been suggested that abnormalities in the cell cycle regulating mechanism such as increased activity of cyclin‐cdk due to mutation of p53, a tumor suppressor gene, and overexpression of cyclin D may be concerned with carcinogenesis of KC. Thus, recent studies indicate that the cyclin‐cdk complex is a common target of proliferation and carcinogenesis in KC.