4 Papers
17 Citations
Kei Haga is an academic researcher from National Cancer Research Institute. The author has contributed to research in topics: Carcinogenesis & Cell growth. The author has an hindex of 4, co-authored 4 publications.
Chat about Author
Papers
Efficient immortalization of primary human cells by p16INK4a-specific short hairpin RNA or Bmi-1, combined with introduction of hTERT.
Kei Haga,Shin Ichi Ohno,Takashi Yugawa,Mako Narisawa-Saito,Masatoshi Fujita,Michiie Sakamoto,Denise A. Galloway,Tohru Kiyono +7 more
TL;DR: Evidence is presented that many human cell types undergo senescence by activation of the p16ink4a/Rb pathway, and that introduction of Bmi‐1 can inhibit p16INK4a expression and extend the life span of human epithelial cells derived from skin, mammary gland and lung.
99
A critical role of MYC for transformation of human cells by HPV16 E6E7 and oncogenic HRAS
Mako Narisawa-Saito,Yuki Inagawa,Yuki Yoshimatsu,Kei Haga,Katsuyuki Tanaka,Nagayasu Egawa,Shin Ichi Ohno,Hitoshi Ichikawa,Takashi Yugawa,Masatoshi Fujita,Tohru Kiyono +10 more
TL;DR: It is shown that transduction of HRAS(G12V) on the background of E6E7 expression causes accumulation of MYC protein and tumorigenic transformation of not only normal HCKs but also other normal primary human cells, including tongue keratinocytes and bronchial epithelial cells as well as hTERT-immortalized foreskin fibroblasts.
ΔNp63α repression of the Notch1 gene supports the proliferative capacity of normal human keratinocytes and cervical cancer cells
Takashi Yugawa,Mako Narisawa-Saito,Yuki Yoshimatsu,Kei Haga,Shin Ichi Ohno,Nagayasu Egawa,Masatoshi Fujita,Tohru Kiyono +7 more
TL;DR: It is suggested that DeltaNp63alpha maintains the self-renewing capacity of normal human keratinocytes and cervical cancer cells partly through transcriptional repression of the Notch1 gene and imply a novel pathogenetical significance of frequently observed overexpression of DeltaN p63alpha together with p53 inactivation in SCCs.
Progerin, the protein responsible for the Hutchinson-Gilford progeria syndrome, increases the unrepaired DNA damages following exposure to ionizing radiation
Asao Noda,Shuji Mishima,Yuko Hirai,Kanya Hamasaki,Reid D. Landes,Hiroshi Mitani,Kei Haga,Tohru Kiyono,Nori Nakamura,Yoshiaki Kodama +9 more
TL;DR: It is suggested that lamin A- or progerin-associated nuclear envelope is involved in cellular aging associated with DNA damage repair as well as normal human cells which undergo replicative senescence.