K
Keishi Makino
Researcher at University of Texas MD Anderson Cancer Center
Publications - 8
Citations - 1711
Keishi Makino is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Kinase & Signal transduction. The author has an hindex of 8, co-authored 8 publications receiving 1647 citations.
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Journal ArticleDOI
Nuclear localization of EGF receptor and its potential new role as a transcription factor
Shiaw Yih Lin,Keishi Makino,Weiya Xia,Angabin Matin,Yong Wen,Ka Yin Kwong,Lilly Y.W. Bourguignon,Mien Chie Hung +7 more
TL;DR: It is demonstrated that nuclear EGFR is strongly correlated with highly proliferating activities of tissues and associated with promoter region of cyclin D1 in vivo, suggesting that EGFR might function as a transcription factor to activate genes required for highly proliferationating activities.
Journal Article
HER-2/neu promotes androgen-independent survival and growth of prostate cancer cells through the Akt pathway.
Yong Wen,Mickey C.T. Hu,Keishi Makino,Bill Spohn,Geoffrey Bartholomeusz,Duen-Hwa Yan,Mien Chie Hung +6 more
TL;DR: It is reported that HER-2/neu activates Akt (protein kinase B) to promote prostate cancer cell survival and growth in the absence of androgen.
Journal ArticleDOI
DOC-2/hDab-2 inhibits ILK activity and induces anoikis in breast cancer cells through an Akt-independent pathway
Shao Chun Wang,Keishi Makino,Weiya Xia,Jeong Soo Kim,Seock Ah Im,Hua Peng,Samuel C. Mok,Sonja E. Singletary,Mien Chie Hung +8 more
TL;DR: It is demonstrated that DOC-2/hDab-2 expression in breast cancer cells resulted in sensitivity to suspension-induced cell death (anoikis), and this event was associated with the down-regulation of the integrin-linked kinase (ILK) activity.
Journal ArticleDOI
Upregulation of IKKα/IKKβ by integrin-linked kinase is required for HER2/neu-induced NF-κB antiapoptotic pathway
TL;DR: The results demonstrate that upregulation of IKKα and IKKβ by the ILK/Akt pathway is required for the HER2/neu-mediated NF-κB antiapoptotic pathway.
Journal Article
E1A inhibition of radiation-induced NF-κB activity through suppression of IKK activity and IκB degradation, independent of Akt activation
Ruping Shao,Eing Mei Tsai,Kevin Wei,Ryan von Lindern,Yun-Houng Chen,Keishi Makino,Mien Chie Hung +6 more
TL;DR: Comparison of the activity of inhibitor of nuclear factor-κB (IκB) kinase (IKK) and the degradation of IκBα in E1A transfectants and parental human cancer cells after ionizing radiation treatment suggests that inhibition of IKK activity and IKKB degradation is the predominant mechanism for E 1A-mediated inhibition of radiation-induced NF-κBs activity.