scispace - formally typeset
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.

Papers
More filters
Journal ArticleDOI

Nuclear localization of EGF receptor and its potential new role as a transcription factor

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.

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

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

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.