H
Hiroaki Kiyokawa
Researcher at Northwestern University
Publications - 93
Citations - 8711
Hiroaki Kiyokawa is an academic researcher from Northwestern University. The author has contributed to research in topics: Cyclin-dependent kinase & Cell cycle. The author has an hindex of 47, co-authored 92 publications receiving 8305 citations. Previous affiliations of Hiroaki Kiyokawa include University of Illinois at Chicago & Memorial Sloan Kettering Cancer Center.
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Journal ArticleDOI
Enhanced Growth of Mice Lacking the Cyclin-Dependent Kinase Inhibitor Function of p27Kip1
Hiroaki Kiyokawa,Rhonda D. Kineman,Katia Manova-Todorova,Vera Soares,Eric S. Hoffman,Masao Ono,Dilruba Khanam,Adrian Hayday,Lawrence A. Frohman,Andrew Koff +9 more
TL;DR: The phenotypes of these mice suggest that loss of p27 causes an alteration in cell proliferation that can lead to specific endocrine dysfunction, and this results reflect a disturbance of the hypothalamic-pituitary-ovarian axis.
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Targeted disruption of CDK4 delays cell cycle entry with enhanced p27(Kip1) activity.
Tateki Tsutsui,Bahar Hesabi,David S. Moons,Pier Paolo Pandolfi,Kimberly S. Hansel,Andrew Koff,Hiroaki Kiyokawa,Hiroaki Kiyokawa +7 more
TL;DR: Results suggest that at least part of CDK4’s participation in the rate-limiting mechanism for the G0-S transition consists of controlling p27 activity, which is opposite to those of p27-deficient mice.
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Cdc2–cyclin E complexes regulate the G1/S phase transition
TL;DR: In vivo results provide strong evidence that Cdc2 may compensate the loss of Cdk2 function, indicating a parallel pathway regulated by p27.
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Requirement for CDK4 kinase function in breast cancer
Qunyan Yu,Ewa Sicinska,Yan Geng,Marie Ahnström,Agnieszka Zagozdzon,Yinxin Kong,Humphrey Gardner,Hiroaki Kiyokawa,Lyndsay Harris,Lyndsay Harris,Olle Stål,Piotr Sicinski +11 more
TL;DR: It is reported that the ability of cyclin D1 to activate cyclin-dependent kinase CDK4 underlies the critical role for cyclinD1 in breast cancer formation and the continued presence ofCDK4-associated kinase activity is required to maintain breast tumorigenesis.
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The absence of p21Cip1/WAF1 alters keratinocyte growth and differentiation and promotes ras-tumor progression.
TL;DR: The results reveal a so far undetected role of p 21 in tumor suppression, demonstrate that this function is specific as it cannot be attributed to the closely related p27 molecule, and point to an essential involvement of p21 in terminal differentiation control, which may account for its role in tumors suppression.