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Shigeki Sekine
Researcher at University of California, San Francisco
Publications - 6
Citations - 1330
Shigeki Sekine is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Hepatocyte & Conditional gene knockout. The author has an hindex of 6, co-authored 6 publications receiving 1215 citations. Previous affiliations of Shigeki Sekine include National Cancer Research Institute.
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Journal ArticleDOI
β-catenin blocks Kras-dependent reprogramming of acini into pancreatic cancer precursor lesions in mice
John P. Morris,David A. Cano,David A. Cano,Shigeki Sekine,Shigeki Sekine,Sam C. Wang,Matthias Hebrok +6 more
TL;DR: It is suggested that beta-catenin signaling is a critical determinant of acinar plasticity and that it is inhibited during Kras-induced fate decisions that specify PDA precursors, highlighting the importance of temporal regulation of embryonic signaling pathways in the development of neoplastic cell fates.
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Hedgehog/Ras interactions regulate early stages of pancreatic cancer.
Marina Pasca di Magliano,Shigeki Sekine,Alexandre N. Ermilov,Jenny Ferris,Andrzej A. Dlugosz,Matthias Hebrok +5 more
TL;DR: A mouse model in which Hedgehog signaling is activated specifically in the pancreatic epithelium indicates the cooperation of Hedgehog and Ras signaling during the earliest stages of PDA formation and marks Hedgehog pathway components as relevant therapeutic targets for both early and advanced stages of pancreatic ductal neoplasia.
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Liver-specific loss of β-catenin blocks glutamine synthesis pathway activity and cytochrome P450 expression in mice
TL;DR: In conclusion, in addition to regulating hepatocyte proliferation, β‐catenin may also control multiple aspects of normal liver function.
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Disruption of Dicer1 Induces Dysregulated Fetal Gene Expression and Promotes Hepatocarcinogenesis
Shigeki Sekine,Shigeki Sekine,Reiko Ogawa,Rie Ito,Nobuyoshi Hiraoka,Michael T. McManus,Yae Kanai,Matthias Hebrok +7 more
TL;DR: Dicer and microRNAs have critical roles in hepatocyte survival, metabolism, developmental gene regulation, and tumor suppression in the liver and can promote hepatocarcinogenesis in cooperation with additional oncogenic stimuli.
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Liver‐specific loss of β‐catenin results in delayed hepatocyte proliferation after partial hepatectomy
TL;DR: The results indicate that β‐Catenin is critical for the proper regulation of hepatocyte proliferation during liver regeneration; however, the activity of β‐catenin/TCF signaling does not correlate with hepatocytes proliferation, suggesting that this regulation might be indirect/secondary.