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您的检索式：作者名="Yuriko Hishida"
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| 1 | αKLOTHO and sTGFβR2 treatment counteract the osteoarthritic phenotype developed in a rat model显示文摘Dear Editor,Homeostasis and repair are critical biological processes that allow for tissue and organ preservation and function in multicellular organisms.Their regulation and extension vary drastically across the animal kingdom,and mammals show limited tissue-specific regenerative capacity that declines with age.During aging,articular cartilage is one of the tissues that undergo substantial changes in the matrix structure,molecular composition,metabolic activity,and mechanical properties(Loeser et al.2016). | Paloma Martinez-Redondo Isabel Guillen-Guillen Noah Davidsohn Chao Wang Javier Prieto Masakazu Kurita Fumiyuki Hatanaka Cuiqing Zhong Reyna Hernandez-Benitez Tomoaki Hishida Takashi Lezaki Akihisa Sakamoto Amy NNemeth Yuriko Hishida Concepcion Rodriguez Esteban Kensaku Shojima Ling Huang Maxim Shokhirev Estrella Nunez-Delicado Josep MCampistol Isabel Guillen-Vicente Elena Rodriguez-Inigo Juan Manuel Lopez-Alcorocho Marta Guillen-Vicente George Church Pradeep Reddy Pedro Guillen-Garcia Guang-Hui Liu Juan Carlos Izpisua Belmonte | 2020 | Protein & Cell2020，11，3： | 2 |
| 2 | Mutations in foregut SOX2^+ cells induce efficient proliferation via CXCR2 pathway显示文摘Identification of the precise molecular pathways involved in oncogene-induced transformation may help us gain a better understanding of tumor initiation and promotion. Here, we demonstrate that SOX2^+ foregut epithelial cells are prone to oncogenic transformation upon mutagenic insults, such as Kras^G12D and p53 deletion. GFP-based lineage-tracing experiments indicate that SOX2^+ cells are the cells-of-origin of esophagus and stomach hyperplasia. Our observations indicate distinct roles for oncogenic KRAS mutation and P53 deletion. p53 homozygous deletion is required for the acquisition of an invasive potential, and Kras^G12D expression, but not p53 deletion, suffices for tumor formation. Global gene expression analysis reveals secreting factors upregulated in the hyperplasia induced by oncogenic KRAS and highlights a crucial role for the CXCR2 pathway in driving hyperplasia. Collectively, the array of genetic models presented here demonstrate that stratified epithelial cells are susceptible to oncogenic insults, which may lead to a better understanding of tumor initiation and aid in the design of new cancer therapeutics. | Tomoaki Hishida Eric Vazquez-Ferrer Yuriko Hishida-Nozaki Ignacio Sancho-Martinez Yuta Takahashi Fumiyuki Hatanaka Jun Wu Alejandro Ocampo Pradeep Reddy Min-Zu Wu Laurie Gerken Reuben J. Shaw Concepcion Rodriguez Esteban Christopher Benner Hiroshi Nakagawa Pedro Guillen Garcia Estrella Nunez Delicado Antoni Castells Josep M. Campistol Guang-Hui Liu Juan Carlos Izpisua Belmonte | 2019 | Protein & Cell2019，10，7： | 1 |
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