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Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie|February 26, 2008
Apoptotic activity of genistein on human lung adenocarcinoma SPC-A-1 cells and preliminary exploration of its mechanisms using microarrayHuafei Zou, Shuxuan Zhan, Kaiming Cao
Plos One|June 30, 2012
Interaction of caveolin-1 with Ku70 inhibits Bax-mediated apoptosisHuafei Zou, Daniela Volonte, Ferruccio Galbiati
Mechanisms of Ageing and Development|November 22, 2011
Caveolin-1, cellular senescence and age-related diseasesHuafei Zou, Elena Stoppani, Daniela Volonte, et al.
Biotechnology Letters|October 10, 2006
Cloning and characterization of a novel small monomeric GTPase, RasL10B, with tumor suppressor potentialHuafei Zou, Lide Hu, Jixi Li, et al.
The Journal of Biological Chemistry|January 6, 2010
Rheb GTPase controls apoptosis by regulating interaction of FKBP38 with Bcl-2 and Bcl-XLDongzhu Ma, Xiaochun Bai, Huafei Zou, et al.
Tetrahedron|December 25, 2018
Design of Stapled Oxyntomodulin Analogs Containing Functionalized Biphenyl Cross-LinkersYulin Tian, Huafei Zou, Peng An, et al.
The Journal of Biological Chemistry|December 17, 2014
Oxidative stress-induced inhibition of Sirt1 by caveolin-1 promotes p53-dependent premature senescence and stimulates the secretion of interleukin 6 (IL-6)Daniela Volonte, Huafei Zou, Janine N Bartholomew, et al.
FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology|October 4, 2008
Human rhomboid family-1 gene RHBDF1 participates in GPCR-mediated transactivation of EGFR growth signals in head and neck squamous cancer cellsHuafei Zou, Sufi M Thomas, Zhen-Wen Yan, et al.
Molecular Cancer Therapeutics|June 6, 2008
Human rhomboid family-1 gene silencing causes apoptosis or autophagy to epithelial cancer cells and inhibits xenograft tumor growthZhenwen Yan, Huafei Zou, Fang Tian, et al.
ACS Medicinal Chemistry Letters|August 16, 2019
Design of a Long-Acting and Selective MEG-Fatty Acid Stapled Prolactin-Releasing Peptide AnalogElsa Pflimlin, Sam Lear, Candy Lee, et al.
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