Increased resistance to apoptosis during differentiation and syncytialization of BeWo choriocarcinoma cells

ISSN Print: 2156-8456
ISSN Online: 2156-8502
www.scirp.net/journal/abb
E-mail: [email protected]

Citations

"Increased resistance to apoptosis during differentiation and syncytialization of BeWo choriocarcinoma cells"
written by Bih-Rong Wei, Chuan Xu, Neal S. Rote,
published by Advances in Bioscience and Biotechnology, Vol.3 No.6A, 2012

has been cited by the following article(s):

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[3]	The supression of DOCK family members by their specific inhibitors induces the cell fusion of human trophoblastic cells
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[4]	Placentation and Barrier Transporters: Regulation by Endogenous and Exogenous Factors
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[5]	Role of Caspases in the Cytotoxicity of NK-92 Cells in Various Models of Coculturing with Trophoblasts
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[6]	РОЛЬ КАСПАЗ В ПРОЯВЛЕНИИ ЦИТОТОКСИЧНОСТИ КЛЕТОК NK-92 В РАЗЛИЧНЫХ МОДЕЛЯХ ИХ СОКУЛЬТИВИРОВАНИЯ С КЛЕТКАМИ ТРОФОБЛАСТА
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[7]	Protein kinases orchestrate cell cycle regulators in differentiating BeWo choriocarcinoma cells
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[8]	Ο ρόλος της αντιπονεκτίνης στην τροφοβλάστη: σχέση με παράγοντες που ενέχονται στη διαφοροποίηση
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[4]	Caspase Activation in Trophoblast Cells after Interacting with Microparticles Produced by Natural Killer Cells in vitro Journal of Evolutionary Biochemistry and Physiology, 2022 DOI:10.1134/S002209302206014X

[5]	Toxicity of anticancer drugs in human placental tissue explants and trophoblast cell lines Archives of Toxicology, 2021 DOI:10.1007/s00204-020-02925-w

[6]	The supression of DOCK family members by their specific inhibitors induces the cell fusion of human trophoblastic cells Biochemical and Biophysical Research Communications, 2020 DOI:10.1016/j.bbrc.2020.06.138

[7]	Role of Caspases in the Cytotoxicity of NK-92 Cells in Various Models of Coculturing with Trophoblasts Biochemistry (Moscow), 2019 DOI:10.1134/S0006297919100079

[8]	Protein kinases orchestrate cell cycle regulators in differentiating BeWo choriocarcinoma cells Molecular and Cellular Biochemistry, 2018 DOI:10.1007/s11010-018-3407-8