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  • Insulin Receptor and GPCR Crosstalk Stimulates YAP via PI3K and PKD in Pancreatic Cancer Cells.

Insulin Receptor and GPCR Crosstalk Stimulates YAP via PI3K and PKD in Pancreatic Cancer Cells.

Molecular cancer research : MCR (2017-04-01)
Fang Hao, Qinhong Xu, Yinglan Zhao, Jan V Stevens, Steven H Young, James Sinnett-Smith, Enrique Rozengurt
摘要

We examined the impact of crosstalk between the insulin receptor and G protein-coupled receptor (GPCR) signaling pathways on the regulation of Yes-associated protein (YAP) localization, phosphorylation, and transcriptional activity in the context of human pancreatic ductal adenocarcinoma (PDAC). Stimulation of PANC-1 or MiaPaCa-2 cells with insulin and neurotensin, a potent mitogenic combination of agonists for these cells, promoted striking YAP nuclear localization and decreased YAP phosphorylation at Ser

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Sigma-Aldrich
神经降压素, ≥90% (HPLC)
Sigma-Aldrich
KU 0063794, ≥98% (HPLC)
Sigma-Aldrich
3-(联苯-4-基)-5-(4-叔丁基苯基)-4-苯基-4H-1,2,4-三唑, 97%
Sigma-Aldrich
kb-NB142-70, ≥97% (HPLC)