p38γ Mitogen-activated Protein Kinase (MAPK) Confers Breast Cancer Hormone Sensitivity by Switching Estrogen Receptor (ER) Signaling from Classical to Nonclassical Pathway via Stimulating ER Phosphorylation and c-Jun Transcription

Lignende værker

• Phosphorylation and Stabilization of Topoisomerase IIα Protein by p38γ Mitogen-activated Protein Kinase Sensitize Breast Cancer Cells to Its Poisons
  af: Qi, Xiaomei, et al.
  Udgivet: (2011)
• p38γ MAPK Cooperates with c-Jun in trans-Activating Matrix Metalloproteinase 9
  af: Loesch, Mathew, et al.
  Udgivet: (2010)
• p38γ Mitogen-activated Protein Kinase Signals through Phosphorylating Its Phosphatase PTPH1 in Regulating Ras Protein Oncogenesis and Stress Response
  af: Hou, Songwang, et al.
  Udgivet: (2012)
• Transcriptional regulation through the estrogen receptor (ER)-α and splice variants of ER-β via classical and nonclassical signal transduction pathways
  af: Hanstein, B, et al.
  Udgivet: (2001)
• The K-Ras effector p38γ MAPK confers intrinsic resistance to tyrosine kinase inhibitors by stimulating EGFR transcription and EGFR dephosphorylation
  af: Yin, Ning, et al.
  Udgivet: (2017)