Inhibition of KCa3.1 suppresses TGF-β1 induced MCP-1 expression in human proximal tubular cells through Smad3, p38 and ERK1/2 signaling pathways

It is well known that TGF-β1 plays a central role in renal fibrosis due in large part to stimulation of inflammatory responses. KCa3.1, a potassium channel protein, has been suggested as a potential therapeutic target for diseases such as sickle cell anemia, autoimmunity, atherosclerosis and more re...

Ausführliche Beschreibung

Gespeichert in:

Bibliographische Detailangaben
Veröffentlicht in:	The international journal of biochemistry & cell biology 2014-02, Vol.47, p.1-10
Hauptverfasser:	Huang, Chunling, Day, Margot L., Poronnik, Philip, Pollock, Carol A., Chen, Xin-Ming
Format:	Artikel
Sprache:	eng
Schlagworte:	Cell signaling Cells, Cultured Chemokine CCL2 - biosynthesis Chemokine CCL2 - genetics Chemokine CCL2 - metabolism Flavonoids - pharmacology Gene Knockdown Techniques Humans Imidazoles - pharmacology Intermediate-Conductance Calcium-Activated Potassium Channels - antagonists & inhibitors Intermediate-Conductance Calcium-Activated Potassium Channels - genetics Intermediate-Conductance Calcium-Activated Potassium Channels - metabolism KCa3.1 Kidney Tubules, Proximal - enzymology Kidney Tubules, Proximal - metabolism MAP Kinase Signaling System - drug effects MCP-1 p38 Mitogen-Activated Protein Kinases - metabolism Phosphorylation Pyrazoles - pharmacology Pyridines - pharmacology RNA, Small Interfering - administration & dosage RNA, Small Interfering - genetics Signal Transduction Smad3 Protein - genetics Smad3 Protein - metabolism TGF-β1 Transfection Transforming Growth Factor beta1 - antagonists & inhibitors Transforming Growth Factor beta1 - genetics Transforming Growth Factor beta1 - metabolism
Online-Zugang:	Volltext
Tags:	Tag hinzufügen Keine Tags, Fügen Sie den ersten Tag hinzu!

Schreiben Sie den ersten Kommentar!