Overexpression of ANO1/TMEM16A, an arterial Ca2+-activated Cl− channel, contributes to spontaneous hypertension

This publication has 37 references indexed in Scilit:

• Protective Role of Acidic pH-Activated Chloride Channel in Severe Acidosis-Induced Contraction from the Aorta of Spontaneously Hypertensive Rats
  PLOS ONE, 2013
• Potent vasorelaxant activity of the TMEM16A inhibitor T16A_inh‐A01
  British Journal of Pharmacology, 2013
• Downregulation of TMEM16A Calcium-Activated Chloride Channel Contributes to Cerebrovascular Remodeling During Hypertension by Promoting Basilar Smooth Muscle Cell Proliferation
  Circulation, 2012
• Ano1 as a regulator of proliferation
  American Journal of Physiology-Gastrointestinal and Liver Physiology, 2011
• TMEM16A Inhibitors Reveal TMEM16A as a Minor Component of Calcium-activated Chloride Channel Conductance in Airway and Intestinal Epithelial Cells
  Journal of Biological Chemistry, 2011
• Expression profile and protein translation of TMEM16A in murine smooth muscle
  American Journal of Physiology-Cell Physiology, 2010
• Absence of Akt1 Reduces Vascular Smooth Muscle Cell Migration and Survival and Induces Features of Plaque Vulnerability and Cardiac Dysfunction During Atherosclerosis
  Arteriosclerosis, Thrombosis, and Vascular Biology, 2009
• Expression Cloning of TMEM16A as a Calcium-Activated Chloride Channel Subunit
  Cell, 2008
• Akt Is a Major Downstream Target of PI3-Kinase Involved in Angiotensin II–Induced Proliferation
  Hypertension, 2003
• Central hemodynamics in the developmental stage of spontaneous hypertension in the unanesthetized rat.
  Hypertension, 1979