Oxidized CaMKII Triggers Atrial Fibrillation Running title :

نویسندگان

  • Anil Purohit
  • Adam G. Rokita
  • Xiaoqun Guan
  • Biyi Chen
  • Olha M. Koval
  • Niels Voigt
  • Stefan Neef
  • Thomas Sowa
  • Zhan Gao
  • Elizabeth D. Luczak
  • Andrew C. Behunin
  • Ramzi N. El-Accaoui
  • Baoli Yang
  • Paari Dominic Swaminathan
  • Robert M. Weiss
  • Long-Sheng Song
  • Lars S. Maier
چکیده

Dept of Internal Medicine, Division of Cardiovascular Medicine and Cardiovascular Research Center, Carver College of Medicine, University of Iowa, Iowa City, IA; Institute of Pharmacology, Faculty of Medicine, University Duisburg-Essen, Essen, Germany, and Division of Experimental Cardiology, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany; Cardiology and Pneumology, German Heart Center, University Hospital Goettingen, Goettingen, Germany; Dept of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX; Dept of Obstetrics and Gynecology; Dept of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA contributed equally

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Oxidized Ca(2+)/calmodulin-dependent protein kinase II triggers atrial fibrillation.

BACKGROUND Atrial fibrillation (AF) is a growing public health problem without adequate therapies. Angiotensin II and reactive oxygen species are validated risk factors for AF in patients, but the molecular pathways connecting reactive oxygen species and AF are unknown. The Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) has recently emerged as a reactive oxygen species-activated proarrh...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2013