An accompanying commentary by Mark Nelson of the University of Vermont provides detail on our current understanding of the molecular underpinnings of hypertension, and places Valverde and colleagues' work in this context.
TITLE: Gain-of-function mutation in the KCNMB1 potassium channel subunit is associated with low prevalence of diastolic hypertension
AUTHOR CONTACT:
Miguel A. Valverde
Universitat Pompeu Fabra, Barcelona, Spain.
Phone: 34-93-542-2832
Fax: 34-93-542-2802
E-mail: miguel.valverde@edu.upf
View the PDF of this article at: https://www.the-jci.org/press/20347.pdf
ACCOMPANYING COMMENTARY: The beta1 subunit of the Ca2+-sensitive K+ channel protects against hypertension
AUTHOR CONTACT:
Mark T. Nelson
University of Vermont, Burlington, Vermont, USA.
Phone: 802-656-2500
Fax: 802-656-4523
E-mail: Mark.Nelson@uvm.edu
View the PDF of this commentary at: https://www.the-jci.org/press/21388.pdf
Bim Notes in the Neuronal Executioner's Song
Brain damage often results after prolonged seizures as well as after brief or repetitive epileptic seizures. Previous work has indicated that loss of neurons in the hippocampus after seizures may be due to onset of programmed cell death. Members of the Bcl-2 family are known to activate a pathway ending in the release of several caspases, including the 'executioner,' caspase-3. David Henshall and colleagues, of Robert S. Dow Neurobiology Laboratories, investigate molecular members of the programmed cell death pathway and show that reduction of Bim (Bcl-2-interacting mediator of cell death) may provide protection from neuronal loss. The researchers examined Bim expression in bot
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Contact: Laurie Goodman
lgoodman@the-jci.org
212-342-4159
Journal of Clinical Investigation
2-Apr-2004