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JCI table of contents: Jan. 25, 2011
Date:1/25/2011
jci.org/articles/view/44470?key=845c740fe207e4a7265b
ACCOMPANYING ARTICLE
TITLE: Defective Tbx2-dependent patterning of the atrioventricular canal myocardium causes accessory pathway formation in mice
AUTHOR CONTACT:
Vincent M. Christoffels
Academic Medical Center, Amsterdam, The Netherlands.
Phone: 0031.20.566.7821; Fax: 31.20.697.6177; E-mail: v.m.christoffels@amc.uva.nl.
View this article at: http://www.jci.org/articles/view/44350?key=c08a399d64c3aa01813d
ACCOMPANYING COMMENTARY
TITLE: Navigational error in the heart leads to premature ventricular excitation
AUTHOR CONTACT:
Issei Komuro
Osaka University Graduate School of Medicine, Osaka, Japan.
Phone: 81.6.6879.3631; Fax: 81.6.6879.3639; E-mail: komuro-tky@umin.ac.jp.
View this article at: http://www.jci.org/articles/view/46038?key=de37f31e59fa64978ae8
IMMUNOLOGY: To modify or not to modify proteins with inflammatory function
A team of researchers, led by Martin Bergo, at the University of Gothenburg, Sweden, has generated in mice surprising data with clinical implications that call into question current dogma that modification of proteins known as Rho proteins by the fat molecule geranylgeranyl are critical to the function of inflammatory cells.
Geranylgeranyl modification of Rho proteins by geranylgeranyltransferase type I (GGTase-I) is considered essential for their function and that of inflammatory cells. Bergo and colleagues therefore hypothesized that mice lacking GGTase-I in immune cells known as macrophages would be protected from inflammatory disease. However, these mice were found to develop severe joint inflammation
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