JCI table of contents: June 14, 2007

quent studies to better understand how the defect of NRG-1beta and Gab1/Gab2 signaling causes DCM, the authors found that angiopoietin 1 expression, which promotes blood vessel formation, is promoted by NRG-1beta and that this interaction is blocked in Gab1/Gab2 double-knockout mice. This lack of response to NRG-1beta may well account for the loss of cardiac contractility and malformed vessels observed in the hearts of these mice and provides insight into the signaling events that underlie DCM.

TITLE: Gab family proteins are essential for postnatal maintenance of cardiac function via neuregulin-1/ErbB signaling

Naoki Mochizuki
National Cardiovascular Center Research Institute, Osaka, Japan.
Phone : 81-6-6833-5012 Ext: 2508; Fax :81-6-6835-5461; E-mail : nmochizu@ri.ncvc.go.jp

Yoshikazu Nakaoka
Osaka University Graduate School of Medicine, Osaka, Japan.
PhoneL 81-6-6879-3835; Fax: 81-6-6879-3839; Email: ynakaoka@imed3.med.osaka-u.ac.jp

View the PDF of this article at: https://www.the-jci.org/article.php?id=30651


Liver protein NCP1L1 is also a target of cholesterol-lowering drug Ezetimibe

Niemann-Pick disease refers to a group of inherited metabolic disorders known as lipid storage diseases in which harmful amounts of fatty substances, such as cholesterol, build up in the spleen, liver, lungs, bone marrow, and brain, causing loss of muscle coordination and brain degeneration. The cholesterol-lowering drug Ezetimibe decreases cholesterol absorption in the intestine by targeting the protein Neimann-Pick C1-like 1 (NPC1L1). However, NPC1L1 is also expressed in the liver. In a study appearing online on June 14 in advance of publication in the July print issue of the Journal of Cli

Contact: Brooke Grindlinger
Journal of Clinical Investigation

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