Abstract:
:Muscle ring finger (MuRF) proteins have been implicated in transmitting mechanical forces to cell signaling pathways through their interactions with the giant protein titin. Recent evidence has linked mechanically-induced stimuli with the control of serum response factor activity and localization through MuRF2. This observation is particularly intriguing in the context of cardiac hypertrophy, where serum response factor transactivation is a key event necessary for the induction of cardiac hypertrophy in response to increased afterload. We have previously reported that MuRF1, which is also a titin-associated protein, exerts antihypertrophic activity in vitro. In the present study, we induced cardiac hypertrophy in mice lacking MuRF1 and MuRF2 to distinguish the physiologic role of these divergent proteins in vivo. We identified for the first time that MuRF1, but not MuRF2, plays a key role in regulating the induction of cardiac hypertrophy, likely by its direct interactions with serum response factor. These studies describe for the first time distinct and nonoverlapping functional characteristics of MuRF1 and MuRF2 in response to cardiac stress in vivo.
journal_name
Circ Resjournal_title
Circulation researchauthors
Willis MS,Ike C,Li L,Wang DZ,Glass DJ,Patterson Cdoi
10.1161/01.RES.0000259559.48597.32subject
Has Abstractpub_date
2007-03-02 00:00:00pages
456-9issue
4eissn
0009-7330issn
1524-4571pii
01.RES.0000259559.48597.32journal_volume
100pub_type
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