Two other VQ motif-containing proteins have been characterized: SIB1 is a nuclear-encoded protein that is targeted to chloroplasts and interacts specifically with plastid RNA polymerase s-factor Sig1, and AtCaMBP25 is a calmodulin-binding protein involved in abiotic stress tolerance. Interestingly, SIB1 was also found to be induced by SA, and to be involved in disease resistance. Thus, the sib1 loss-of-function mutation is compromised in the induction of some defense-related genes triggered by pathogen infection, whereas over-expression of SIB1 activates defense-related gene expression following pathogen infection, leading to enhanced resistance to infection by P. syringae. It is thus tempting to speculate that like MKS1 and SIB1, other VQ domain-containing proteins also play roles in basal resistance. Sanggenone-D Future studies, including double mutant analysis and protein interaction experiments, will clarify the role this protein family may exert in plant immunity and whether MKS1 and SIB1 play similar roles in the MPK4 regulatory node. Despite important advances in medical as well as surgical and device treatment, chronic heart failure remains an important worldwide health problem with a poor prognosis. Since it is characterized by loss of cardiomyocytes combined with impaired function of the remaining cells and often decreased blood flow, cell transplantation and gene therapy have been tried and have proved to be promising strategies. In particular, transplantation of mesenchymal stem cells, bone marrow mononuclear cells and skeletal myoblasts, as well as gene therapy with hepatocyte Kaempferol growth factor, insulin-like growth factor and vascular endothelial growth factor, have been demonstrated to improve cardiac function and to ameliorate many of the underlying pathophysiological features. Integrin-linked kinase is a widely expressed serine/ threonine protein kinase and an important biomechanical sensor which becomes activated upon cell-matrix interaction, thereby exerting a variety of biological functions including induction of angiogenesis and regulation of cardiac contractility, ventricular hypertrophy, cell proliferation, survival and differentiation. Deletion of ILK from the murine heart results in dilated cardiomyopathy and spontaneous heart failure. We have previously shown that ILK gene therapy can attenuate ventricular remodeling and improve cardiac function in a rat model of myocardial infarction.