|1.||Brancaccio, Mara: 11 articles (03/2015 - 01/2003)|
|2.||Tarone, Guido: 11 articles (03/2015 - 01/2003)|
|3.||Sbroggiò, Mauro: 5 articles (01/2014 - 05/2005)|
|4.||Silengo, Lorenzo: 5 articles (10/2011 - 01/2003)|
|5.||Ferretti, Roberta: 4 articles (11/2011 - 09/2003)|
|6.||Regitz-Zagrosek, Vera: 3 articles (01/2014 - 06/2007)|
|7.||Lembo, Giuseppe: 3 articles (01/2009 - 01/2003)|
|8.||Accornero, Federica: 3 articles (06/2008 - 05/2005)|
|9.||De Acetis, Marika: 3 articles (05/2005 - 01/2003)|
|10.||Hirsch, Emilio: 2 articles (01/2014 - 01/2003)|
03/01/2012 - "In the present study, we investigated the possible role that melusin plays during cardiac remodeling after myocardial infarction (MI). "
01/01/2014 - "Here, we evaluated the consequences of melusin overexpression in the setting of myocardial infarction (MI) using a comprehensive multicentre approach. "
03/01/2012 - "Altered melusin pathways involved in cardiac remodeling following acute myocardial infarction."
01/01/2014 - "Melusin protects from cardiac rupture and improves functional remodelling after myocardial infarction."
01/01/2014 - "At 2 weeks after MI, melusin overexpression conferred a favourable adaptive remodelling characterized by reduced left ventricle dilatation and better preserved contractility in the presence of a comparable degree of hypertrophy. "
01/01/2014 - "Melusin is a muscle-specific chaperone protein whose expression is required for a compensatory hypertrophy response to pressure overload. "
11/01/2011 - "Melusin, however, organizes ERK signal transduction in cardiomyocytes and regulates cardiac compensatory hypertrophy in response to different stress stimuli."
10/15/2011 - "Finally, analysis of isolated neonatal cardiomyocytes indicates that both FAK and IQGAP1 regulate melusin-dependent cardiomyocyte hypertrophy and survival through ERK1/2 activation."
01/01/2009 - "Melusin is a muscle specific signaling protein, required for compensatory hypertrophy response in pressure-overloaded heart. "
01/10/2013 - "In this report, we confirm the low prevalence of mutations and single nucleotide polymorphisms in the coding sequence of the human melusin gene in patients with DCM, ruling out the possibility that genetic variations in this myocardially transcribed gene may have a significant impact on the epidemiology of DCM-induced heart failure."
03/01/2012 - "We also showed a dynamic change in melusin during heart failure progression; it had an initial decline which was evident at 3 weeks and increased subsequently, reaching peak levels at 6 weeks. "
05/27/2005 - "We have previously shown that genetic ablation of melusin, a muscle specific beta 1 integrin interacting protein, accelerates left ventricle (LV) dilation and heart failure in response to pressure overload. "
01/01/2003 - "Melusin, a muscle-specific integrin beta1-interacting protein, is required to prevent cardiac failure in response to chronic pressure overload."
|4.||Cardiomegaly (Heart Hypertrophy)
05/27/2005 - "Echocardiography analysis indicated that melusin over-expression induced a mild cardiac hypertrophy in basal conditions (30% increase in interventricular septum thickness) with no obvious structural and functional alterations. "
05/27/2005 - "Here we show that melusin expression was increased during compensated cardiac hypertrophy in mice subjected to 1 week pressure overload, but returned to basal levels in LV that have undergone dilation after 12 weeks of pressure overload. "
09/11/2003 - "Melusin is a muscle specific protein required for heart hypertrophy in response to mechanical overload. "
06/01/2007 - "The role of melusin, a necessary component in pressure-induced left-ventricular hypertrophy (LVH) in mice, has not yet been determined in human cardiac hypertrophy. "
|5.||Dilated Cardiomyopathy (Cardiomyopathy, Congestive)
01/10/2013 - "Identification of a missense mutation in the melusin-encoding ITGB1BP2 gene in a patient with dilated cardiomyopathy."
05/27/2005 - "Cardiac overexpression of melusin protects from dilated cardiomyopathy due to long-standing pressure overload."
01/01/2003 - "Melusin-null mice showed normal cardiac structure and function in physiological conditions, but when subjected to pressure overload--a condition that induces a hypertrophic response in wild-type controls--they developed an abnormal cardiac remodeling that evolved into dilated cardiomyopathy and contractile dysfunction. "
|1.||Molecular Chaperones (Chaperone, Molecular)
|2.||Heat-Shock Proteins (Heat-Shock Protein)