Cardiomyopathy, Dilated
|
0.210 |
Biomarker
|
group |
MGD |
|
|
|
Patent ductus arteriosus
|
0.200 |
Biomarker
|
disease |
MGD |
|
|
|
Seizures
|
0.100 |
GeneticVariation
|
phenotype |
CLINVAR |
|
|
|
Poor school performance
|
0.100 |
GeneticVariation
|
phenotype |
CLINVAR |
|
|
|
Cardiomyopathy, Dilated
|
0.210 |
AlteredExpression
|
group |
BEFREE |
Myocardin and HOP mRNA levels were estimated by both northern blot hybridization and semiquantitative RT-PCR in human ventricular preparations in end-stage failure due to dilated cardiomyopathy (DCM), as well as in nonfailing donor hearts.
|
12920479 |
2003 |
Cardiomyopathy, Familial Idiopathic
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
Myocardin and HOP mRNA levels were estimated by both northern blot hybridization and semiquantitative RT-PCR in human ventricular preparations in end-stage failure due to dilated cardiomyopathy (DCM), as well as in nonfailing donor hearts.
|
12920479 |
2003 |
Heart failure
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
A possible dual consequence of increased myocardin and decreased HOP expression levels on serum response factor-dependent cardiac-specific expression in the normal heart and at heart failure is discussed.
|
12920479 |
2003 |
Congestive heart failure
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
A possible dual consequence of increased myocardin and decreased HOP expression levels on serum response factor-dependent cardiac-specific expression in the normal heart and at heart failure is discussed.
|
12920479 |
2003 |
Cardiomegaly
|
0.300 |
Biomarker
|
phenotype |
CTD_human |
Myocardin induces cardiomyocyte hypertrophy.
|
16556869 |
2006 |
Cardiac Hypertrophy
|
0.300 |
Biomarker
|
phenotype |
CTD_human |
Myocardin induces cardiomyocyte hypertrophy.
|
16556869 |
2006 |
Hypertrophic disorder of skin, unspecified
|
0.010 |
AlteredExpression
|
group |
BEFREE |
Consistent with a role for myocardin as a transducer of hypertrophic signals, forced expression of myocardin in cardiomyocytes is sufficient to substitute for hypertrophic signals and induce cardiomyocyte hypertrophy and the fetal cardiac gene program.
|
16556869 |
2006 |
Neoplasms
|
0.050 |
AlteredExpression
|
group |
BEFREE |
Myocardin expression is reduced in multiple types of human tumors.
|
17292825 |
2007 |
Malignant Neoplasms
|
0.030 |
AlteredExpression
|
group |
BEFREE |
Restoration of myocardin expression in sarcoma cells results in differentiation and inhibition of malignant growth, whereas inactivation of myocardin in normal fibroblasts increases their proliferative potential.
|
17292825 |
2007 |
Malignant transformation
|
0.020 |
Biomarker
|
phenotype |
BEFREE |
Collectively, our results demonstrate that myocardin is an important suppressive modifier of the malignant transformation process.
|
17292825 |
2007 |
Alzheimer's Disease
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Thus, SRF-MYOCD overexpression in small cerebral arteries appears to initiate independently of Abeta a pathogenic pathway mediating arterial hypercontractility and CBF dysregulation, which are associated with Alzheimer's dementia.
|
17215356 |
2007 |
Heart Block
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Forced myocardin expression also endowed human MSFs with the ability to transmit an action potential and to repair an artificially created conduction block in cardiomyocyte cultures.
|
17579192 |
2007 |
Infarction
|
0.010 |
Biomarker
|
phenotype |
LHGDN |
Fibroblasts from human postmyocardial infarction scars acquire properties of cardiomyocytes after transduction with a recombinant myocardin gene.
|
17579192 |
2007 |
Dementia due to Alzheimer's disease (disorder)
|
0.010 |
Biomarker
|
disease |
BEFREE |
MYOCD in vivo gene transfer to mouse pial arteries increased contractile protein content and diminished CBF responses produced by brain activation in wild-type mice and in two AD models, the Dutch/Iowa/Swedish triple mutant human amyloid beta-peptide (Abeta)-precursor protein (APP)- expressing mice and APPsw(+/-) mice.Silencing Srf had the opposite effect.
|
17215356 |
2007 |
Congenital heart disease
|
0.310 |
GeneticVariation
|
group |
BEFREE |
We identified a rare human sequence variation in MYOCD in a patient with congenital heart disease that resulted in a missense mutation at codon 259 (K259R).
|
18852265 |
2008 |
Hypertrophic Cardiomyopathy
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Thus, a myocardin promoter allelic variant existing in the normal Cretan population was associated with decreased left ventricular mass in HCM patients and decreased myocardin mRNA levels in peripheral blood.
|
18028454 |
2008 |
Neoplasms
|
0.050 |
AlteredExpression
|
group |
BEFREE |
We show here by array-based comparative genomic hybridization, fluorescence in situ hybridization, and expression analysis approaches that MYOCD gene is highly amplified and overexpressed in human retroperitoneal leiomyosarcomas (LMS), a very aggressive well-differentiated tumor.
|
19276386 |
2009 |
Malignant Neoplasms
|
0.030 |
AlteredExpression
|
group |
BEFREE |
Regulation of myocardin-related transcriptional coactivators through cofactor interactions in differentiation and cancer.
|
19625774 |
2009 |
leiomyosarcoma
|
0.030 |
AlteredExpression
|
disease |
BEFREE |
We show here by array-based comparative genomic hybridization, fluorescence in situ hybridization, and expression analysis approaches that MYOCD gene is highly amplified and overexpressed in human retroperitoneal leiomyosarcomas (LMS), a very aggressive well-differentiated tumor.
|
19276386 |
2009 |
LATERAL MENINGOCELE SYNDROME
|
0.030 |
Biomarker
|
disease |
BEFREE |
Collectively, these results show that human retroperitoneal LMS differentiation is dependent on MYOCD amplification/overexpression, suggesting that in these well-differentiated LMS, differentiation could be a consequence of an acquired genomic alteration.
|
19276386 |
2009 |
LIMB-MAMMARY SYNDROME
|
0.030 |
Biomarker
|
disease |
BEFREE |
Collectively, these results show that human retroperitoneal LMS differentiation is dependent on MYOCD amplification/overexpression, suggesting that in these well-differentiated LMS, differentiation could be a consequence of an acquired genomic alteration.
|
19276386 |
2009 |