About Enhancer
| Enhancer ID: | E_01_0749 |
| Species: | human |
| Position : | chr18:47806131-47808131   |
| Biosample name: | |
| Experiment class : | High+Lowthroughput |
| Enhancer type: | Enhancer |
| Disease: | Heart disease |
| Pubmed ID: | 30141986 |
| Enhancer experiment: | weston blot,RNA sequencing analysis |
| Enhancer experiment description: | LVAD support was associated with CaMKII? activation, increased nuclear myocyte enhancer factor 2, sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05). Active CaMKII? activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33). |
About Target gene
| Target gene : | HDAC5 |
| Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
| Less strong evidence: | RNA-Seq |
| Target gene experiment description: | LVAD support was associated with CaMKII? activation, increased nuclear myocyte enhancer factor 2, sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05). Active CaMKII? activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33).;LVAD support was associated with CaMKII? activation, increased nuclear myocyte enhancer factor 2, sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05). Active CaMKII? activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33). |
About TF
| TF name : | SMAD2 |
| TF experiment: | weston blot,RNA sequencing analysis |
| TF experiment description: | LVAD support was associated with CaMKII? activation, increased nuclear myocyte enhancer factor 2, sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05). Active CaMKII? activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33).;LVAD support was associated with CaMKII? activation, increased nuclear myocyte enhancer factor 2, sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05). Active CaMKII? activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33). |
About Function
| Enhancer function : | LVAD support was associated with CaMKII? activation, increased nuclear myocyte enhancer factor 2, sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05). Active CaMKII? activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33). |
| Enhancer function experiment: | Immunohistochemical staining |
| Enhancer function experiment description: |
LVAD support was associated with CaMKII? activation, increased nuclear myocyte enhancer factor 2, sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05). Active CaMKII? activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33). |
About SNP
| SNP ID: | -- |
Upstream Pathway Annotation of TF
Enhancer associated network
The number on yellow line represents the distance between enhancer and
target gene