| Interacting proteins: Q96IK5 and P50402 |
Pubmed |
SVM Score :0.65769442 |
| Although GCL alone can not explain the disease mechanism , our results strongly support gene expression models for Emery Dreifuss muscular dystrophy by showing that emerin binds directly to a transcriptional repressor , GCL , and by suggesting that emerin repressor complexes might be regulated by BAF . 0.65769442^^^ |
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| Interacting proteins: Q96IK5 and P50402 |
Pubmed |
SVM Score :0.0 |
| The Delta 95 99 mutation was relatively uninformative , as this mutation also disrupts emerin binding to lamin A and a different transcription repressor named germ cell less ( GCL ) . ^^^ In striking contrast , emerin mutant S54F , which binds normally to barrier to autointegration factor , lamin A and GCL , selectively disrupted emerin binding to Btf . ^^^ |
|
| Interacting proteins: Q96IK5 and P50402 |
Pubmed |
SVM Score :0.0 |
| Other partners for emerin include nesprin 1alpha and transcriptional regulators such as germ cell less ( GCL ) . ^^^ Emerin and lamin A together form stable complexes with either BAF or GCL in vitro . ^^^ BAF , however , competes with GCL for binding to emerin in vitro . ^^^ |
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| Interacting proteins: Q96IK5 and P50402 |
Pubmed |
SVM Score :0.0 |
| The phosphorylation sites Y 74 / Y 75 ( human / mouse emerin ) , Y 85 / Y 86 , Y 94 / Y 95 , and Y 105 / Y 106 are located in regions previously shown to be critical for interactions of emerin with lamin A , actin or the transcriptional regulators GCL and Btf , while the residues Y 161 and Y 167 are in a region linked to binding lamin A or actin . ^^^ |
|
| Interacting proteins: Q96IK5 and P50402 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q96IK5 and P50402 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q96IK5 and P50402 |
Pubmed |
SVM Score :0.0 |
| NA |
|