a component
| complexing with ATF7IP/MDB1 (complex facilitating the formation of heterochromatic domains, and emphasizing the role of MCAF/AM family proteins in epigenetic control) |
|
complex at least composed of the CAF-1 subunit CHAF1A, MBD1 and SETDB1 |
|
associating with CHAF1B-CBX5 chaperone complex and monomethylating K9 on non nucleosomal histone H3, thus providing H3K9me1 for subsequent trimethylation by SUV39H1/H2 in pericentric regions |
|
forms a multimeric complex with SUV39H1 and other H3K9 methyltransferases |
|
OLIG2-SETDB1 complex can mediate transcriptional repression in oligodendrocytes progenitor cells (OPCs), affecting myelination |
protein
| TRIM28, ERG |
|
interacting with ESCO2 |
|
interacting with CBX1, CBX5, DNMT3A, HDAC1, HDAC2 |
|
interacting with SIN3A, SIN3B, DNMT3B and SUMO2 |
|
can bind to HIV-1 Tat and methylate it, thus regulating the transcriptional activity of the viral LTR |
|
nuclear interacting partner of AKT1 |
|
ZNF274 binding sites co-localize with SETDB1, TRIM28, and H3K9me3 at the 3prime ends of zinc finger genes |
|
JARID2 functions as a transcriptional repressor of target genes, including NOTCH1, through a novel process involving the modification of H3K9 methylation via specific interaction with SETDB1 during heart development |
|
MAT2A interacts with histone methyltransferase SETDB1 and inhibits PTGS2 gene expression |
|
associates with histone deacetylase 4 to bind and inhibit the activity of RUNX2, a hypertrophy-promoting transcription factor |
|
SETDB1-TIAM1 compounds were involved in a novel pathway, which regulated epigenetic modification of gene expression in hepatocellular carcinoma (HCC) |
Other morbid association(s)
|
Type | Gene Modification | Chromosome rearrangement | Protein expression | Protein Function
|
---|
constitutional
|  
|  
| --over
|  
|
markedly increased in Huntington's disease | tumoral
|  
| amplification
|  
|  
|
focally amplified in non-small-cell lung cancer, small-cell lung cancer, ovarian cancer, hepatocellular carcinoma and breast cancer | tumoral
|  
|  
| --over
|  
|
may potentially contribute to melanoma formation by abrogating oncogene-induced senescence | |