+ |
ASXL3 | down-regulates activity
binding
|
KDM1A |
0.27 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266764 |
|
|
Homo sapiens |
|
pmid |
sentence |
25450400 |
Here, we showed that ASXL3 interacts with HP1α and LSD1, leading to transcriptional repression. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
ASXL3 | up-regulates activity
binding
|
BRD4 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266762 |
|
|
Homo sapiens |
Small Cell Lung Cancer Cell |
pmid |
sentence |
32669118 |
We report a critical link between BAP1 complex and BRD4, which is bridged by the physical interaction between ASXL3 and BRD4 in an SCLC subtype (SCLC-A), which expresses a high level of ASCL1. We further showed that ASXL3 functions as an adaptor protein, which directly interacts with BRD4's extra-terminal (ET) domain via a novel BRD4 binding motif (BBM), and maintains chromatin occupancy of BRD4 to active enhancers. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
ASXL3 | down-regulates activity
binding
|
CBX5 |
0.254 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266763 |
|
|
Homo sapiens |
HEP-3B Cell |
pmid |
sentence |
25450400 |
Here, we showed that ASXL3 interacts with HP1α and LSD1, leading to transcriptional repression. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
ASXL3 | down-regulates activity
binding
|
NR1H3 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266765 |
|
|
Homo sapiens |
HEP-3B Cell |
pmid |
sentence |
25450400 |
We determined that ASXL3 depletion augments the ligand-induced transcriptional activities of LXRα and TRβ, which were repressed by ASXL3 overexpression. The ligand-dependent interactions of ASXL3 with LXRα and TRβ were demonstrated by the GST pull-down and immunoprecipitation analyses. We confirmed that ASXL3 suppresses the expression of LXRα target genes through its recruitment to the LXR-response elements. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
ASXL3 | down-regulates activity
binding
|
THRB |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266766 |
|
|
Homo sapiens |
HEP-3B Cell |
pmid |
sentence |
25450400 |
We determined that ASXL3 depletion augments the ligand-induced transcriptional activities of LXRα and TRβ, which were repressed by ASXL3 overexpression. The ligand-dependent interactions of ASXL3 with LXRα and TRβ were demonstrated by the GST pull-down and immunoprecipitation analyses. We confirmed that ASXL3 suppresses the expression of LXRα target genes through its recruitment to the LXR-response elements. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
BAP1 | up-regulates activity
binding
|
ASXL3 |
0.546 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266761 |
|
|
Homo sapiens |
Small Cell Lung Cancer Cell |
pmid |
sentence |
32669118 |
We report a critical link between BAP1 complex and BRD4, which is bridged by the physical interaction between ASXL3 and BRD4 in an SCLC subtype (SCLC-A), which expresses a high level of ASCL1. We further showed that ASXL3 functions as an adaptor protein, which directly interacts with BRD4's extra-terminal (ET) domain via a novel BRD4 binding motif (BBM), and maintains chromatin occupancy of BRD4 to active enhancers. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
ASXL3 | down-regulates activity
binding
|
THR |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-270302 |
|
|
Homo sapiens |
HEP-3B Cell |
pmid |
sentence |
25450400 |
We determined that ASXL3 depletion augments the ligand-induced transcriptional activities of LXRα and TRβ, which were repressed by ASXL3 overexpression. The ligand-dependent interactions of ASXL3 with LXRα and TRβ were demonstrated by the GST pull-down and immunoprecipitation analyses. We confirmed that ASXL3 suppresses the expression of LXRα target genes through its recruitment to the LXR-response elements. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |