+ |
ASXL2 | up-regulates quantity by expression
transcriptional regulation
|
TET2 |
0.344 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-260074 |
|
|
Homo sapiens |
|
pmid |
sentence |
28516957 |
Interestingly, this identified a number of genes known to promote leukemogenesis (either alone or in the context of AML1-ETO leukemia) as differentially expressed by ASXL2 loss. These include downregulation of TET2 as well as NOTCH2 with ASXL2 loss in human AML1-ETO-expressing cells, downregulation of which have been previously shown to functionally promote myeloid leukemogenesis when altered in expression |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, IDH-TET in AML |
+ |
ASXL2 | up-regulates activity
binding
|
PPARG |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-260063 |
|
|
Homo sapiens |
|
pmid |
sentence |
21047783 |
ASXL2, which does not bind HP1, promotes differentiation by binding to PPARγ and increasing the level of methylated H3K4, leading to the elevation of PPARγ activity. Our genome-wide analysis confirmed the physiological roles of ASXL1 and ASXL2 in adipogenesis at the molecular level, supporting the hypothesis that ASXL1 is an authentic corepressor of PPARγ, whereas ASXL2 is a PPARγ coactivator, and that together ASXL1 and ASXL2 fine-tune adipogenesis via differential regulation of PPARγ. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |