+ |
CCNA1 | down-regulates quantity by repression
transcriptional regulation
|
WT1 |
0.399 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255905 |
|
|
Homo sapiens |
|
pmid |
sentence |
19082485 |
This study identified WT1 as a repressed target of cyclin A1 and suggests that the suppression of WT1 in cyclin A1-overexpressing leukemias might play a role in the growth and suppression of apoptosis in these leukemic cells. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML |
+ |
CCNA1 | up-regulates
|
Proliferation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255734 |
|
|
Homo sapiens |
ML-1 Cell |
pmid |
sentence |
15829981 |
SiRNA mediated silencing of cyclin A1 in highly cyclin A1 expressing ML1 leukemic cells significantly slowed S phase entry, decreased proliferation and inhibited colony formation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, ASXL1 in AML, FLT3 in AML, Onco-fusion proteins in AML |
+ |
PML-RARalpha | up-regulates activity
|
CCNA1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256373 |
|
|
Homo sapiens |
|
pmid |
sentence |
11090075 |
We show that the ectopic expression of PML-RARα is sufficient to elevate levels of cyclin A1 in U937 myeloid leukemia cells and cyclin A1 is negatively regulated by the RARα pathway. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3 in AML, Onco-fusion proteins in AML |
+ |
CCNA1 | up-regulates
|
G1/S_transition |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252255 |
|
|
|
|
pmid |
sentence |
15829981 |
Cyclin A1 contributes to G1 to S cell cycle progression in somatic cells. Cyclin A1 overexpression enhances S phase entry consistent with an oncogenic function. Finally, cyclin A1 might be a therapeutic target since its silencing inhibited leukemia cell growth. |
|
Publications: |
1 |
+ |
RARA | down-regulates quantity by repression
transcriptional regulation
|
CCNA1 |
0.246 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-249636 |
|
|
Homo sapiens |
NB-4 Cell |
pmid |
sentence |
11090075 |
RARα is involved in the regulation of cyclin A1. Further studies using ligands selective for various retinoic acid receptors suggested that cyclin A1 expression is negatively regulated by activated RARα. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, ASXL1 in AML |
+ |
SMARCB1 | down-regulates
|
CCNA1 |
0.342 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-92779 |
|
|
Homo sapiens |
|
pmid |
sentence |
12226744 |
We show that the ectopic expression of wild-type hsnf5/ini1, but not that of truncated versions, leads to a cell cycle arrest by inhibiting the entry into s phase of mrt cells. This g1 arrest is associated with down-regulation of a subset of e2f targets including cyclin a, e2f1 and cdc6. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PML-RARalpha | up-regulates quantity by expression
transcriptional regulation
|
CCNA1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255725 |
|
|
Homo sapiens |
|
pmid |
sentence |
11090075 |
Overexpression of cyclin A1 observed in APL cells is caused by the expression of the aberrant fusion proteins, PML-RARα and PLZF-RARα. PML-RARα itself can lead to activation of the cyclin A1 promoter.Since both fusion proteins disrupt the normal RARα function, our results strongly suggested that the RARα pathway negatively regulates the expression of cyclin A1 and that this negative regulation is disrupted by the aberrant fusion proteins. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, FLT3 in AML, Onco-fusion proteins in AML |
+ |
CCNA1 | up-regulates
|
Cell_growth |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-249637 |
|
|
|
|
pmid |
sentence |
15829981 |
Cyclin A1 contributes to G1 to S cell cycle progression in somatic cells. Cyclin A1 overexpression enhances S phase entry consistent with an oncogenic function. Finally, cyclin A1 might be a therapeutic target since its silencing inhibited leukemia cell growth. |
|
Publications: |
1 |