+ |
AR | up-regulates quantity by expression
transcriptional regulation
|
UBE2C |
0.408 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251543 |
|
|
Homo sapiens |
|
pmid |
sentence |
19632176 |
The evolution of prostate cancer from an androgen-dependent state (ADPCa) to one that is androgen-independent (AIPCa) marks its lethal progression. The androgen receptor (AR) is essential in both, though its function in AIPCa is poorly understood. We have defined the direct AR-dependent target genes in both AIPCa and ADPCa by generating AR-dependent gene expression profiles and AR cistromes. In contrast to ADPCa, AR selectively up-regulates M-phase cell cycle genes in AIPCa including UBE2C, a gene that inactivates the M-phase checkpoint. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Prostate Cancer |
+ |
Ub:E1 (UBA1 substrate) | up-regulates activity
ubiquitination
|
UBE2C |
0.716 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271322 |
|
|
Homo sapiens |
|
pmid |
sentence |
34199813 |
The ubiquitination process is mediated sequentially by three classes of enzymes consisting of a Ub-activating enzyme E1, a Ub-conjugating enzyme E2, and a Ub ligase E3. Ub is first activated by E1 in an adenosine 5′-triphosphate (ATP)-dependent manner t |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
Ub:E1 (UBA6 substrate) | up-regulates activity
ubiquitination
|
UBE2C |
0.598 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-271356 |
|
|
Homo sapiens |
|
pmid |
sentence |
34199813 |
The ubiquitination process is mediated sequentially by three classes of enzymes consisting of a Ub-activating enzyme E1, a Ub-conjugating enzyme E2, and a Ub ligase E3. Ub is first activated by E1 in an adenosine 5′-triphosphate (ATP)-dependent manner t |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
UBE2C | down-regulates
|
Mitotic_checkpoint |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251544 |
|
|
Homo sapiens |
|
pmid |
sentence |
19632176 |
The evolution of prostate cancer from an androgen-dependent state (ADPCa) to one that is androgen-independent (AIPCa) marks its lethal progression. The androgen receptor (AR) is essential in both, though its function in AIPCa is poorly understood. We have defined the direct AR-dependent target genes in both AIPCa and ADPCa by generating AR-dependent gene expression profiles and AR cistromes. In contrast to ADPCa, AR selectively up-regulates M-phase cell cycle genes in AIPCa including UBE2C, a gene that inactivates the M-phase checkpoint. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Prostate Cancer |