Protein Variants | Comment | Organism |
---|---|---|
additional information | treatment with uPAR siRNA significantly increases the G0-G1 population by 27% in the CFPAC-1 cells and 20.4% in the PANC-1 cells, compared to control, PAI-2 or uPA siRNA, overview. uPA siRNA treatment reduces cell migration by approximately 25% for CFPAC-1 and 18% for PANC-1 cells. Transfection with PAI-2 siRNA has no effect on cell migration compared to non-silencing siRNA controls | Homo sapiens |
Inhibitors | Comment | Organism | Structure |
---|---|---|---|
plasminogen activator inhibitor-2 | i.e. PAI-2 | Homo sapiens |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
CFPAC-1 cell | - |
Homo sapiens | - |
PANC-1 cell | - |
Homo sapiens | - |
pancreatic adenocarcinoma cell | - |
Homo sapiens | - |
Synonyms | Comment | Organism |
---|---|---|
uPA | - |
Homo sapiens |
Urokinase-type plasminogen activator | - |
Homo sapiens |
Organism | Comment | Expression |
---|---|---|
Homo sapiens | inhibitors of p-ERK and p-p38 downregulate uPA in CFPAN-1 and PANC-1 cells, but these inhibitors affect uPAR considerably more than uPA | down |
General Information | Comment | Organism |
---|---|---|
malfunction | pancreatic ductal adenocarcinoma, PDAC, expresses high levels of urokinase-type plasminogen activator, its receptor uPAR, and plasminogen activator inhibitor-2, which may play an important role in PDAC progression. Proliferation and migration of pancreatic adenocarcinoma cells via regulation of ERK/p38 signaling is inhibited by suppression of urokinase plasminogen activator receptor. Effects of uPAR in the uPA system on cancer cell development and progression, overview | Homo sapiens |