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Literature summary for 3.4.21.73 extracted from

  • Xue, A.; Xue, M.; Jackson, C.; Smith, R.C.
    Suppression of urokinase plasminogen activator receptor inhibits proliferation and migration of pancreatic adenocarcinoma cells via regulation of ERK/p38 signaling (2009), Int. J. Biochem. Cell Biol., 41, 1731-1738.
    View publication on PubMed

Protein Variants

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

Inhibitors Comment Organism Structure
plasminogen activator inhibitor-2 i.e. PAI-2 Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
CFPAC-1 cell
-
Homo sapiens
-
PANC-1 cell
-
Homo sapiens
-
pancreatic adenocarcinoma cell
-
Homo sapiens
-

Synonyms

Synonyms Comment Organism
uPA
-
Homo sapiens
Urokinase-type plasminogen activator
-
Homo sapiens

Expression

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

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