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JUN — PLAUR

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: JUN → Complex of PLAU-PLAUR (increases, PLAU/PLAUR Activity)
  Evidence: In addition to the influence on the protein kinase system, uPA can regulate gene expression. The binding of uPA to uPAR has been shown to stimulate downstream up-regulation of various transcription factors: AP1 in the HT-1080 cell line [54] and c-Jun, c-Myc, and c-fos factors in SaOS2 cells [55]. Recently, the possibility of signal transduction into the cell by the receptor systems associated with urokinase endocytosis was shown [56].

Text-mined interactions from Literome

Okan et al., Oncogene 2001 : The small-GTPase RalA activates transcription of the urokinase plasminogen activator receptor ( uPAR ) gene via an AP1 dependent mechanism ... Here we show that uPAR transcription is stimulated by V12 H-Ras, the effector loop mutant V12 H-Ras G37 and constitutively-active RalA 72L. RalA dependent transcription required the presence of the ATF2-like AP1-site at -70 bp and the c-Jun binding motif at -184 bp in the uPAR promoter ... These data provide evidence for the existence of a novel signalling pathway that links RalA to the activation of uPAR transcription via a c-Src intermediate and activation of AP1
Kim et al., Int J Oncol 2005 (Neoplasm Invasiveness...) : Transient transfection studies using AP-1 decoy confirmed that the activation of AP-1 is involved in PMS induced uPAR upregulation
Leupold et al., Mol Cancer Res 2007 (Colorectal Neoplasms...) : The present study was conducted ( a ) to investigate if, in particular, AP-1 related transcriptional mediators are required for Src induced u-PAR-gene expression, ( b ) to show in vivo relevance of AP-1 mediated Src induced u-PAR gene expression for invasion/intravasation and for resected tissues from colorectal cancer patients
Baek et al., Oncol Rep 2008 (Carcinoma...) : Suppression of the EGF induced uPAR promoter activity by the AP-1 decoy oligonuclotide, as well as expression vectors encoding mutated-type NF-kappaB inducting kinase and I-kappaB, confirmed that the activation of AP-1 and NF-kappaB are essential for the EGF induced uPAR upregulation
Khoi et al., Toxicol Appl Pharmacol 2012 (MAP Kinase Signaling System) : Studies with expression vectors encoding mutated NF-?B signaling molecules and AP-1 decoy confirmed that NF-?B and AP-1 were essential for the nicotine stimulated uPAR expression
Dear et al., FEBS Lett 1997 (Fibrosarcoma...) : Since transcription factors bound to AP-1 recognition sequences within the PAI-2 gene promoter play a role in basal and phorbol ester mediated induction of PAI-2 gene expression, we hypothesised that u-PA/u-PAR mediated modulation of AP-1 activity would in turn influence constitutive and inducible PAI-2 gene expression