Gene interactions and pathways from curated databases and text-mining

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JUN — SP1

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Lim et al., J Virol 2000 (Astrocytoma) : We postulate that a Tat mediated increase in SP1 binding activities augments the binding of AP1 and NF-kappaB, leading to synergistic activation of the MCP-1 promoter
García-Lora et al., Cancer Immunol Immunother 2001 : Here we report that PSK enhanced AP-1 and CRE binding activities, whereas IL-2 increased AP-1 and SP-1 and modified GAS/ISRE, IRF-1 and STAT5
Chamboredon et al., Oncogene 2005 : Extensive analysis, conducted in CEFs and in Sp1/3-deficient Drosophila SL2 cells, further showed that ( i ) high constitutive activity of -433/+11 requires a direct binding of the ubiquitous Sp1 and/or Sp3 transcription factors acting on two distinct motifs, that is, a proximal TCC-rich region and an upstream GC box, and that ( ii ) repression by v-Jun does not require any direct binding of the oncoprotein to the DNA, but an indirect binding within a v-Jun-Sp1/3-DNA chromatin associated complex
Xing et al., J Cell Mol Med 2009 : These findings indicate that the up-regulation of the eNOS gene transactivity by LPC involves the enhancement of SP1 transcription factor by the activation of JNK and ERK1/2 signalling pathways and AP1 transcription factor by the activation of JNK signalling pathway
Clerc et al., Virology 2009 : In conclusion, we demonstrate that the repression of c-Jun activity in vivo is mainly due to the HBZ-SP1 mediated sequestration of c-Jun to the HBZ-NBs
Chai et al., Hepatology 2012 (Cholestasis...) : In HepG2 cells, TNFa treatment induced SP1 and MRP3/ABCC3 expression in a dose- and time dependent manner, where increased phosphorylation of c-Jun NH2-terminal kinase/stress activated protein kinase ( JNK/SAPK ) was also detected