Gene interactions and pathways from curated databases and text-mining

◀ Back to NOTCH1

JUN — NOTCH1

Text-mined interactions from Literome

Talora et al., Genes Dev 2002 (Cell Transformation, Neoplastic...) : Increased Notch1 signaling, but not Notch2, causes a dramatic down-modulation of HPV-driven transcription of the E6/E7 viral genes, through suppression of AP-1 activity by up-regulation of the Fra-1 family member and decreased c-Fos expression
Chu et al., J Biol Chem 2004 : Evidence that C promoter binding factor 1 binding is required for Notch-1 mediated repression of activator protein-1
Jang et al., J Cell Physiol 2004 (Leukemia, Erythroblastic, Acute) : We show that : ( 1 ) downregulation of Notch-1 sensitizes MEL cells to apoptosis induced by a Ca ( 2+ ) influx or anti-neoplastic drugs ; ( 2 ) Notch-1 downregulation induces phosphorylation of c-Jun N-terminal kinase (JNK) while constitutive activation of Notch-1 or prolonged exposure to a soluble Notch ligand abolishes it ; ( 3 ) Notch-1 has dose- and time dependent effects on the levels of apoptotic inhibitor Bcl-x ( L ) and cell cycle regulators p21 ( cip1/waf1 ), p27 ( kip1 ), and Rb ; and ( 4 ) Notch-1 activation by a cell associated ligand is accompanied by rapid and transient induction of NF-kappaB DNA binding activity
Wang et al., Int J Gynecol Cancer 2007 (Carcinoma...) : Increased Notch1 signaling induced a downmodulation of human papillomavirus transcription through suppression of activator protein (AP)-1 activity by upregulation of c-Jun and the decreased expression of c-Fos
Henken et al., Cellular oncology (Dordrecht) 2012 (Cell Transformation, Neoplastic...) : Moderate Notch expression led to an increased AP-1 transcriptional activity and DNA binding activity, but did not affect complex composition
Ordentlich et al., Mol Cell Biol 1998 : We provide evidence that Notch and Deltex may act on E47 by inhibiting signaling through Ras because ( i ) full E47 activity was found to be dependent on Ras and ( ii ) both Notch and Deltex inhibited GAL4-Jun , a hybrid transcription factor whose activity is dependent on signaling from Ras to SAPK/JNK