◀ Back to JUN
ATF1 — JUN
Pathways - manually collected, often from reviews:
-
NCI Pathway Database ErbB1 downstream signaling:
ATF1 (ATF1)
→
JUN (JUN)
(transcription, activates)
Gupta et al., J Biol Chem 2002*, Han et al., Mol Cell Biol 1992*, Hurst et al., Nucleic Acids Res 1991*, Quantin et al., Nature 1988*, Clarke et al., Mol Cell Biol 1998*
Evidence: genetic interaction
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Mao et al., J Immunol 2001
:
Furthermore, the bZip elements of the two promoters bind different transcription factors, as the GL epsilon promoter binds and is activated by
AP-1 , whereas the gamma1 promoter binds and is
activated by
activating transcription factor 2
Adiseshaiah et al., J Immunol 2006
(MAP Kinase Signaling System) :
Our findings collectively indicate that ERK signaling plays key roles in both Elk1, CREB, and
ATF-1 activation and the subsequent recruitment of
c-Jun to the FRA-1 promoter in response to TNF-alpha in pulmonary epithelial cells
Lu et al., J Dermatol 2013
:
Importantly,
JUN may
regulate activating transcription factor 3 expression to involve cell proliferation process ; STAT1 and STAT3 can inhibit tissue inhibitor of metalloproteinases-3 expression to modulate the cell adhesion molecule pathway ; NF-?B and E2F1 can downregulate cyclin D1, but upregulate proliferating cell nuclear antigen expression to promote the cell cycle pathway