Gene interactions and pathways from curated databases and text-mining

◀ Back to SP1

SP1 — TFAP2A

Pathways - manually collected, often from reviews:

  • FastForward regulation: SP1 → TFAP2A (transcriptional regulation, unknown)
    Evidence: DNABINDING

Text-mined interactions from Literome

Pena et al., Mol Endocrinol 1999 (Choriocarcinoma) : Activator protein-2 mediates transcriptional activation of the CYP11A1 gene by interaction with Sp1 rather than binding to DNA ... AP-2 induced Sp1/Sp3 activity independently of AP-2 binding to DNA using a GAL4 paradigm ... AP-2 induced Sp1/ Sp3-GAL4 activity 3- to 4-fold, requiring both the amino and extreme carboxy terminus of AP-2 ... The induction of Sp1 activity by AP-2 may contribute to the induction of other genes that bind Sp1
Fujiwara et al., Biosci Biotechnol Biochem 2000 (Melanoma) : We demonstrated here that the AP-2 like CCCCACCC sequence is involved in the UV-mediated activation and Sp1 binds to the sequence
Uchida et al., J Biol Chem 2002 : These results suggest that AP-2 and Sp1 regulate basal promoter activity, and Sp1 is also involved in PKA mediated expression of the rat SPT gene in concert with the transcriptional coactivator CBP
Zhang et al., Peptides 2008 : Thus, the synergistic activation of the human AM gene promoter by Sp1 and AP-2alpha may be mediated by the binding of Sp1 to the promoter region ( -70/-29 ) and the interaction with AP-2alpha , which binds to the promoter region ( -103/-71 )
Costa et al., Endocr Relat Cancer 2008 (Breast Neoplasms...) : Using glutathione S-transferase pull-down assays combined with electrophoretic mobility shift assay and chromatin immunoprecipitation, we demonstrated that by interacting with Sp1, C/EBPbeta, and AP-2 , PPARgamma can prevent Sp1/AP-2 protein-protein association and inhibit binding of Sp1 and C/EBPbeta to DNA, thus reducing IR gene transcription
Chen et al., Mol Cell Biol 1997 : These results suggest that the relatively low Sp1/AP-2 ratio as well as the polyamine mediated inhibition of Sp1 binding to the E motif may account, in part, for the suppression of the K3 gene in corneal epithelial basal cells, while the elevated Sp1/AP-2 ratio may be involved in activating the K3 gene in differentiated corneal epithelial cells
Piao et al., Endocrinology 1997 (Choriocarcinoma) : Second, the binding of AP-2 to its motif in the region from -62 to -53 led to reduced binding of Sp1 and Sp3, and furthermore, mutation of the AP-2 element increased promoter activity to 260 % in JEG-3 cells