Gene interactions and pathways from curated databases and text-mining

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SP1 — TP53

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

Kanaya et al., Clin Cancer Res 2000 : These findings suggest that p53 repressed telomerase activity through down-regulation of hTERT transcription and that interaction of p53 with Sp1 or other transcription factors may be involved in this regulation
Lee et al., Oncogene 2000 (Carcinoma, Hepatocellular...) : Wild-type p53 inhibited binding of transcription factors Sp1 and TBP on the P4 promoter, while p53mt249 enhanced the formation of transcriptional complexes through enhanced DNA-protein ( Sp1 or TBP ) and protein-protein ( Sp1 and TBP ) interactions ... p53mt249 stimulates transcription factor Sp1 phosphorylation which might be a cause of increased transcription factor binding on the P4 promoter while wild-type p53 does not
Xu et al., Oncogene 2000 (Breast Neoplasms...) : Finally, wt p53 inhibited Sp1 binding to the hTERT proximal promoter by forming a p53-Sp1 complex
Amini et al., J Biol Chem 2004 : Expression of p53 further enhanced the level of Vpr-Sp1 mediated transcription activation of p21 through the sequence spanning -84 to -74 and increased the DNA binding activity of Sp1 in the presence of Vpr. Results from glutathione S-transferase pull-down assay showed the association of Vpr with p53 in extracts containing Sp1
Pietrzak et al., Biol Chem 2008 : As shown by electrophoretic mobility shift assays, Sp1 binding to the sites located in the -295 to +16 MCL-1 promoter fragment was decreased in the presence of p53
Bheda et al., Oncogene 2008 : Wild-type p53 suppressed Sp1- and YY1 mediated induction of the EGFR promoter ... We conclude that acute loss of p53 in normal HKc induces EGFR expression by a mechanism that involves YY1 and Sp1 and does not require p53 binding to the EGFR promoter
Króliczak et al., Acta biochimica Polonica 2008 (Neoplasms) : Sp1 and NFkappaB binding to the probes resembling their putative binding sites present in the S100A6 promoter was decreased in the presence of wild type p53
Lin et al., Cancer Res 2010 (Lung Neoplasms) : Low level of exogenous Sp1 enhanced the repressive activity of endogenous p53 on the DNMT1 promoter whereas high level of Sp1 upregulated DNMT1 gene expression level in A549 ( p53 wild-type ) cells
Fuchs-Young et al., Breast Cancer Res Treat 2011 (Cell Transformation, Neoplastic...) : Previous studies from our laboratory have shown that p53 regulates ER expression transcriptionally, by binding the ER promoter and forming a complex with CARM1, CBP, c-Jun, RNA polymerase II and Sp1
Hwang et al., Proc Natl Acad Sci U S A 2011 (Neoplasm Invasiveness) : Wild-type p53 negatively regulates MET expression by two mechanisms : ( i ) transactivation of MET targeting miR-34, and ( ii ) inhibition of SP1 binding to MET promoter
Dhar et al., Cancer Res 2011 (Carcinoma, Squamous Cell...) : Exposure to DMBA and TPA activated p53 and decreased MnSOD expression via p53 mediated suppression of Sp1 binding to the MnSOD promoter in normal appearing skin and benign papillomas
Gu et al., J Cell Physiol 2012 (Breast Neoplasms) : Oldenlandia diffusa extracts exert antiproliferative and apoptotic effects on human breast cancer cells through ERa/Sp1 mediated p53 activation
Chew et al., J Biol Chem 2012 : Sulforaphane induction of p21 ( Cip1 ) cyclin dependent kinase inhibitor expression requires p53 and Sp1 transcription factors and is p53 dependent
Gualberto et al., J Biol Chem 1995 : The presence of Sp1 increased p53 binding to its recognition sequence in the HIV-1 LTR, and experiments in Drosophila cells show that Sp1 is necessary for full transactivation by mutant p53
Bargonetti et al., Cell Mol Biol Incl Cyto Enzymol 1997 : p53 represses Sp1 DNA binding and HIV-LTR directed transcription
Ohlsson et al., Endocrinology 1998 (Osteosarcoma) : p53 regulates insulin-like growth factor-I (IGF-I) receptor expression and IGF-I induced tyrosine phosphorylation in an osteosarcoma cell line : interaction between p53 and Sp1