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NFYC — SP1

Pathways - manually collected, often from reviews:

• FastForward regulation: NFYA, NFYB, NFYC → SP1 (transcriptional regulation, unknown) Nicolás et al., Biochem J 2003*
  Evidence: DNABINDING
• FastForward regulation: SP1 → NFYC (transcriptional regulation, unknown)
  Evidence: DNABINDING
• Reactome Reaction: SP1 → NFYC (reaction) Xiong et al., Proc Natl Acad Sci U S A 2000*, Amemiya-Kudo et al., J Lipid Res 2002*, Shin et al., J Nutr 2007, Rome et al., Physiol Genomics 2008, Reed et al., PLoS Genet 2008, Choi et al., J Biol Chem 2008*, Bennett et al., J Biol Chem 1995*, Inoue et al., J Biochem 1998, Pai et al., J Biol Chem 1998
• Reactome Reaction: SP1 → NFYC (indirect_complex) Xiong et al., Proc Natl Acad Sci U S A 2000*, Amemiya-Kudo et al., J Lipid Res 2002*, Shin et al., J Nutr 2007, Rome et al., Physiol Genomics 2008, Reed et al., PLoS Genet 2008, Choi et al., J Biol Chem 2008*, Bennett et al., J Biol Chem 1995*, Inoue et al., J Biochem 1998, Pai et al., J Biol Chem 1998

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: SP1 — NFYC (direct interaction, two hybrid) Bandyopadhyay et al., Nat Methods 2010
• IRef Intact Interaction: SP1 — NFYC (physical association, two hybrid pooling approach) Bandyopadhyay et al., Nat Methods 2010

Text-mined interactions from Literome

Molander et al., Mol Biol Rep 2001 : Furthermore, transfection of NF-Y failed to enhance transcriptional activity when the Sp1 binding sites were deleted from the promoter, suggesting an important role for Sp1 in this NF-Y controlled transcription
Nicolás et al., Biochem J 2003 : Whereas overexpression of NF-Y or E2F had an additive effect on Sp1 overexpression, the activation of Sp1 transcription due to Sp1 was counteracted by Sp3 overexpression
Zhao et al., BMC cancer 2005 : Mdm2 may directly repress activation by both pRB and Sp1 , or activation by NF-Y
Oleaga et al., Mol Nutr Food Res 2013 : Incubation with 3-methyl-epicatechin led to an increase in HNF-3ß mRNA, HNF-3ß, ER-a, Sp1 , and NFY protein levels and the activation of ApoAI transcription mediated by NFY , Sp1, and ER-a