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PRKCZ — SP1

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: SP1 → PRKCZ (increases, PRKCZ Activity, SP1 Activity) Pal et al., J Biol Chem 2001*
  Evidence: It has been shown through electrophoretic mobility shift assay that Ras promoted the PKCzeta-induced binding of Sp1 to the VPF/VEGF promoter.
• OpenBEL Selventa BEL large corpus: SP1 → PRKCZ (increases, PRKCZ Activity, SP1 Activity) Neid et al., J Biol Chem 2004*
  Evidence: Modified assertion
• OpenBEL Selventa BEL large corpus: SP1 → PRKCZ (increases, SP1 Activity) Tan et al., Circ Res 2008*
  Evidence: Here we have used a variety of approaches to identify 3 amino acids (Thr668, Ser670, and Thr681) in the zinc finger domain of Sp1 that are modified by PKC-zeta

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: SP1 — PRKCZ (physical association, affinity chromatography technology) Zhang et al., Mol Cell Biol 2006*
• IRef Biogrid Interaction: SP1 — PRKCZ (direct interaction, enzymatic study) Tan et al., Circ Res 2008*

Text-mined interactions from Literome

Zhang et al., Mol Cell Biol 2006 : Phosphatidylinositol 3-kinase/protein kinase Czeta induced phosphorylation of Sp1 and p107 repressor release have a critical role in histone deacetylase inhibitor mediated derepression [ corrected ] of transcription of the luteinizing hormone receptor gene
Kim et al., Endothelium : journal of endothelial cell research 2008 : The aim of this study was to determine if changes in levels of Sp1 phosphorylation induced by protein kinase Czeta (PKCzeta) in ECs exposed to SS but not CS are important for MT1-MMP expression