◀ Back to NFKB1
NFKB1 — SP1
Pathways - manually collected, often from reviews:
-
FastForward regulation:
SP1
→
NFKB1
(transcriptional regulation, unknown)
Evidence: DNABINDING
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Lim et al., J Virol 2000
(Astrocytoma) :
We postulate that a Tat mediated increase in
SP1 binding activities
augments the binding of AP1 and
NF-kappaB , leading to synergistic activation of the MCP-1 promoter
Gu et al., Blood 2002
(Precursor Cell Lymphoblastic Leukemia-Lymphoma) :
MDM2
induces NF-kappaB/p65 expression transcriptionally through
Sp1 binding sites : a novel, p53 independent role of MDM2 in doxorubicin resistance in acute lymphoblastic leukemia
Sheng et al., FEBS Lett 2006
:
Analysis of the hTERT promoter occupancy in vivo using chromatin immunoprecipitation assays, however, did not
detect an increased binding of
NFkappaB to the hTERT promoter in the activated T cells, although an increased binding of cMyc and
Sp1 was detected
Caposio et al., J Biol Chem 2007
:
Using transient transfection and luciferase assay, electrophoretic mobility shift assay, and chromatin immunoprecipitation, we demonstrate indeed that activation of the
NF-kappaB response is
mediated by IFI16 induced block of
Sp1-like factor recruitment to the promoter of the IkappaBalpha gene, encoding the main NF-kappaB inhibitor
Mertens et al., PLoS Pathog 2009
(Abdominal Abscess) :
In CD8 ( + ) CD28 ( - ) T cells,
Sp1 enhances Zap-70 phosphorylation and increasingly
involves NF-kappaB which ultimately results in protection versus apoptosis and cell death and promotes survival and accumulation of the CD8 ( + ) CD28 ( - ) population
Kim et al., Mol Cancer Ther 2010
(Carcinoma, Hepatocellular...) :
beta-Ionone enhances TRAIL induced apoptosis in hepatocellular carcinoma cells through
Sp1 dependent upregulation of DR5 and downregulation of
NF-kappaB activity
Jutooru et al., J Biol Chem 2010
(Pancreatic Neoplasms) :
Results of Sp1, Sp3, and Sp4 knockdown by RNA interference demonstrate that both p50 and p65 are Sp-regulated genes and that inhibition of constitutive or tumor necrosis factor induced
NFkappaB by curcumin is
dependent on down-regulation of
Sp1 , Sp3, and Sp4 proteins by this compound
Neish et al., J Biol Chem 1995
:
The cytokine induced enhancer of the VCAM1 gene requires constitutively bound
Sp1 and
induced heterodimeric
NF-kappa B for maximal promoter activity
Pindolia et al., Hematopathol Mol Hematol 1996
:
Whereas AP-1 and
SP-1 are constitutively expressed in stromal cells,
NF-kB is
detected only after stimulation with IL-1
Yurochko et al., J Virol 1997
(Cytomegalovirus Infections) :
Therefore, to detail the role that
Sp1 plays in the regulation of
NF-kappaB during infection, we initially examined Sp1 levels for changes during infection ... Last, to further dissect the role of HCMV in the
Sp1 mediated induction of
NF-kappaB , we examined the role that the viral IE genes played in Sp1 regulation ... These data supported our hypothesis that
Sp1 was
involved in the upregulation of
NF-kappaB during HCMV infection through the Sp1 binding sites in the p65 and p105/p50 promoters and additionally demonstrated a potential viral mechanism that might be responsible for the upregulation of Sp1 activity