| Interaction ID | Mol A | Type | Species | Verb | Nature | Mol B | Type | Species |   |
|---|
|
| 21474 | NF-kappa-B | Multi subunit | Homo sapiens-e | Decreases activity | direct | PPARG | Protein | Homo sapiens-e | | | Unlike suppression of the PPAR-gamma
transactivation function by mitogen-activated protein
kinase-induced growth factor signalling through
phosphorylation of the A/B domain, NF-kappaB blocks
PPAR-gamma binding to DNA by forming a complex with
PPAR-gamma and its AF-1-specific co-activator PGC-2. | | | |
Interaction id | 21474 | |
MOLECULE A | |
Id | TRHsM00001 |
Type | Multi subunit |
Species | Homo sapiens-e | |
Attribute |
--
|
Structure Details | -- |
Disease Details | -- | |
MOLECULE B | |
Id | 5468 |
Type | Protein |
Species | Homo sapiens-e | |
Attribute | -- |
Structure Details | -- |
Disease Details | -- | | Kinetics | - | |
|
General Information |
Interaction term | Decreases activity (
direct ) | |
Pathway | Protein Kinase Cascade:I-Kappab Kinase/Nf-Kappab CascadeCell Differentiation | |
Experimental location and method | - cell::Pluripotent mesenchymal stem cells
| |
References | |
PubMed Id | 12598905 | |
Author | Suzawa M, Takada I, Yanagisawa J, Ohtake F, Ogawa S,
Yamauchi T, Kadowaki T, Takeuchi Y, Shibuya H, Gotoh Y,
Matsumoto K, Kato S | |
Title | Cytokines suppress adipogenesis and PPAR-gamma function
through the TAK1/TAB1/NIK cascade. |
|
|
| | |
| 103171 | IL1B | Protein | Homo sapiens-e | Decreases expression | indirect | PPARG | Protein | Homo sapiens | | | RT-PCR and Western blot analysis revealed
that PPARgamma expression was decreased by IL-1beta. | | | |
Interaction id | 103171 | |
MOLECULE A | |
Id | 3553 |
Type | Protein |
Species | Homo sapiens-e | |
Attribute |
--
|
Structure Details | -- |
Disease Details | -- | |
MOLECULE B | |
Id | 5468 |
Type | Protein |
Species | Homo sapiens | |
Attribute | -- |
Structure Details | -- |
Disease Details | -- | | Kinetics | - | |
|
General Information |
Interaction term | Decreases expression (
indirect ) | |
Pathway | Cytokine And Chemokine Mediated Signaling
Pathway:IL1 Signaling Pathway | |
Disease Details | | |
Experimental location and method | - Experimental method::Blotting, Western
- species::Human
- cell::Chondrocytes
| |
References | |
PubMed Id | 11457450 | |
Author | Boyault S, Simonin MA, Bianchi A, Compe E, Liagre B,
Mainard D, Becuwe P, Dauca M, Netter P, Terlain B, Bordji K | |
Title | 15-Deoxy-delta12,14-PGJ2, but not troglitazone, modulates
IL-1beta effects in human chondrocytes by inhibiting NF-kappaB
and AP-1 activation pathways. |
|
|
| | |
| 126670 | CCL2 | Protein | Homo sapiens-e | Decreases expression | indirect | PPARG | RNA | Homo sapiens | | | Here we show that primary cultures of human
preadipocytes constitutively produce three chemokines,
interleukin-8 (IL-8), macrophage inflammatory protein-1alpha
(MIP-1alpha) and monocyte chemotactic protein-1 (MCP-1),
while their level of expression is low in mature adipocytes.
/ Prolonged stimulation of cultured human adipocytes with
exogenous chemokines leads to a decrease in lipid content in
association with the downregulation of PPARgamma mRNA expression. | | | |
Interaction id | 126670 | |
MOLECULE A | |
Id | 6347 |
Type | Protein |
Species | Homo sapiens-e | |
Attribute |
--
|
Structure Details | -- |
Disease Details | -- | |
MOLECULE B | |
Id | 5468 |
Type | RNA |
Species | Homo sapiens | |
Attribute | -- |
Structure Details | -- |
Disease Details | -- | | Kinetics | - | |
|
General Information |
Interaction term | Decreases expression (
indirect ) | |
Pathway | Cytokine And Chemokine Mediated Signaling Pathway | |
Disease Details | | disease: :Obesity:Diabetes Mellitus:Cachexia |
| |
Experimental location and method | - species::Human
- cell::Cultured Adipocytes
| |
References | |
PubMed Id | 11325518 | |
Author | Gerhardt CC, Romero IA, Cancello R, Camoin L, Strosberg AD | |
Title | Chemokines control fat accumulation and leptin secretion by
cultured human adipocytes. |
|
|
| | |
| 138183 | PLA2G4A | Protein | Homo sapiens | Increases activity | indirect | PPARG | Protein | Homo sapiens | | | Overexpression of cPLA(2), but not group IIA
sPLA(2) in the HepG2 cells, caused a significantly increased
PPAR-alpha/gamma-mediated reporter activity. / Antisense
inhibition of cPLA(2) resulted in a significantly decreased
PPAR-alpha/gamma activity. The PPAR-alpha/gamma-induced gene
transcription in the HepG2 cells was inhibited by the
cPLA(2) inhibitors methyl arachidonyl fluorophosphonate and
arachidonyltrifluoromethyl ketone, but not by the sPLA(2)
inhibitor LY311727. / The cPLA(2)-mediated PPAR activation
was likely mediated by arachidonic acid and prostaglandin
E(2). / The cPLA(2) thus may represent a potential
therapeutic target for the control of PPAR-related liver and
metabolic disorders such as obesity, lipid metabolic
disorders, diabetes mellitus, and atherosclerosis. | | | |
Interaction id | 138183 | |
MOLECULE A | |
Id | 5321 |
Type | Protein |
Species | Homo sapiens | |
Attribute |
--
|
Structure Details | -- |
Disease Details | -- | |
MOLECULE B | |
Id | 5468 |
Type | Protein |
Species | Homo sapiens | |
Attribute | -- |
Structure Details | -- |
Disease Details | -- | |
Regulator | |
Regulation | Negative | | Description | Methyl arachidonyl fluorophosphonate;Arachidonyltrifluoromethane |
|
| | Kinetics | - | |
|
General Information |
Interaction term | Increases activity (
indirect ) | |
Pathway | Transmembrane receptor activity:PLC activating
metabotropic glutamate receptor activityProstanoid receptor activity:Prostaglandin E
receptor activityLipid Metabolism | |
Disease Details | | disease: :Diabetes
Mellitus:Obesity:Arteriosclerosis:Liver Diseases |
| |
Experimental location and method | - Experimental method::Reporter gene assay
- Experimental method::Transcript silencing
- species::Human
- cell::HepG2 cells
| |
Comments | |
Property | | Transcript silenced molecule:PLA2G4A;Molecular
weight of molecule:PLA2G4A(85-kDa) |
| |
References | |
PubMed Id | 11897617 | |
Author | Han C, Demetris AJ, Michalopoulos G, Shelhamer JH, Wu T | |
Title | 85-kDa cPLA(2) plays a critical role in PPAR-mediated gene
transcription in human hepatoma cells. |
|
|
| | |
| 215029 | PPARG | Protein | Homo sapiens-e | Decreases activity | direct | BACE1 | DNA | Homo sapiens-e | | | Nonsteroidal anti-inflammatory drugs repress
beta-secretase gene promoter activity by the activation of
PPARgamma. / Conversely, overexpression of PPARgamma, as
well as NSAIDs and PPARgamma activators, reduced BACE1 gene
promoter activity. These results suggested that PPARgamma
could be a repressor of BACE1. We then identified a
PPARgamma responsive element (PPRE) in the BACE1 gene
promoter. Mutagenesis of the PPRE abolished the binding of
PPARgamma to the PPRE and increased BACE1 gene promoter
activity. / Interestingly, brain extracts from AD patients
showed decreased PPARgamma expression and binding to PPRE in
the BACE1 gene promoter. | | | |
Interaction id | 215029 | |
MOLECULE A | |
Id | 5468 |
Type | Protein |
Species | Homo sapiens-e | |
Attribute |
--
|
Structure Details | -- |
Disease Details | disease: :Alzheimer Diseaseexpression: :Low | |
MOLECULE B | |
Id | 23621 |
Type | DNA |
Species | Homo sapiens-e | |
Attribute | -- |
Structure Details | -- |
Disease Details | -- | |
Regulator | |
Regulation | Positive | | Description | Nonsteroidal anti-inflammatory drug |
|
| | Kinetics | - | |
|
General Information |
Interaction term | Decreases activity (
direct ) | |
Pathway | Ligand-dependent nuclear receptor
activity:Peroxisome proliferator associated receptor activity | |
Disease Details | | disease: :Alzheimer Disease |
| |
Experimental location and method | - Experimental method::Mutation analysis
| |
Comments | |
Property | | Mutated molecule:BACE1(PPARgamma responsive element) |
Domain_motif_site_residue | | [US:PPARgamma responsive element](23621) |
| |
References | |
PubMed Id | 16407166 | |
Author | Sastre M, Dewachter I, Rossner S, Bogdanovic N, Rosen E,
Borghgraef P, Evert BO, Dumitrescu-Ozimek L, Thal DR, Landreth
G, Walter J, Klockgether T, van Leuven F, Heneka MT | |
Title | Nonsteroidal anti-inflammatory drugs repress beta-secretase
gene promoter activity by the activation of PPARgamma. |
|
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