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Statistic
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Details for phenotype: regulation of inflammatory response
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EndoNet ID: ENP00300
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Name
regulation of inflammatory response
General information
This phenotype is not pathologic
Links to other resources
GO
regulation of inflammatory response
MeSH term
68007249
Phenotype triggers
more activity (high ligand concentration, overexpression) of
Lysophosphatidic acid receptor 3
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in
microglial_cell_in_central_nervous_system
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It is notable that LPA3 is upregulated in lipopolysaccharide-stimulated microglia, suggesting a role for LPA signaling in activated microglia during neuroinflammation.
[1]
normal activity of
PRLR
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in
prostate
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The effects of PRL on prostate include involvement in estrogen-induced inflammation.
[2]
Estradiol-induced inflammation in the rat lateral prostate is mediated at least in part by the release of PRL from the pituitary.
[2]
normal activity of
ER-alpha
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in
macrophage
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ER alpha is critical for maintenance of macrophage metabolism and for macrophage IL-4 responsiveness.
[3]
ER alpha is necessary for the repression of inflammation, maintenance of oxidative metabolsim and full phagocytic activity in isolated macrophages.
[3]
normal activity of
ER-beta
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in
microglial_cell_in_central_nervous_system
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ER beta specific ligands potently inhibit transcriptional activation of inflammatory response genes in microglia and astrocytes.
[4]
normal activity of
Sphingosine 1-phosphate receptor 3
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in
smooth_muscle_cell
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In vascular smooth muscle cells, S1P stimulates DNA synthesis in association with ERK activation, and may play a central role in excessive fibroproliferative and inflammatory response to vascular injury that are hallmarks of atherosclerois progression.
[5]
normal activity of
Sphingosine 1-phosphate receptor 1
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in
smooth_muscle_cell
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In vascular smooth muscle cells, S1P stimulates DNA synthesis in association with ERK activation, and may play a central role in excessive fibroproliferative and inflammatory response to vascular injury that are hallmarks of atherosclerois progression.
[5]
a central role for S1P1 in vascular smooth muscle cell migration was established by the phenotype of S1P1-deficient mice in which those cells do not migrate properly to surround and reinforce nascent vessels.
[6]
Reference