EndoNet

Hormone: ADM
Hormone: pentraxin 3
- PTX3 is made by diverse cell types, most prominently endothelial cells, macrophages and dendritic cells, in response to primary inflammatory signals (e.g. interleukin-1 (IL-1), tumour necrosis factor (TNF), lipopolysaccharide (LPS)). [1]
- PTX3 is produced by a variety of cells and tissues, most notably dendritic cells and macrophages, in response to Toll-like receptor (TLR) engagement and inflammatory cytokines. [2]
Hormone: TNF-alpha
- In man, the secretion of TNFalpha is reported to be mainly due to the cells of the stromal vascular and matrix fractions, including the macrophages. [3]
Influenced by:
- TLR2
  in alveolar_macrophage
  SP-A significantly reduced PGN-elicited tumor necrosis factor alpha (TNF-alpha) secretion by rat alveolar macrophages. The inhibitory effect on TNF-alpha secretion was dependent upon SP-A concentrations in physiological range. [4]
  Direct interaction of SP-A with TLR2 alters PGN-induced cell signaling. [4]
Hormone: MIG
Hormone: IL-18
Hormone: IL-12A
Hormone: C-C motif chemokine 2
Hormone: GRObeta
- [5]
Hormone: MDC
Hormone: IL-1F5
Hormone: PARC
- Specifically induced in macrophages by IL-4, IL-13, and IL-10. Expression is inhibited by IFN-gamma while glucocorticoids exert a slightly positive synergistic effect in combination with IL-4. [6]
Hormone: resistin
- Human resistin mRNA and protein were found to be expressed in human primary monocyte-derived macrophages, and levels were downregulated after 96-h treatment with rosiglitazone. [7]
Hormone: adipsin
Hormone: eotaxin
- Human eotaxin is an 8,3-kDa, 74-amino-acid residue, nonglycosylated polypeptide secreted by endothelial cells, fibroblasts, macrophages, ciliated and nonciliated bronchial epithelial cells, smooth muscle cells, chondrocytes, and eosinophils. [8]
Hormone: CD40-L
Hormone: tenascin-C
Hormone: APRIL
Hormone: BAFF
Hormone: thymosin beta-4
Hormone: TIMP-1
Hormone: osteopontin
- Osteopontin is exceptionally highly expressed in adipose tissue macrophages in humans and mice. [9]
Hormone: IFN-beta
- Human monocyte-derived macrophages express IFN-alpha, IFN-beta, IL-28, IL-29, TNF-alpha and the chemokines CCL5 and CXCL10 after herpes simplex virus 1 (HSV-1) infection. [10]
Influenced by:
- TLR4
  in macrophage
  With LPS in the presence of LPS-binding protein TLR4 activates the common MyD88-dependent signaling pathway as well as a MyD88-independent pathway leading to interferon-beta production. [11]
Hormone: interleukin 6
Hormone: IFN-alpha
Influenced by:
- TLR4
  in macrophage
Hormone: IP-10
Hormone: IL-29
Hormone: RANTES
Hormone: IL-10
Hormone: IL-1 alpha
Hormone: PAF
Influenced by:
- TNFR1
  in macrophage
  TNF induce PAF synthesis by monocyte/macrophages. [12]
- IL-1RII
  in macrophage
  IL-1 induce PAF synthesis by monocyte/macrophages. [12]
Hormone: IL-12
Hormone: FGF-2
Hormone: CD5L
Hormone: elastase-2
Hormone: elafin
Hormone: TXA2
Hormone: ATP-binding cassette sub-family A member 1
Hormone: APOE
Influenced by:
- ApoA-I receptor
  in macrophage
  ApoA-I stimulates secretion of apoE from macrophage foam cells, although the mechanism of this process is not understood. [13]
  ApoA-I stimulates secretion of apoE independently of both ABCA1-mediated cholesterol efflux and of lipid binding by its terminus. [13]
Hormone: cholesterol
Influenced by:
- ATP-binding cassette sub-family A member 1
  in macrophage
  It is likely that ABCA1 is the cAMP-inducible apolipoprotein receptor that promotes secretion of lipids from macrophages. [14]
  There was an investigation whether ABCA1 expression is also responsible for the apoA-I-mediated cholesterol efflux induced by cAMP in macrophages and whether this involves direct binding of apoA-I to plasma membrane ABCA1. [14]
Hormone: TGF-beta 1
- Subtype THP-1 cells secrete TGF-beta1 into the medium by forming a functional complex with the latent TGF-beta1-binding protein. We conclude that subtype THP-1 cells could not take up Ac-LDL because ScR was inhibited (leading to a loss of function) caused by the secreted TGF-beta1. [15]
Hormone: CCL1
Influenced by:
- AhR
  in macrophage
  Polycyclic aromatic hydrocarbons (PAHs) induce expression of the chemokine CCL1 in an AhR- and calcium-dependent manner. [16]
Hormone: IL-1 beta
- IL-1β is abundantly secreted by activated macrophages and blood monocytes. [17]
- IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
- Pro-IL-1β is then cleaved by caspase- to biologically-active mature IL-1β. [18]
Influenced by:
- TLR4
  in macrophage
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
- TLR8
  in macrophage
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
- TLR9
  in macrophage
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
- TLR7
  in macrophage
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
- TLR10
  in macrophage
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
- TLR6
  in macrophage
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
- TLR2
  in macrophage
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
- TLR3
  in macrophage
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
- TLR5
  in macrophage
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
- TLR1
  in macrophage
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
Hormone: MMP-3
Influenced by:
- basigin
  in brain
  CD147/Basigin induces matrix metalloproteinase expression in neighbouring fibroblasts, leading to tumor cell invasion [19]
Hormone: MMP-7
Hormone: ICAM-1

Receptor: glucocorticoid receptor
Induced phenotype:
- hypertension
  
  Oxidative stress and nitric oxide deficiency are emerging as key components in the pathogenesis of glucocorticoid-induced hypertension. [20]
  This highlights the role of inflammation and oxidative stress in the pathogenesis of glucocorticoid-induced hypertension and this is consistent with a role for macrophages in this pathology. [21]
- abdominal obesity-metabolic syndrome
  
  Glucocorticoids play a role in adipocyte maturation, function and distribution. Differentiating adipocytes produce increasing levels of the enzyme 11-beta-hydroxysteroid dehydrogenase 1 to convert inactive cortisone into cortisol, in turn amplifying local glucocorticoid levels. [22]
  Many findings implicate macrophages, GR and 11βHSD1 in the pro-inflammatory phenotype of metabolic dysfunction. [21]
- negative regulation of immune response
  
  A recent study exploring the effect of corticosterone on isolated peritoneal macrophages has demonstrated that high corticosterone concentrations suppress macrophage immune functions. [23]
  Responses to high corticosteroid levels are a consequence of GR activation. [23]
- osteoporosis
  
  Glucocorticoids suppress osteoblast activity in vivo. [24]
  Glucocorticoid signalling via GR inhibits proliferation of osteoclastogenic cells, apoptosis of mature osteoclasts and osteoclast function in vitro and in vivo, by altering the activity rather than the number of osteoclasts. Glucocorticoid-induced bone mass reduction is not only mediated by directly inhibiting osteoblasts, but also by inhibiting osteoclast activity, which in turn disrupts the remodelling cycle and suppresses osteoblast activity . [25]
- atherosclerosis
  
  Atherosclerosis is a progressive disease characterised by an inflammatory event in which monocyte-derived macrophages play a central role. [26]
  Glucocorticoid treatment has been shown to reduce macrophage accumulation in a model of cholesterol-induced atherosclerosis. [27]
  Glucocorticoid treatment has been shown to decrease neointimal proliferation following balloon angioplasty. [28]
  Effects of glucocorticoids on etiology and progression of atherosclerosis are only partially mediated through GR. [21]
Receptor: GR-beta
Receptor: PPARgamma1
- The peroxisome proliferation-activated receptor gamma (PPARγ) is expressed in many cell types including mammary epithelium, ovary, macrophages, and B- and T-cells [29]
Receptor: TLR4
Influences:
- IFN-beta
  
  With LPS in the presence of LPS-binding protein TLR4 activates the common MyD88-dependent signaling pathway as well as a MyD88-independent pathway leading to interferon-beta production. [11]
- IFN-alpha
- IL-1 beta
  
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
Receptor: ferroportin-1
Receptor: PPAR-gamma1
Receptor: vitronectin receptor
Induced phenotype:
- positive regulation of macrophage derived foam cell
  
  AlphaVbeta3 integrin regulates macrophage functional maturation into foam cells in a persistent manner [30]
Receptor: LXR-alpha
Receptor: basigin
Receptor: LRP5
Receptor: TNFR1
Influences:
- PAF
  
  TNF induce PAF synthesis by monocyte/macrophages. [12]
Receptor: PAF-R
Receptor: IL-1RII
Influences:
- PAF
  
  IL-1 induce PAF synthesis by monocyte/macrophages. [12]
Receptor: IgE Fc receptor, alpha-subunit
Receptor: IL-15R alpha
Receptor: ADAM17
Receptor: sialoadhesin
Induced phenotype:
- cell-cell interactions of macrophages during inflammatory reactions
  
  aken together, these observations indicate that Sn has evolved primarily to mediate extracellular functions, namely cell-cell or cell-matrix interactions. [31]
Receptor: MRC2
Receptor: ApoA-I receptor
Influences:
- APOE
  
  ApoA-I stimulates secretion of apoE from macrophage foam cells, although the mechanism of this process is not understood. [13]
  ApoA-I stimulates secretion of apoE independently of both ABCA1-mediated cholesterol efflux and of lipid binding by its terminus. [13]
Receptor: ATP-binding cassette sub-family A member 1
Influences:
- cholesterol
  
  It is likely that ABCA1 is the cAMP-inducible apolipoprotein receptor that promotes secretion of lipids from macrophages. [14]
  There was an investigation whether ABCA1 expression is also responsible for the apoA-I-mediated cholesterol efflux induced by cAMP in macrophages and whether this involves direct binding of apoA-I to plasma membrane ABCA1. [14]
Receptor: AhR
Influences:
- CCL1
  
  Polycyclic aromatic hydrocarbons (PAHs) induce expression of the chemokine CCL1 in an AhR- and calcium-dependent manner. [16]
Receptor: TLR8
Influences:
- IL-1 beta
  
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
Receptor: TLR9
Influences:
- IL-1 beta
  
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
Receptor: TLR7
Influences:
- IL-1 beta
  
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
Receptor: TLR10
Influences:
- IL-1 beta
  
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
Receptor: TLR6
Influences:
- IL-1 beta
  
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
Receptor: TLR2
Influences:
- IL-1 beta
  
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
Receptor: TLR3
Influences:
- IL-1 beta
  
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
Receptor: TLR5
Influences:
- IL-1 beta
  
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
Receptor: TLR1
Influences:
- IL-1 beta
  
  IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
Receptor: CD72
Induced phenotype:
- macrophage activation during immune response
  
  CD100/Sema4D induces immune response through CD72, it appears to play a role in monocyte activation. [32]
  The negative regulator CD100/Sema4D regulates B cell response through shutting off CD72-mediated negative signaling. [33]
Influences:
- IFN-gamma
  
  Activated NK cells express CD100 and produce soluble CD100. They interact with macrophages by several routs among which is the CD100-CD72 interaction. Such interaction lead to IFNgamma secretion which in turn activates other cells of the immune system. [34]
- SEMA4D
  
  Activated NK cells express CD100 and produce soluble CD100. They interact with macrophages by several routs among which is the CD100-CD72 interaction. Such interaction lead to soluble CD100 secretion which in turn activates other cells of the immune system. [34]
Receptor: PRLR
Induced phenotype:
- macrophage activation during immune response
  
  It has been shown that macrophage activation and superoxide anion production responsible for killing pathogenic organisms are effects mediated by the PRLR. [35]
  Activation of macrophages was originally thought to be an action of GH. However, it has been shown that macrophage activation is an effect mediated by the prolactin receptor. [36]
Receptor: Sphingosine 1-phosphate receptor 1
Induced phenotype:
- negative regulation of cytokine production
  
  Peritoneal macrophages from low-density lipoprotein-receptor-deficient mice, which are a model for atherosclerosis, that had been treated with FTY720 (FTY720 is a sphingosine analogue that could be phosphorylated by SPHKs to produce a S1PR ligand with potent effects, including S1PR agonism and the downregulation of S1PR expression) had a markedly decreased production of inflammatory tumour-necrosis factor (TNF), TNF receptor (TNFR) and IL-6 in response to LPS. [37]
Receptor: Sphingosine 1-phosphate receptor 2
Induced phenotype:
- negative regulation of cytokine production
  
  Peritoneal macrophages from low-density lipoprotein-receptor-deficient mice, which are a model for atherosclerosis, that had been treated with FTY720 (FTY720 is a sphingosine analogue that could be phosphorylated by SPHKs to produce a S1PR ligand with potent effects, including S1PR agonism and the downregulation of S1PR expression) had a markedly decreased production of inflammatory tumour-necrosis factor (TNF), TNF receptor (TNFR) and IL-6 in response to LPS. [37]
Receptor: Probable G-protein coupled receptor 132
Induced phenotype:
- regulation of innate immune response
  
  Innate immune responses of macrophages may be regulated via G2A in response to local fluctuations in lysolipids encountered during infection and inflammation. It is possible that LPC produced at sites of inflammation and from disintegrating apoptotic/necrotic cell membranes may be a novel “molecular pattern” recognized by G2A to modulate innate immune processes and the initiation and/or resolution of inflammatory responses. [38]
- atherosclerosis
  
  The key role of LPC as a major antigenic component of oxLDL has implicated this bioactive lipid in atherosclerosis, the primary cause of heart disease and stroke. [38]
  Aspects of immune function as potential targets of LPC action play some role in atherogenesis. Macrophage responses to oxLDL such as migration and activation are likely determined to a significant extent by its LPC content, and may therefore be mediated to some degree via G2A and/or GPR4. [38]
Receptor: G-protein coupled receptor 4
Induced phenotype:
- atherosclerosis
  
  The key role of LPC as a major antigenic component of oxLDL has implicated this bioactive lipid in atherosclerosis, the primary cause of heart disease and stroke. [38]
  Aspects of immune function as potential targets of LPC action play some role in atherogenesis. Macrophage responses to oxLDL such as migration and activation are likely determined to a significant extent by its LPC content, and may therefore be mediated to some degree via G2A and/or GPR4. [38]
Receptor: Psychosine receptor
Induced phenotype:
- Krabbe disease
  
  The secondary accumulation of Psy in macrophages probably induces the formation of globoid cells. [39]
Receptor: mineralcorticoid receptor
Induced phenotype:
- positive regulation of immune response
  
  A recent study exploring the effect of corticosterone on isolated peritoneal macrophages has demonstrated that low corticosterone concentrations enhance macrophage immune functions. [23]
  The effects of low corticosterone concentrations are mediated via MR. [23]
- fibrosis
  
  In renal disease models, reduced monocyte/macrophage infiltration is accompanied by a substantial reduction in fibrosis. MR signalling and macrophages appear to be important in inflammatory conditions in the kidney. [21]
  Activation of an MR, in the context of inappropriate sodium status, has major cardiovascular pathophysiological consequences including cardiac fibrosis. [21]
  In cardiac disease models, reduced monocyte/macrophage infiltration is accompanied by a substantial reduction in fibrosis. MR signalling and macrophages appear to be important in inflammatory conditions in the heart. [21]
  Selective deletion of MR from macrophages protected against mineralocorticoid-mediated cardiac fibrosis, despite normal macrophage recruitment. [21]
- production of molecular mediator involved in inflammatory
  
  Inflammation may be a key mechanism translating MR signalling into cardiac and vascular remodelling. [21]
  Mineralocorticoid/salt-induced pathology is characterised by an early vascular inflammatory response with elevated cardiac expression of inflammatory mediators such as monocytes/macrophages, MCP-1 and adhesion molecules (ICAM-1 and VCAM-1), prior to the onset of collagen deposition. [40]
  mineralocorticoid/salt treatment is also associated with increased monocyte/macrophage infiltration and expression of inflammatory markers such as osteopontin, MCP-1, IL-6 and IL-1β in the kidney. [41]
  MR antagonism prevents inflammation-induced peritoneal fibrosis and reduces macrophage infiltration and expression of MCP-1, TGF-β, PAI-1 and Sgk-1. [42]
- atherosclerosis
  
  Aldosterone treatment increases oxidative stress in macrophages derived from ApoE-deficient mice. [43]
  Aldosterone activation of MR in endothelial cells specifically modulates ICAM-1 expression and promotes leukocyte adhesion, supporting a role for MR signalling in endothelial cells in the initial stages of atherosclerosis. These findings highlight a key role for both macrophage and endothelial MR signalling in atherosclerosis. [44]
- hypertension
  
  Activation of an MR, in the context of inappropriate sodium status, has major cardiovascular pathophysiological consequences including hypertension. [21]
  Chronic inappropriate activation of an MR is well recognised to promote hypertension. Excess plasma mineralocorticoids promote sodium and water retention and potassium secretion leading to the maintenance of blood pressure at a higher set point. [45]
  MR antagonists have been shown to be effective anti-hypertensive agents in essential hypertension, suggesting a role for MR signalling in hypertension. [46]
Receptor: ER-alpha
Induced phenotype:
- regulation of inflammatory response
  
  ER alpha is critical for maintenance of macrophage metabolism and for macrophage IL-4 responsiveness. [47]
  ER alpha is necessary for the repression of inflammation, maintenance of oxidative metabolsim and full phagocytic activity in isolated macrophages. [47]
Receptor: progesterone receptor
Receptor: VDR
Induced phenotype:
- negative regulation of macrophage derived foam cell differentiation
  
  Activation of vitamin D receptor signaling prevents foam cell formation by reducing modified LDL cholesterol uptake in macrophages. [48]
Receptor: thyroid hormone receptor beta 2
Receptor: THRB1
Receptor: THRA1
Receptor: thyroid hormone receptor alpha2
Receptor: RAR
Induced phenotype:
- Positive regulator of inflammatory cytokine production
  
  Inflammatory cytokine production is impaired in RAR-deficient macrophages. [49]
Receptor: RAR-beta
Receptor: RXR-alpha
Receptor: CMKLR1
- We have previously described ChemR23 as a human orphan G protein–coupled receptor expressed in macrophages and immature DCs [50]
Induced phenotype:
- chemotaxis of macrophages
  
  Human recombinant chemerin promoted in vitro migration of macrophages was observed. [50]

EndoNet

The information resource about the endocrine network in human.

Details for anatomical structure: macrophage

Synonyms

General information

Links to other resources

Related structures

Larger structures

Substructures

Secreted hormones

Hormone: ADM ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_0_toolsBtn',{id:'j_idt91:0:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_0_j_idt99',{id:'j_idt91:0:j_idt99',target:'j_idt91:0:toolsBtn',dynamic:true});});

Hormone: pentraxin 3 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_1_toolsBtn',{id:'j_idt91:1:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_1_j_idt99',{id:'j_idt91:1:j_idt99',target:'j_idt91:1:toolsBtn',dynamic:true});});

Hormone: TNF-alpha ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_2_toolsBtn',{id:'j_idt91:2:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_2_j_idt99',{id:'j_idt91:2:j_idt99',target:'j_idt91:2:toolsBtn',dynamic:true});});

Influenced by:

Hormone: MIG ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_3_toolsBtn',{id:'j_idt91:3:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_3_j_idt99',{id:'j_idt91:3:j_idt99',target:'j_idt91:3:toolsBtn',dynamic:true});});

Hormone: IL-18 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_4_toolsBtn',{id:'j_idt91:4:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_4_j_idt99',{id:'j_idt91:4:j_idt99',target:'j_idt91:4:toolsBtn',dynamic:true});});

Hormone: IL-12A ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_5_toolsBtn',{id:'j_idt91:5:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_5_j_idt99',{id:'j_idt91:5:j_idt99',target:'j_idt91:5:toolsBtn',dynamic:true});});

Hormone: C-C motif chemokine 2 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_6_toolsBtn',{id:'j_idt91:6:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_6_j_idt99',{id:'j_idt91:6:j_idt99',target:'j_idt91:6:toolsBtn',dynamic:true});});

Hormone: GRObeta ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_7_toolsBtn',{id:'j_idt91:7:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_7_j_idt99',{id:'j_idt91:7:j_idt99',target:'j_idt91:7:toolsBtn',dynamic:true});});

Hormone: MDC ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_8_toolsBtn',{id:'j_idt91:8:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_8_j_idt99',{id:'j_idt91:8:j_idt99',target:'j_idt91:8:toolsBtn',dynamic:true});});

Hormone: IL-1F5 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_9_toolsBtn',{id:'j_idt91:9:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_9_j_idt99',{id:'j_idt91:9:j_idt99',target:'j_idt91:9:toolsBtn',dynamic:true});});

Hormone: PARC ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_10_toolsBtn',{id:'j_idt91:10:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_10_j_idt99',{id:'j_idt91:10:j_idt99',target:'j_idt91:10:toolsBtn',dynamic:true});});

Hormone: resistin ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_11_toolsBtn',{id:'j_idt91:11:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_11_j_idt99',{id:'j_idt91:11:j_idt99',target:'j_idt91:11:toolsBtn',dynamic:true});});

Hormone: adipsin ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_12_toolsBtn',{id:'j_idt91:12:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_12_j_idt99',{id:'j_idt91:12:j_idt99',target:'j_idt91:12:toolsBtn',dynamic:true});});

Hormone: eotaxin ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_13_toolsBtn',{id:'j_idt91:13:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_13_j_idt99',{id:'j_idt91:13:j_idt99',target:'j_idt91:13:toolsBtn',dynamic:true});});

Hormone: CD40-L ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_14_toolsBtn',{id:'j_idt91:14:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_14_j_idt99',{id:'j_idt91:14:j_idt99',target:'j_idt91:14:toolsBtn',dynamic:true});});

Hormone: tenascin-C ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_15_toolsBtn',{id:'j_idt91:15:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_15_j_idt99',{id:'j_idt91:15:j_idt99',target:'j_idt91:15:toolsBtn',dynamic:true});});

Hormone: APRIL ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_16_toolsBtn',{id:'j_idt91:16:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_16_j_idt99',{id:'j_idt91:16:j_idt99',target:'j_idt91:16:toolsBtn',dynamic:true});});

Hormone: BAFF ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_17_toolsBtn',{id:'j_idt91:17:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_17_j_idt99',{id:'j_idt91:17:j_idt99',target:'j_idt91:17:toolsBtn',dynamic:true});});

Hormone: thymosin beta-4 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_18_toolsBtn',{id:'j_idt91:18:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_18_j_idt99',{id:'j_idt91:18:j_idt99',target:'j_idt91:18:toolsBtn',dynamic:true});});

Hormone: TIMP-1 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_19_toolsBtn',{id:'j_idt91:19:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_19_j_idt99',{id:'j_idt91:19:j_idt99',target:'j_idt91:19:toolsBtn',dynamic:true});});

Hormone: osteopontin ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_20_toolsBtn',{id:'j_idt91:20:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_20_j_idt99',{id:'j_idt91:20:j_idt99',target:'j_idt91:20:toolsBtn',dynamic:true});});

Hormone: IFN-beta ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_21_toolsBtn',{id:'j_idt91:21:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_21_j_idt99',{id:'j_idt91:21:j_idt99',target:'j_idt91:21:toolsBtn',dynamic:true});});

Influenced by:

Hormone: interleukin 6 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_22_toolsBtn',{id:'j_idt91:22:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_22_j_idt99',{id:'j_idt91:22:j_idt99',target:'j_idt91:22:toolsBtn',dynamic:true});});

Hormone: IFN-alpha ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_23_toolsBtn',{id:'j_idt91:23:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_23_j_idt99',{id:'j_idt91:23:j_idt99',target:'j_idt91:23:toolsBtn',dynamic:true});});

Influenced by:

Hormone: IP-10 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_24_toolsBtn',{id:'j_idt91:24:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_24_j_idt99',{id:'j_idt91:24:j_idt99',target:'j_idt91:24:toolsBtn',dynamic:true});});

Hormone: IL-29 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_25_toolsBtn',{id:'j_idt91:25:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_25_j_idt99',{id:'j_idt91:25:j_idt99',target:'j_idt91:25:toolsBtn',dynamic:true});});

Hormone: RANTES ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_26_toolsBtn',{id:'j_idt91:26:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_26_j_idt99',{id:'j_idt91:26:j_idt99',target:'j_idt91:26:toolsBtn',dynamic:true});});

Hormone: IL-10 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_27_toolsBtn',{id:'j_idt91:27:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_27_j_idt99',{id:'j_idt91:27:j_idt99',target:'j_idt91:27:toolsBtn',dynamic:true});});

Hormone: IL-1 alpha ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_28_toolsBtn',{id:'j_idt91:28:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_28_j_idt99',{id:'j_idt91:28:j_idt99',target:'j_idt91:28:toolsBtn',dynamic:true});});

Hormone: PAF ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_29_toolsBtn',{id:'j_idt91:29:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_29_j_idt99',{id:'j_idt91:29:j_idt99',target:'j_idt91:29:toolsBtn',dynamic:true});});

Influenced by:

Hormone: IL-12 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_30_toolsBtn',{id:'j_idt91:30:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_30_j_idt99',{id:'j_idt91:30:j_idt99',target:'j_idt91:30:toolsBtn',dynamic:true});});

Hormone: FGF-2 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_31_toolsBtn',{id:'j_idt91:31:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_31_j_idt99',{id:'j_idt91:31:j_idt99',target:'j_idt91:31:toolsBtn',dynamic:true});});

Hormone: CD5L ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_32_toolsBtn',{id:'j_idt91:32:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_32_j_idt99',{id:'j_idt91:32:j_idt99',target:'j_idt91:32:toolsBtn',dynamic:true});});

Hormone: elastase-2 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_33_toolsBtn',{id:'j_idt91:33:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_33_j_idt99',{id:'j_idt91:33:j_idt99',target:'j_idt91:33:toolsBtn',dynamic:true});});

Hormone: elafin ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_34_toolsBtn',{id:'j_idt91:34:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_34_j_idt99',{id:'j_idt91:34:j_idt99',target:'j_idt91:34:toolsBtn',dynamic:true});});

Hormone: TXA2 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_35_toolsBtn',{id:'j_idt91:35:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_35_j_idt99',{id:'j_idt91:35:j_idt99',target:'j_idt91:35:toolsBtn',dynamic:true});});

Hormone: ATP-binding cassette sub-family A member 1 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_36_toolsBtn',{id:'j_idt91:36:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_36_j_idt99',{id:'j_idt91:36:j_idt99',target:'j_idt91:36:toolsBtn',dynamic:true});});

Hormone: APOE ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_37_toolsBtn',{id:'j_idt91:37:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_37_j_idt99',{id:'j_idt91:37:j_idt99',target:'j_idt91:37:toolsBtn',dynamic:true});});

Influenced by:

Hormone: cholesterol ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_38_toolsBtn',{id:'j_idt91:38:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_38_j_idt99',{id:'j_idt91:38:j_idt99',target:'j_idt91:38:toolsBtn',dynamic:true});});

Influenced by:

Hormone: TGF-beta 1 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_39_toolsBtn',{id:'j_idt91:39:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_39_j_idt99',{id:'j_idt91:39:j_idt99',target:'j_idt91:39:toolsBtn',dynamic:true});});

Hormone: CCL1 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_40_toolsBtn',{id:'j_idt91:40:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_40_j_idt99',{id:'j_idt91:40:j_idt99',target:'j_idt91:40:toolsBtn',dynamic:true});});

Influenced by:

Hormone: IL-1 beta ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_41_toolsBtn',{id:'j_idt91:41:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_41_j_idt99',{id:'j_idt91:41:j_idt99',target:'j_idt91:41:toolsBtn',dynamic:true});});

Influenced by:

Hormone: MMP-3 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_42_toolsBtn',{id:'j_idt91:42:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_42_j_idt99',{id:'j_idt91:42:j_idt99',target:'j_idt91:42:toolsBtn',dynamic:true});});

Influenced by:

Hormone: MMP-7 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_43_toolsBtn',{id:'j_idt91:43:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_43_j_idt99',{id:'j_idt91:43:j_idt99',target:'j_idt91:43:toolsBtn',dynamic:true});});

Hormone: ICAM-1 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_44_toolsBtn',{id:'j_idt91:44:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_44_j_idt99',{id:'j_idt91:44:j_idt99',target:'j_idt91:44:toolsBtn',dynamic:true});});

Receptors

Receptor: glucocorticoid receptor ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt139_0_toolsBtn',{id:'j_idt139:0:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt139_0_j_idt145',{id:'j_idt139:0:j_idt145',target:'j_idt139:0:toolsBtn',dynamic:true});});

Induced phenotype:

Receptor: GR-beta ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt139_1_toolsBtn',{id:'j_idt139:1:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt139_1_j_idt145',{id:'j_idt139:1:j_idt145',target:'j_idt139:1:toolsBtn',dynamic:true});});

Receptor: PPARgamma1 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt139_2_toolsBtn',{id:'j_idt139:2:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt139_2_j_idt145',{id:'j_idt139:2:j_idt145',target:'j_idt139:2:toolsBtn',dynamic:true});});

Receptor: TLR4 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt139_3_toolsBtn',{id:'j_idt139:3:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt139_3_j_idt145',{id:'j_idt139:3:j_idt145',target:'j_idt139:3:toolsBtn',dynamic:true});});

Influences:

Receptor: ferroportin-1 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt139_4_toolsBtn',{id:'j_idt139:4:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt139_4_j_idt145',{id:'j_idt139:4:j_idt145',target:'j_idt139:4:toolsBtn',dynamic:true});});

Receptor: PPAR-gamma1 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt139_5_toolsBtn',{id:'j_idt139:5:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt139_5_j_idt145',{id:'j_idt139:5:j_idt145',target:'j_idt139:5:toolsBtn',dynamic:true});});

Receptor: vitronectin receptor ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt139_6_toolsBtn',{id:'j_idt139:6:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt139_6_j_idt145',{id:'j_idt139:6:j_idt145',target:'j_idt139:6:toolsBtn',dynamic:true});});

Induced phenotype:

Receptor: LXR-alpha ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt139_7_toolsBtn',{id:'j_idt139:7:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt139_7_j_idt145',{id:'j_idt139:7:j_idt145',target:'j_idt139:7:toolsBtn',dynamic:true});});

Receptor: basigin ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt139_8_toolsBtn',{id:'j_idt139:8:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt139_8_j_idt145',{id:'j_idt139:8:j_idt145',target:'j_idt139:8:toolsBtn',dynamic:true});});

Receptor: LRP5 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt139_9_toolsBtn',{id:'j_idt139:9:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt139_9_j_idt145',{id:'j_idt139:9:j_idt145',target:'j_idt139:9:toolsBtn',dynamic:true});});

Receptor: TNFR1 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt139_10_toolsBtn',{id:'j_idt139:10:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt139_10_j_idt145',{id:'j_idt139:10:j_idt145',target:'j_idt139:10:toolsBtn',dynamic:true});});

Influences:

Hormone: ADM

Hormone: pentraxin 3

Hormone: TNF-alpha

Hormone: MIG

Hormone: IL-18

Hormone: IL-12A

Hormone: C-C motif chemokine 2

Hormone: GRObeta

Hormone: MDC

Hormone: IL-1F5

Hormone: PARC

Hormone: resistin

Hormone: adipsin

Hormone: eotaxin

Hormone: CD40-L

Hormone: tenascin-C

Hormone: APRIL

Hormone: BAFF

Hormone: thymosin beta-4

Hormone: TIMP-1

Hormone: osteopontin

Hormone: IFN-beta

Hormone: interleukin 6

Hormone: IFN-alpha

Hormone: IP-10

Hormone: IL-29

Hormone: RANTES

Hormone: IL-10

Hormone: IL-1 alpha

Hormone: PAF

Hormone: IL-12

Hormone: FGF-2

Hormone: CD5L

Hormone: elastase-2

Hormone: elafin

Hormone: TXA2

Hormone: ATP-binding cassette sub-family A member 1

Hormone: APOE

Hormone: cholesterol

Hormone: TGF-beta 1

Hormone: CCL1

Hormone: IL-1 beta

Hormone: MMP-3

Hormone: MMP-7

Hormone: ICAM-1

Receptor: glucocorticoid receptor

Receptor: GR-beta

Receptor: PPARgamma1

Receptor: TLR4

Receptor: ferroportin-1

Receptor: PPAR-gamma1

Receptor: vitronectin receptor

Receptor: LXR-alpha

Receptor: basigin

Receptor: LRP5

Receptor: TNFR1

Receptor: PAF-R

Receptor: IL-1RII

Receptor: IgE Fc receptor, alpha-subunit

Receptor: IL-15R alpha

Receptor: ADAM17

Receptor: sialoadhesin

Receptor: MRC2

Receptor: ApoA-I receptor

Receptor: ATP-binding cassette sub-family A member 1

Receptor: AhR

Receptor: TLR8

Receptor: TLR9

Receptor: TLR7

Receptor: TLR10

Receptor: TLR6

Receptor: TLR2

Receptor: TLR3

Receptor: TLR5

Receptor: TLR1

Receptor: CD72

Receptor: PRLR

Receptor: Sphingosine 1-phosphate receptor 1

Receptor: Sphingosine 1-phosphate receptor 2

Receptor: Probable G-protein coupled receptor 132