Details for anatomical structure: hepatocyte

Related structures
Hormones
Receptors
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EndoNet ID: ENC00249

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Synonyms

hepatocyte, parenchymal liver cell, hepatic cell, Epitheliocytus hepatis

General information

Cell of the liver parenchyme; the hepatocytes are responsible for almost all the functions of the liver; builds the blood-bile barrier

Links to other resources

Cytomer

cy0011233

Larger structures

Substructures

Secreted hormones

Hormone: osteopontin
Hormone: complement factor B
Hormone: CRP
- Great quantities of serum CRP are produced by the liver during the acute phase response. [1]
Hormone: IL-8
- A proinflammatory cytokine gene program that includes C-X-C and C-C chemokines (IL-8, GRO-alpha, GRO-beta, GRO-gamma, ENA-78 and RANTES) and the cytokines TNF-alpha and M-CSF was upregulated in human hepatocytes after stimulation with IL-1a or TNF-alpha or bacterial invasion. In contrast, expression of hematopoietic/ lymphoid growth factors [2]
Hormone: HGF
- Forced HGF expression by cultured human hepatocytes had a mitogenic effect. [3]
Hormone: VEGF-121
- VEGF-121, VEGF-165 and VEGF-189 were detected in 14 of the 15 HCC samples and in all the corresponding non-cancerous tissue samples. [4]
Hormone: VEGF-189
Hormone: IGFBP-2
Hormone: IGFBP-3
Hormone: IGFBP-4
Hormone: IGFBP-1 isoform a
- Hepatocytes have been shown to express IGFBP-1 through IGFBP-4 mRNAs and release the corresponding proteins. [5]
Hormone: IL-1 beta
- Interleukin-1 (IL-1) is a proinflammatory cytokine that participates in the activation of the acute-phase plasma protein genes in hepatic cells during infection and injury. [6]
Influenced by:
- EGFR isoform a
  in hepatocyte
  Induced IL-1alpha release from hepatocyte is contingent on both TNF and autocrine TGF-alpha. [7]
- TNFR1
  in hepatocyte
  Induced IL-1alpha release from hepatocyte is contingent on both TNF and autocrine TGF-alpha. [7]
- TNFR2
  in hepatocyte
  Induced IL-1alpha release from hepatocyte is contingent on both TNF and autocrine TGF-alpha. [7]
Hormone: IL-7
Hormone: TGF-beta 1
- Cytokines from the TGF-beta family play a role in liver development, by induction of Vg1. [8]
- In the normal adult liver,sinusoidal endothelial cells and Kupffer cells have relatively high, constitutive levels of mRNA for TGF-beta1 and lower but detectable levels for TGF-beta2 and TGF-beta3, whereas stellate cells express very little TGF-beta in the normal state,and hepatocytes essentially none. [9]
Hormone: APOA1
Hormone: APOE
Hormone: apolipoprotein A-II
Hormone: APOC1
Hormone: IL-15
Hormone: APOC2
Hormone: APOC3
Hormone: APOA4
Hormone: hepcidin
- Studies in knockout mice and cell culture assays indicate that C/EBP-alpha induces and HNF4-alpha reduces hepcidin mRNA expression. [10]
- The physiological equilibrium of hepcidin is affected by different pathologies. Elevated hepcidin levels are associated with secondary iron overload, type IV hereditary hemochromatosis(HH) and chronic infectious or inflammatory diseases resulting in "anaemia of inflammation". Decreased hepcidin levels are observed during conditions of increased iron absorption such as hypoxia, iron deficiency anaemias and in HH (type l,ll,lll) and thalassemia. [10]
Influenced by:
- transferrin receptor 2
  in hepatocyte
- IL-6R
  in hepatocyte
  Hepcidin mRNA expression can be induced in response to the inflammatory cytokine IL-6 (Interleukin-6). [10]
Hormone: apo B-100
Influenced by:
- LDL-R
  in hepatocyte
  Apolipoprotein B (apoB) is required for the hepatic assembly and secretion of very low density lipoprotein (VLDL). The LDL receptor (LDLR) promotes post-translational degradation of apoB and thereby reduces VLDL particle secretion. [11]
  LDLR directs apoB to degradation in a post-ER compartment. Furthermore, the reuptake mechanism of degradation occurs via internalization of apoB through a constitutive endocytic pathway and apoE through a ligand-dependent pathway. [11]
- Sterol O-acyltransferase 1
  in hepatocyte
  Cholesteryl esters play an important role in regulating the assembly and secretion of apoB-containing lipoproteins. [12]
- PPAR-alpha
  in hepatocyte
  The peroxisome proliferator-activated receptor (PPAR) agonist WY 14,643 increased the secretion of apolipoprotein (apo) B-100, but not that of apoB-48, and decreased triglyceride biosynthesis and secretion from primary rat hepatocytes. These effects resulted in decreased secretion of apoB-100-very low density lipoprotein (VLDL) and an increased secretion of apoB-100 on low density lipoproteins/intermediate density lipoproteins. [13]
- autocrine motility factor receptor
  in hepatocyte
  Tumor autocrine motility factor receptor, also known as gp78, is an endoplasmic reticulum (ER)-associated E3. This E3 is involved in the ER-associated degradation of nascent apoB. [14]
Hormone: apolipoprotein A-related gene C
Hormone: adipsin
Hormone: chondromodulin 2
Hormone: sNRP1
Hormone: APOA1(1-242)
Hormone: erythropoietin
Hormone: cardiotrophin 1
- CT-1 is up-regulated during liver regeneration and exerts potent antiapoptotic effects on hepatocytic cells. [15]
Hormone: RANTES
- [16]
Hormone: GROalpha
Hormone: TNF-alpha
Hormone: M-CSF
Hormone: GRObeta
Hormone: GROgamma
Hormone: SCF
Hormone: FGF-19
Influenced by:
- bile acid receptor
  in hepatocyte
  FXR induces expression of FGF-19 in primary cultures of human hepatocytes. [17]
Hormone: VEGF-165
- VEGF protein was strongly expressed in both well-differentiated HCC cells and non-cancerous hepatocytes. [4]
Hormone: APOA5
- APOA5 is expressed in human hepatoma HepG2 cells with levels comparable with human primary hepatocytes. [18]
Influenced by:
- THRA1
  in hepatocyte
  Treatment with T3 significantly increased APOA5 mRNA levels at 6 h, and a 2-fold induction was achieved after 24 h of T3 addition. [18]
- THRB1
  in hepatocyte
  T3-activated TRbeta1 enhanced the activity of APOA5 DR4-driven promoter constructs. [18]
  Treatment with T3 significantly increased APOA5 mRNA levels at 6 h, and a 2-fold induction was achieved after 24 h of T3 addition. [18]
- bile acid receptor
  in hepatocyte
  Bile acids induce human apoAV promoter activity via FXR. [19]
- LXR-alpha
  in hepatocyte
  Co-transfection of SREBP-1c downregulates APOA5 promoter activity. [20]
- PPAR-alpha
  in hepatocyte
  Overexpression of PPAR-alpha enhances the activity of the human ApoA5 gene promoter. [19]
Hormone: angiotensinogen
- Freshly isolated human hepatocytes expressed higher levels of angiotensinogen and lower levels of renin and ACE compared with activated HSCs. [21]
- Hepatocytes are the main source of angiotensinogen in the human liver. [21]
Influenced by:
- angiotensin II type 1 receptor
  in hepatocyte
  Angiotensin II stimulates the hepatic synthesis and secretion of angiotensinogen, the substrate of renin. This effect is mainly related to a transient inhibition of adenylylcyclase. [22]
Hormone: renin
Hormone: cholesterol
Influenced by:
- LXR-alpha
  in hepatocyte
  Liver X receptor (LXR) alpha and beta are the nuclear receptors responsible for regulation of cholesterol metabolism. In physiological conditions, high intracellular cholesterol levels cause increased synthesis of oxysterols, which activate LXR, thus triggering a transcriptional response for cholesterol secretion and catabolism. [23]
- LXR-beta
  in hepatocyte
  Liver X receptor (LXR) alpha and beta are the nuclear receptors responsible for regulation of cholesterol metabolism. In physiological conditions, high intracellular cholesterol levels cause increased synthesis of oxysterols, which activate LXR, thus triggering a transcriptional response for cholesterol secretion and catabolism. [23]
Hormone: CBG
- CBG is secreted from hepatocytes as a 383-amino-acid peptide after cleavage of a 22-amino-acid signal peptide and circulates at concentrations ranging from 30 to 52 pg/ml. [24]
Influenced by:
- glucocorticoid receptor
  in hepatocyte
  Levels of CBG are decreased by glucocorticoids. The effects of glucocorticoids on CBG synthesis are glucocorticoid receptor dependent. [24]
- ER-alpha
  in liver
  Our results show that o,p′-DDD (mitotane) increases CBG expression and secretion by an ERα-dependent mechanism. [25]
Hormone: IGF-1
Influenced by:
- glucocorticoid receptor
  in hepatocyte
  IGF-1 is synthesized in hepatocytes upon GH stimulation. [26]
Hormone: apo B-48
Influenced by:
- LDL-R
  in hepatocyte
  Apolipoprotein B (apoB) is required for the hepatic assembly and secretion of very low density lipoprotein (VLDL). The LDL receptor (LDLR) promotes post-translational degradation of apoB and thereby reduces VLDL particle secretion. [11]
  LDLR directs apoB to degradation in a post-ER compartment. Furthermore, the reuptake mechanism of degradation occurs via internalization of apoB through a constitutive endocytic pathway and apoE through a ligand-dependent pathway. [11]
- Sterol O-acyltransferase 1
  in hepatocyte
  Cholesteryl esters play an important role in regulating the assembly and secretion of apoB-containing lipoproteins. [12]
Hormone: Dynamin-2
Hormone: TGF-alpha
Influenced by:
- TNFR1
  in hepatocyte
  In primary hepatocyte cultures, TNF not only potentiates growth factor-stimulated proliferation, but acts as a mitogen itself through the induced release of autocrine transforming growth factor- (TGF-) and its activation of serine-threonine protein kinase B (PKB)/Akt and extracellular signal-regulated kinase (ERK). [7]
- TNFR2
  in hepatocyte
  In primary hepatocyte cultures, TNF not only potentiates growth factor-stimulated proliferation, but acts as a mitogen itself through the induced release of autocrine transforming growth factor- (TGF-) and its activation of serine-threonine protein kinase B (PKB)/Akt and extracellular signal-regulated kinase (ERK). [7]
Hormone: IL-1 alpha
Influenced by:
- EGFR isoform a
  in hepatocyte
  Induced IL-1alpha release from hepatocyte is contingent on both TNF and autocrine TGF-alpha. [7]
- TNFR1
  in hepatocyte
  Induced IL-1alpha release from hepatocyte is contingent on both TNF and autocrine TGF-alpha. [7]
- TNFR2
  in hepatocyte
  Induced IL-1alpha release from hepatocyte is contingent on both TNF and autocrine TGF-alpha. [7]
Hormone: IL-1RA
Influenced by:
- TNFR1
  in hepatocyte
  TNF induces the release of IL-1ra. [7]
- TNFR2
  in hepatocyte
  TNF induces the release of IL-1ra. [7]
Hormone: fetuin-A
- Ahsg (fetuin-A) is a 55-59kDa phosphorylated glycoprotein synthesized in the adult predominantly by hepatocytes, from which it enters the circulation. [27]
Hormone: fibrinogen
Influenced by:
- IL-6R
  in hepatocyte
  We determined the role of IL-6-receptor-gp130-Stat3 signaling in IL-6 activation of the γFBG promoter in liver and lung epithelial cells. [28]

Receptors

Receptor: LXR-beta
Influences:
- cholesterol
  
  Liver X receptor (LXR) alpha and beta are the nuclear receptors responsible for regulation of cholesterol metabolism. In physiological conditions, high intracellular cholesterol levels cause increased synthesis of oxysterols, which activate LXR, thus triggering a transcriptional response for cholesterol secretion and catabolism. [23]
Receptor: H1
Receptor: H2
Receptor: histamine H4 receptor
Receptor: ferroportin-1
Receptor: transferrin receptor 2
Influences:
- hepcidin
Receptor: IL-6R
Influences:
- hepcidin
  
  Hepcidin mRNA expression can be induced in response to the inflammatory cytokine IL-6 (Interleukin-6). [10]
- SAA1
- fibrinogen
  
  We determined the role of IL-6-receptor-gp130-Stat3 signaling in IL-6 activation of the γFBG promoter in liver and lung epithelial cells. [28]
Receptor: transferrin receptor 1
Induced phenotype:
- regulation of iron ion transmembrane transport
  
  Absorbed iron is bound to circulating transferrin and passes initially through the portal system of the liver, which is the major site of iron storage. Hepatocytes take up transferrin-bound iron via the classical transferrin receptor (TfR1) but likely in greater amounts by the homologous protein, TfR2. [29]
Receptor: RXR-alpha
Receptor: SR-BI
Receptor: BMP receptor type II
Receptor: hepatocyte growth factor receptor
Receptor: CAR
Receptor: glucocorticoid receptor
Influences:
- IGF-1
  
  IGF-1 is synthesized in hepatocytes upon GH stimulation. [26]
- CBG
  
  Levels of CBG are decreased by glucocorticoids. The effects of glucocorticoids on CBG synthesis are glucocorticoid receptor dependent. [24]
Receptor: VDR
- VDR protein and mRNA were identified in primary human hepatocytes. [30]
Induced phenotype:
- negative regulation of bile acid biosynthetic process
  
  Lithocholic acid acetate or 1α, 25-dihydroxy-vitamin D3-activated VDR strongly inhibites cholesterol 7α-hydroxylase mRNA expression and reduces bile acid synthesis in human hepatocytes. [30]
Receptor: PPAR-alpha
- PPARα is expressed at high levels in organs that carry out significant catabolism of fatty acids such as the brown adipose tissue, liver, heart, kidney, and intestine [31]
Influences:
- APOA5
  
  Overexpression of PPAR-alpha enhances the activity of the human ApoA5 gene promoter. [19]
- apo B-100
  
  The peroxisome proliferator-activated receptor (PPAR) agonist WY 14,643 increased the secretion of apolipoprotein (apo) B-100, but not that of apoB-48, and decreased triglyceride biosynthesis and secretion from primary rat hepatocytes. These effects resulted in decreased secretion of apoB-100-very low density lipoprotein (VLDL) and an increased secretion of apoB-100 on low density lipoproteins/intermediate density lipoproteins. [13]
Receptor: TNFR1
Induced phenotype:
- antagonizing IL-1alpha/beta ligand activity
  
  TNF induces the release of IL-1ra, which antagonizes IL-1alpha/beta ligand activity. [7]
- positive regulation of apoptosis
  
  TNF-induced autocrine TGF- and IL-1alpha/beta contribute to multiple intracellular signaling pathways that govern hepatocyte apoptosis. [7]
  Autocrine IL-1alpha/beta regulates proapoptotic signaling through JNK and p38 pathways. [7]
- positive regulation of cell proliferation
  
  TNF-induced autocrine TGF- and IL-1alpha/beta contribute to multiple intracellular signaling pathways that govern hepatocyte proliferation. [7]
  101 Autocrine TGF-alpha regulates pro-proliferative/antiapoptotic signaling through the ERK and, in the absence of Adenoviral infection, Akt pathways. 2452 [32]
Influences:
- TGF-alpha
  
  In primary hepatocyte cultures, TNF not only potentiates growth factor-stimulated proliferation, but acts as a mitogen itself through the induced release of autocrine transforming growth factor- (TGF-) and its activation of serine-threonine protein kinase B (PKB)/Akt and extracellular signal-regulated kinase (ERK). [7]
- IL-1 alpha
  
  Induced IL-1alpha release from hepatocyte is contingent on both TNF and autocrine TGF-alpha. [7]
- IL-1 beta
  
  Induced IL-1alpha release from hepatocyte is contingent on both TNF and autocrine TGF-alpha. [7]
- IL-1RA
  
  TNF induces the release of IL-1ra. [7]
Receptor: fas receptor
Receptor: EGFR isoform a
Influences:
- IL-1 alpha
  
  Induced IL-1alpha release from hepatocyte is contingent on both TNF and autocrine TGF-alpha. [7]
- IL-1 beta
  
  Induced IL-1alpha release from hepatocyte is contingent on both TNF and autocrine TGF-alpha. [7]
Receptor: RXR-beta
Receptor: LXR-alpha
Influences:
- APOA5
  
  Co-transfection of SREBP-1c downregulates APOA5 promoter activity. [20]
- cholesterol
  
  Liver X receptor (LXR) alpha and beta are the nuclear receptors responsible for regulation of cholesterol metabolism. In physiological conditions, high intracellular cholesterol levels cause increased synthesis of oxysterols, which activate LXR, thus triggering a transcriptional response for cholesterol secretion and catabolism. [23]
Receptor: growth hormone receptor
Receptor: bile acid receptor
Influences:
- FGF-19
  
  FXR induces expression of FGF-19 in primary cultures of human hepatocytes. [17]
- APOA5
  
  Bile acids induce human apoAV promoter activity via FXR. [19]
- fetuin-B
  
  FXR agonists induce fetuin-B expression in human primary hepatocytes. [33]
Receptor: PXR
Receptor: FGFR-4
Receptor: LRP5
Receptor: THRB1
Influences:
- APOA5
  
  T3-activated TRbeta1 enhanced the activity of APOA5 DR4-driven promoter constructs. [18]
  Treatment with T3 significantly increased APOA5 mRNA levels at 6 h, and a 2-fold induction was achieved after 24 h of T3 addition. [18]
Receptor: THRA1
Influences:
- APOA5
  
  Treatment with T3 significantly increased APOA5 mRNA levels at 6 h, and a 2-fold induction was achieved after 24 h of T3 addition. [18]
Receptor: LDL-R
Influences:
- apo B-48
  
  Apolipoprotein B (apoB) is required for the hepatic assembly and secretion of very low density lipoprotein (VLDL). The LDL receptor (LDLR) promotes post-translational degradation of apoB and thereby reduces VLDL particle secretion. [11]
  LDLR directs apoB to degradation in a post-ER compartment. Furthermore, the reuptake mechanism of degradation occurs via internalization of apoB through a constitutive endocytic pathway and apoE through a ligand-dependent pathway. [11]
- apo B-100
  
  Apolipoprotein B (apoB) is required for the hepatic assembly and secretion of very low density lipoprotein (VLDL). The LDL receptor (LDLR) promotes post-translational degradation of apoB and thereby reduces VLDL particle secretion. [11]
  LDLR directs apoB to degradation in a post-ER compartment. Furthermore, the reuptake mechanism of degradation occurs via internalization of apoB through a constitutive endocytic pathway and apoE through a ligand-dependent pathway. [11]
Receptor: angiotensin receptor 2
Receptor: angiotensin II type 1 receptor
Influences:
- angiotensinogen
  
  Angiotensin II stimulates the hepatic synthesis and secretion of angiotensinogen, the substrate of renin. This effect is mainly related to a transient inhibition of adenylylcyclase. [22]
Receptor: VPAC1
Induced phenotype:
- regulation of cell proliferation
  
  The fact that VIP exerts a mitogenic action on rat hepatocytes strongly suggests that PACAP could be also involved in the control of liver cell proliferation via stimulation of adenylate cyclase. [34]
Receptor: GL-R
Induced phenotype:
- glycogenolysis
  
  Glucagon stimulates glycogenolysis in liver, resulting in elevation of plasma glucose. [35]
- gluconeogenesis
  
  Glucagon stimulates gluconeogenesis in liver, resulting in elevation of plasma glucose. [35]
- maintainence of serum glucose concentration
  
  Glucagon has a critical role in maintaining serum glucose concentration. [35]
Receptor: V1a
Receptor: Sterol O-acyltransferase 1
Influences:
- apo B-100
  
  Cholesteryl esters play an important role in regulating the assembly and secretion of apoB-containing lipoproteins. [12]
- apo B-48
  
  Cholesteryl esters play an important role in regulating the assembly and secretion of apoB-containing lipoproteins. [12]
Receptor: autocrine motility factor receptor
Influences:
- apo B-100
  
  Tumor autocrine motility factor receptor, also known as gp78, is an endoplasmic reticulum (ER)-associated E3. This E3 is involved in the ER-associated degradation of nascent apoB. [14]
Receptor: TNFR2
Induced phenotype:
- antagonizing IL-1alpha/beta ligand activity
  
  TNF induces the release of IL-1ra, which antagonizes IL-1alpha/beta ligand activity. [7]
- positive regulation of cell proliferation
  
  TNF-induced autocrine TGF- and IL-1alpha/beta contribute to multiple intracellular signaling pathways that govern hepatocyte proliferation. [7]
  Autocrine TGF-alpha regulates pro-proliferative/antiapoptotic signaling through the ERK and, in the absence of Adenoviral infection, Akt pathways. [32]
- positive regulation of apoptosis
  
  TNF-induced autocrine TGF- and IL-1alpha/beta contribute to multiple intracellular signaling pathways that govern hepatocyte apoptosis. [7]
  Autocrine IL-1alpha/beta regulates proapoptotic signaling through JNK and p38 pathways. [7]
Influences:
- TGF-alpha
  
  In primary hepatocyte cultures, TNF not only potentiates growth factor-stimulated proliferation, but acts as a mitogen itself through the induced release of autocrine transforming growth factor- (TGF-) and its activation of serine-threonine protein kinase B (PKB)/Akt and extracellular signal-regulated kinase (ERK). [7]
- IL-1 beta
  
  Induced IL-1alpha release from hepatocyte is contingent on both TNF and autocrine TGF-alpha. [7]
- IL-1 alpha
  
  Induced IL-1alpha release from hepatocyte is contingent on both TNF and autocrine TGF-alpha. [7]
- IL-1RA
  
  TNF induces the release of IL-1ra. [7]
Receptor: PLXNB1
Receptor: leptin receptor
Induced phenotype:
- negative regulation of insulin receptor signaling pathway
  
  Exposure of hepatic cells to leptin, at concentrations comparable with those present in obese individuals, caused attenuation of several insulin-induced activities, including tyrosine phosphorylation of the insulin receptor substrate-1 (IRS-1), association of the adapter molecule growth factor receptor-bound protein 2 with IRS-1, and down-regulation of gluconeogenesis. In contrast, leptin increased the activity of IRS-1-associated phosphatidylinositol 3-kinase. These in vitro studies raise the possibility that leptin modulates insulin activities in obese individuals. [36]
Receptor: PRLR
Induced phenotype:
- increase in glycogen phosphorylase-a activation
  
  PRL at physiological concentrations produced a 4-fold increase in glycogen phosphorylase-a activation in isolated hepatocytes. [37]
- positive regulation of cell proliferation
  
  PRL plays an important role in the turnover of hepatocytes. There was a striking increase in the number of mitotic figures in livers of transgenic mice expressing hGH, which binds equally well to PRL and GH receptors. [38]

Reference

EndoNet

The information resource about the endocrine network in human.

Details for anatomical structure: hepatocyte

Synonyms

General information

Links to other resources

Related structures

Larger structures

Substructures

Secreted hormones

Hormone: osteopontin 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: complement factor B 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: CRP 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});});

Hormone: IL-8 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: HGF 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: VEGF-121 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: VEGF-189 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: IGFBP-2 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: IGFBP-3 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: IGFBP-4 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: IGFBP-1 isoform a 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: IL-1 beta 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});});

Influenced by:

Hormone: IL-7 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: TGF-beta 1 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: APOA1 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: APOE 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: apolipoprotein A-II 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: APOC1 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: IL-15 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: APOC2 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: APOC3 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: APOA4 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});});

Hormone: hepcidin 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});});

Influenced by:

Hormone: apo B-100 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: apolipoprotein A-related gene C 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: adipsin 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: chondromodulin 2 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: sNRP1 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: APOA1(1-242) 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: erythropoietin 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});});

Hormone: cardiotrophin 1 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: RANTES 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: GROalpha 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: TNF-alpha 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: M-CSF 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: GRObeta 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: GROgamma 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: SCF 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});});

Hormone: FGF-19 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: VEGF-165 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: APOA5 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: angiotensinogen 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: renin 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});});

Hormone: cholesterol 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});});

Influenced by:

Hormone: CBG 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});});

Influenced by:

Hormone: IGF-1 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_45_toolsBtn',{id:'j_idt91:45:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_45_j_idt99',{id:'j_idt91:45:j_idt99',target:'j_idt91:45:toolsBtn',dynamic:true});});

Influenced by:

Hormone: apo B-48 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_46_toolsBtn',{id:'j_idt91:46:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_46_j_idt99',{id:'j_idt91:46:j_idt99',target:'j_idt91:46:toolsBtn',dynamic:true});});

Influenced by:

Hormone: Dynamin-2 ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_47_toolsBtn',{id:'j_idt91:47:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_47_j_idt99',{id:'j_idt91:47:j_idt99',target:'j_idt91:47:toolsBtn',dynamic:true});});

Hormone: TGF-alpha ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_48_toolsBtn',{id:'j_idt91:48:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_48_j_idt99',{id:'j_idt91:48:j_idt99',target:'j_idt91:48:toolsBtn',dynamic:true});});

Influenced by:

Hormone: IL-1 alpha ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_49_toolsBtn',{id:'j_idt91:49:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_49_j_idt99',{id:'j_idt91:49:j_idt99',target:'j_idt91:49:toolsBtn',dynamic:true});});

Influenced by:

Hormone: IL-1RA ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_50_toolsBtn',{id:'j_idt91:50:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_50_j_idt99',{id:'j_idt91:50:j_idt99',target:'j_idt91:50:toolsBtn',dynamic:true});});

Influenced by:

Hormone: fetuin-A ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_51_toolsBtn',{id:'j_idt91:51:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_51_j_idt99',{id:'j_idt91:51:j_idt99',target:'j_idt91:51:toolsBtn',dynamic:true});});

Hormone: fibrinogen ui-buttonPrimeFaces.cw('CommandButton','widget_j_idt91_52_toolsBtn',{id:'j_idt91:52:toolsBtn'}); $(function(){PrimeFaces.cw('OverlayPanel','widget_j_idt91_52_j_idt99',{id:'j_idt91:52:j_idt99',target:'j_idt91:52:toolsBtn',dynamic:true});});

Influenced by:

Receptors

Receptor: LXR-beta 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});});

Influences:

Hormone: osteopontin

Hormone: complement factor B

Hormone: CRP

Hormone: IL-8

Hormone: HGF

Hormone: VEGF-121

Hormone: VEGF-189

Hormone: IGFBP-2

Hormone: IGFBP-3

Hormone: IGFBP-4

Hormone: IGFBP-1 isoform a

Hormone: IL-1 beta

Hormone: IL-7

Hormone: TGF-beta 1

Hormone: APOA1

Hormone: APOE

Hormone: apolipoprotein A-II

Hormone: APOC1

Hormone: IL-15

Hormone: APOC2

Hormone: APOC3

Hormone: APOA4

Hormone: hepcidin

Hormone: apo B-100

Hormone: apolipoprotein A-related gene C

Hormone: adipsin

Hormone: chondromodulin 2

Hormone: sNRP1

Hormone: APOA1(1-242)

Hormone: erythropoietin

Hormone: cardiotrophin 1

Hormone: RANTES

Hormone: GROalpha

Hormone: TNF-alpha

Hormone: M-CSF

Hormone: GRObeta

Hormone: GROgamma

Hormone: SCF

Hormone: FGF-19

Hormone: VEGF-165

Hormone: APOA5

Hormone: angiotensinogen

Hormone: renin

Hormone: cholesterol

Hormone: CBG

Hormone: IGF-1

Hormone: apo B-48

Hormone: Dynamin-2

Hormone: TGF-alpha

Hormone: IL-1 alpha

Hormone: IL-1RA

Hormone: fetuin-A

Hormone: fibrinogen

Receptor: LXR-beta

Receptor: H1

Receptor: H2

Receptor: histamine H4 receptor

Receptor: ferroportin-1

Receptor: transferrin receptor 2

Receptor: IL-6R

Receptor: transferrin receptor 1

Receptor: RXR-alpha

Receptor: SR-BI

Receptor: BMP receptor type II

Receptor: hepatocyte growth factor receptor

Receptor: CAR

Receptor: glucocorticoid receptor

Receptor: VDR

Receptor: PPAR-alpha

Receptor: TNFR1

Receptor: fas receptor

Receptor: EGFR isoform a

Receptor: RXR-beta

Receptor: LXR-alpha

Receptor: growth hormone receptor

Receptor: bile acid receptor

Receptor: PXR

Receptor: FGFR-4

Receptor: LRP5

Receptor: THRB1