Ignet

Gene Information

Gene symbol: FOS

Gene name: FBJ murine osteosarcoma viral oncogene homolog

HGNC ID: 3796

Synonyms: c-fos, AP-1

Related Genes

#	Gene Symbol	Number of hits
1	AGTR1	1 hits
2	ALB	1 hits
3	CFH	1 hits
4	CREB1	1 hits
5	CSF2	1 hits
6	EDN1	1 hits
7	EGFR	1 hits
8	JUN	1 hits
9	MAPK1	1 hits
10	MAPK10	1 hits
11	MAPK8	1 hits
12	NFKB1	1 hits
13	NPHS1	1 hits
14	PRKCA	1 hits
15	PTK2	1 hits
16	RHOD	1 hits
17	STX2	1 hits
18	TEC	1 hits
19	TGFB1	1 hits
20	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	31399972	Aldosterone acts on renal vessels, renal cells (glomerular mesangial cells, podocytes, vascular smooth muscle cells, tubular epithelial cells, and interstitial fibroblasts), and infiltrating inflammatory cells, inducing reactive oxygen species (ROS) production, upregulated epithelial growth factor receptor (EGFR), and type 1 angiotensin (AT1) receptor expressions, and activating nuclear factor kappa B (NF-κB), activator protein-1 (AP-1), and EGFR to further promote cell proliferation, apoptosis, and proliferation.
2	31399972	Phenotypic transformation of epithelial cells stimulates the expression of transforming growth factor-β (TGF-β), connective tissue growth factor (CTGF), osteopontin (OPN), and plasminogen activator inhibitor-1 (PAI-1), eventually leading to renal fibrosis.
3	30642982	Cadmium Induces Glomerular Endothelial Cell-Specific Expression of Complement Factor H via the -1635 AP-1 Binding Site.
4	30642982	Cadmium Induces Glomerular Endothelial Cell-Specific Expression of Complement Factor H via the -1635 AP-1 Binding Site.
5	30642982	Cadmium Induces Glomerular Endothelial Cell-Specific Expression of Complement Factor H via the -1635 AP-1 Binding Site.
6	30642982	Cadmium Induces Glomerular Endothelial Cell-Specific Expression of Complement Factor H via the -1635 AP-1 Binding Site.
7	30642982	Cd activates the JNK pathway and increases c-Jun and c-Fos in human renal glomerular endothelial cells.
8	30642982	Cd activates the JNK pathway and increases c-Jun and c-Fos in human renal glomerular endothelial cells.
9	30642982	Cd activates the JNK pathway and increases c-Jun and c-Fos in human renal glomerular endothelial cells.
10	30642982	Cd activates the JNK pathway and increases c-Jun and c-Fos in human renal glomerular endothelial cells.
11	30642982	A JNK inhibitor, SP600125, specifically abolishes Cd-induced CFH production.
12	30642982	A JNK inhibitor, SP600125, specifically abolishes Cd-induced CFH production.
13	30642982	A JNK inhibitor, SP600125, specifically abolishes Cd-induced CFH production.
14	30642982	A JNK inhibitor, SP600125, specifically abolishes Cd-induced CFH production.
15	30642982	By chromatin immunoprecipitation assay and EMSA, the -1635 AP-1 motif on human CFH promoter was identified as the binding element for c-Jun and c-Fos.
16	30642982	By chromatin immunoprecipitation assay and EMSA, the -1635 AP-1 motif on human CFH promoter was identified as the binding element for c-Jun and c-Fos.
17	30642982	By chromatin immunoprecipitation assay and EMSA, the -1635 AP-1 motif on human CFH promoter was identified as the binding element for c-Jun and c-Fos.
18	30642982	By chromatin immunoprecipitation assay and EMSA, the -1635 AP-1 motif on human CFH promoter was identified as the binding element for c-Jun and c-Fos.
19	30642982	In a luciferase activity assay, mutation of the AP1 site eliminates Cd-induced increase of CFH promoter activity.
20	30642982	In a luciferase activity assay, mutation of the AP1 site eliminates Cd-induced increase of CFH promoter activity.
21	30642982	In a luciferase activity assay, mutation of the AP1 site eliminates Cd-induced increase of CFH promoter activity.
22	30642982	In a luciferase activity assay, mutation of the AP1 site eliminates Cd-induced increase of CFH promoter activity.
23	30642982	Thus, the -1635 AP-1 motif on the CFH promoter region mediates Cd-inducible CFH gene expression.
24	30642982	Thus, the -1635 AP-1 motif on the CFH promoter region mediates Cd-inducible CFH gene expression.
25	30642982	Thus, the -1635 AP-1 motif on the CFH promoter region mediates Cd-inducible CFH gene expression.
26	30642982	Thus, the -1635 AP-1 motif on the CFH promoter region mediates Cd-inducible CFH gene expression.
27	23010541	Rapamycin enhanced podocyte NF-κB and CREB activities but then it decreased AP-1 binding activity.
28	17148661	Stx-2 enhanced ET-1 mRNA and protein expression via activation of nuclear factor kappaB (NF-kappaB) and activator protein-1 (Ap-1) to the extent that transfection with the dominant-negative mutant of IkappaB-kinase 2 or with Ap-1 decoy oligodeoxynucleotides reduced ET-1 mRNA levels.
29	17148661	We propose a role for p38 and p42/44 mitogen-activated protein kinases (MAPKs) in mediating NF-kappaB-dependent gene transcription induced by Stx-2, based on data that Stx-2 phosphorylated p38 and p42/44 MAPKs and that MAPK inhibitors reduced transcription of NF-kappaB promoter/luciferase reporter gene construct induced by Stx-2.
30	17148661	Stx-2 caused F-actin redistribution and intercellular gaps via production of ET-1 acting on ETA receptor, because cytoskeleton changes were prevented by ETA receptor blockade.
31	17148661	Exogenous ET-1 induced cytoskeleton rearrangement and intercellular gaps via phosphatidylinositol-3 kinase and Rho-kinase pathway and increased protein permeability across the podocyte monolayer.
32	16452496	Immunofluorescence studies of podocyte-associated proteins nephrin and podocin revealed diminished and discontinuous staining patterns in rats with PAN nephrosis, indicating severe podocyte injury.
33	16452496	Fluvastatin also mitigated tubulointerstitial damage in PAN nephrosis, with the repression of PAN-induced NF-kappaB and activator protein-1 activation in the kidneys.
34	15855633	Both Y27632, which inhibits Rho kinase-dependent stress fiber formation, and jasplakinolide, an F-actin stabilizer, decreased NF-kappaB and Ap-1 activity and reduced ET-1 expression.
35	15855633	Both Y27632, which inhibits Rho kinase-dependent stress fiber formation, and jasplakinolide, an F-actin stabilizer, decreased NF-kappaB and Ap-1 activity and reduced ET-1 expression.
36	15855633	Both Y27632, which inhibits Rho kinase-dependent stress fiber formation, and jasplakinolide, an F-actin stabilizer, decreased NF-kappaB and Ap-1 activity and reduced ET-1 expression.
37	15855633	This suggested a role for the cytoskeleton, through activated Rho, in the regulation of the ET-1 peptide.
38	15855633	This suggested a role for the cytoskeleton, through activated Rho, in the regulation of the ET-1 peptide.
39	15855633	This suggested a role for the cytoskeleton, through activated Rho, in the regulation of the ET-1 peptide.
40	15855633	Focal adhesion kinase (FAK), an integrin-associated nonreceptor tyrosine kinase, was phosphorylated by albumin treatment via Rho kinase-triggered actin reorganization.
41	15855633	Focal adhesion kinase (FAK), an integrin-associated nonreceptor tyrosine kinase, was phosphorylated by albumin treatment via Rho kinase-triggered actin reorganization.
42	15855633	Focal adhesion kinase (FAK), an integrin-associated nonreceptor tyrosine kinase, was phosphorylated by albumin treatment via Rho kinase-triggered actin reorganization.
43	15855633	FAK activation led to NF-kappaB- and Ap-1-dependent ET-1 expression.
44	15855633	FAK activation led to NF-kappaB- and Ap-1-dependent ET-1 expression.
45	15855633	FAK activation led to NF-kappaB- and Ap-1-dependent ET-1 expression.
46	15855633	These data suggest that reorganization of the actin cytoskeletal network in response to protein load is implicated in modulation of the ET-1 gene via Rho kinase-dependent FAK activation of NF-kappaB and Ap-1 in differentiated podocytes.
47	15855633	These data suggest that reorganization of the actin cytoskeletal network in response to protein load is implicated in modulation of the ET-1 gene via Rho kinase-dependent FAK activation of NF-kappaB and Ap-1 in differentiated podocytes.
48	15855633	These data suggest that reorganization of the actin cytoskeletal network in response to protein load is implicated in modulation of the ET-1 gene via Rho kinase-dependent FAK activation of NF-kappaB and Ap-1 in differentiated podocytes.
49	12424224	Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria.
50	12424224	Podocin interacts with the C-terminal domain of nephrin and facilitates nephrin-dependent signaling.
51	12424224	NEPH1 triggers AP-1 activation similarly to nephrin but requires the presence of Tec family kinases for efficient transactivation.
52	12424224	We conclude that NEPH1 defines a new family of podocin-binding molecules that are potential candidates for hereditary nephrotic syndromes not linked to either NPHS1 or NPHS2.
53	11779150	High glucose induced VEGF expression via PKC and ERK in glomerular podocytes.
54	11779150	Using a differentiated mouse podocyte cell line, we investigated the roles of protein kinase C (PKC) and extracellular signal-regulated kinase (ERK) on the expression of VEGF under high glucose conditions.
55	11779150	High glucose induced up-regulation of VEGF mRNA and protein expression in podocytes via activation of PKC (PKC-alpha and -betaII isoforms) and ERK.
56	11779150	High glucose and the PKC stimulator, phorbol 12-myristate 13-acetate (PMA) induced activator protein-1 (AP-1)-dependent transcriptional activity and expression of VEGF.
57	11779150	These observations suggested that high glucose-induced VEGF expression in podocytes was largely mediated through PKC and ERK pathways that may be involved in diabetic nephropathy.
58	11752025	Reactive oxygen species alter gene expression in podocytes: induction of granulocyte macrophage-colony-stimulating factor.
59	11752025	One differentially expressed clone was identified as the proinflammatory cytokine granulocyte macrophage-colony-stimulating factor (GM-CSF).
60	11752025	GM-CSF release by podocytes was also stimulated by lipopolysaccharide (LPS), interleukin-1 (IL-1), and phorbolester (PMA).
61	11752025	Dimethyl-thio-urea significantly inhibited the LPS-, IL-1-, and PMA-induced GM-CSF production.
62	11752025	Activation of the transcription factor nuclear factor-kappaB (NF-kappaB) but not activator protein-1 was involved in the upregulation of ROS-induced GM-CSF production.
63	11752025	ROS also partially mediate the effects of PMA and IL-1 on podocyte GM-CSF production.
64	11576932	In mesangial and endothelial cells, the AGE-RAGE interaction caused enhanced formation of oxygen radicals with subsequent activation of nuclear factor-kappaB and release of pro-inflammatory cytokines (interleukin-6, tumor necrosis factor-alpha), growth factors (transforming growth factor-beta1 [TGF-beta1], insulin-like growth factor-1), and adhesion molecules (vascular cell adhesion molecule-1, intercellular adhesion molecule-1).
65	11576932	In tubular cells, incubation with AGE albumin was followed by stimulation of the mitogen-activating protein (MAP) kinase pathway and its downstream target, the activating protien-1 (AP-1) complex, TGF-beta1 overexpression, enhanced protein kinase C activity, decreased cell proliferation, and impaired protein degradation rate, in part caused by decreased cathepsin activities.
66	11576932	The pathogenic relevance of AGEs was further verified by in vivo experiments in euglycemic rats and mice by the parenteral administration of AGE albumin, leading in the glomeruli to TGF-beta1 overproduction, enhanced gene expression of ECM proteins, and morphological lesions similar to those of DN.