Ignet

Gene Information

Gene symbol: FN1

Gene name: fibronectin 1

HGNC ID: 3778

Synonyms: MSF, CIG, LETS, GFND2, FINC

Related Genes

#	Gene Symbol	Number of hits
1	ACTC1	1 hits
2	AHSG	1 hits
3	AKT1	1 hits
4	ALB	1 hits
5	APBB1	1 hits
6	APP	1 hits
7	C1QA	1 hits
8	CCL2	1 hits
9	CD68	1 hits
10	CD80	1 hits
11	CLU	1 hits
12	COL1A1	1 hits
13	COL4A1	1 hits
14	CST3	1 hits
15	EGFR	1 hits
16	GSK3B	1 hits
17	HTATIP	1 hits
18	ICAM1	1 hits
19	IL6	1 hits
20	LEP	1 hits
21	MMP9	1 hits
22	NPHS1	1 hits
23	NPHS2	1 hits
24	PTK2	1 hits
25	PXN	1 hits
26	SERPINE1	1 hits
27	SMAD3	1 hits
28	SMAD4	1 hits
29	STAT3	1 hits
30	TGFA	1 hits
31	TGFB1	1 hits
32	TRAF6	1 hits
33	TRO	1 hits
34	VCL	1 hits
35	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	9740168	Cryofibrinogen is a cold insoluble complex of fibrin, fibrinogen, and fibrin split products with albumin, cold insoluble globulin, factor VIII, and plasma proteins.
2	11035540	Retinal mRNA was prepared from STZ-diabetic and non-diabetic FVB mice at 4, 8, 12 and 16 weeks and cDNA encoding basement membrane components was quantitated using MIMIC constructs that compete for the same primer pairs. alpha1 (IV) collagen, the beta1 and gamma1 chains of laminin, fibronectin, and vitronectin mRNAs were quantitated.
3	11035540	The magnitude of change was greatest for alpha1 (IV) collagen (2.4-fold) and beta1 laminin (2. 5-fold) at 8 weeks, and least for fibronectin (1.6-fold).
4	12411472	Leptin induces endothelial cell migration through Akt, which is inhibited by PPARgamma-ligands.
5	12411472	The antidiabetic thiazolidinediones (TZD) inhibit leptin gene expression and vascular smooth muscle cell migration through activation of the peroxisome proliferator-activated receptor-gamma (PPARgamma).
6	12411472	Because activation of two signaling pathways, the phosphatidylinositol-3 kinase (PI3K)-->Akt-->eNOS and the ERK1/2 MAPK pathway, is known to be involved in cell migration, we used the pharmacological inhibitors wortmannin and PD98059 to determine if chemotactic signaling by leptin involves Akt or ERK1/2, respectively.
7	12411472	Treatment with the TZD-PPARgamma-ligands TRO and CIG significantly inhibited the chemotactic response toward leptin.
8	12411472	Both PPARgamma-ligands inhibited leptin-stimulated Akt and eNOS phosphorylation, but neither attenuated ERK 1/2 activation in response to leptin.
9	12411472	The inhibition of Akt-phosphorylation was accompanied by a PPARgamma-ligand-mediated upregulation of PTEN, a phosphatase that functions as a negative regulator of PI3K-->Akt signaling.
10	12411472	These experiments provide the first evidence that activation of Akt and ERK 1/2 are crucial events in leptin-mediated signal transduction leading to EC migration.
11	12411472	Moreover, inhibition of leptin-directed migration by the PPARgamma-ligands TRO and CIG through inhibition of Akt underscores their potential in the prevention of diabetes-associated complications.
12	12411472	Leptin induces endothelial cell migration through Akt, which is inhibited by PPARgamma-ligands.
13	12411472	The antidiabetic thiazolidinediones (TZD) inhibit leptin gene expression and vascular smooth muscle cell migration through activation of the peroxisome proliferator-activated receptor-gamma (PPARgamma).
14	12411472	Because activation of two signaling pathways, the phosphatidylinositol-3 kinase (PI3K)-->Akt-->eNOS and the ERK1/2 MAPK pathway, is known to be involved in cell migration, we used the pharmacological inhibitors wortmannin and PD98059 to determine if chemotactic signaling by leptin involves Akt or ERK1/2, respectively.
15	12411472	Treatment with the TZD-PPARgamma-ligands TRO and CIG significantly inhibited the chemotactic response toward leptin.
16	12411472	Both PPARgamma-ligands inhibited leptin-stimulated Akt and eNOS phosphorylation, but neither attenuated ERK 1/2 activation in response to leptin.
17	12411472	The inhibition of Akt-phosphorylation was accompanied by a PPARgamma-ligand-mediated upregulation of PTEN, a phosphatase that functions as a negative regulator of PI3K-->Akt signaling.
18	12411472	These experiments provide the first evidence that activation of Akt and ERK 1/2 are crucial events in leptin-mediated signal transduction leading to EC migration.
19	12411472	Moreover, inhibition of leptin-directed migration by the PPARgamma-ligands TRO and CIG through inhibition of Akt underscores their potential in the prevention of diabetes-associated complications.
20	16741042	Inhibition of mitogen-activated protein kinase with pharmacological inhibitors and protein kinase B with dominant negative transfections prevented glucose- and ET-1-mediated FN and ED-B FN expression.
21	16741042	We then determined the functional significance of ED-B in ECs and show that ED-B FN is involved in vascular endothelial growth factor expression and cellular proliferation.
22	16741042	Inhibition of mitogen-activated protein kinase with pharmacological inhibitors and protein kinase B with dominant negative transfections prevented glucose- and ET-1-mediated FN and ED-B FN expression.
23	16741042	We then determined the functional significance of ED-B in ECs and show that ED-B FN is involved in vascular endothelial growth factor expression and cellular proliferation.
24	18723004	Quantitative PCR confirmed altered regulation in 6 of 7 Alzheimer-related genes (Apbb1, C1qa, Clu, App, Cst3, Fn1, Htatip) in iron-deficient rats relative to iron-sufficient controls at P15.
25	18793745	The examples of such candidate proteins include several hubs, focal adhesion kinase PTK2 and the extracellular proteins fibronectin FN1, paxillin PXN, and vinculin VCL.
26	19211686	Real-time PCR demonstrated increased glomerular expression of Col4a1, Fn1, and Tgfb1.
27	20947626	Here, we used centrifugation to separate a fetuin-mineral complex (FMC) composed of fetuin-A, fibrinogen, fibronectin-1, and calcium from the serum of hemodialysis patients.
28	20947626	Moreover, the magnitude of cinacalcet-induced reduction in parathyroid hormone correlated with the decrease in RR but not with changes in serum or supernatant fetuin-A.
29	21910999	As a result, five shared risk feature genes, CD80, EGFR, FN1, GSK3B and TRAF6 were found and proven to be associated with rheumatoid arthritis by previous reports.
30	22736507	Liquid chromatography-tandem mass spectroscopy-based analysis revealed increases in urinary proteins that are early indicators of DN (e.g., cystatin C, clusterin, cathepsin B, retinol binding protein 4, and peroxiredoxin-1) in the STZ group, which were blocked by suramin.
31	22736507	Endothelial intracellular adhesion molecule-1 (ICAM-1) activation, leukocyte infiltration, and inflammation; transforming growth factor-β1 (TGF-β1) signaling; TGF-β1/SMAD-3-activated fibrogenic markers fibronectin-1, α-smooth muscle actin, and collagen 1A2; activation of proinflammatory and profibrotic transcription factors nuclear factor-κB (NF-κB) and signal transducer and activator of transcription factor-3 (STAT-3), respectively, were all increased in STZ rats and suramin blocked these changes.
32	22736507	In conclusion, delayed administration of suramin attenuated 1) urinary markers of DN, 2) inflammation by blocking NF-κB activation and ICAM-1-mediated leukocyte infiltration, and 3) fibrosis by blocking STAT-3 and TGF-β1/SMAD-3 signaling.
33	23454124	Emerging evidence shows that transient hyperglycemic exposure of human endothelial cells induces histone 3 lysine 4 mono-methylation (H3K4me1) on the promoter and persistent mRNA expression of RelA and IL-8 genes, suggesting that epigenetic histone modification and chromatin structure remodeling is a key event underlying metabolic memory.
34	23454124	To address this, we used type 1 diabetes mouse model induced by streptozocin to be hyperglycemic for 8 weeks, and isolated endothelial cells that were used either freshly after isolation or after 2 to 3-week cell culture in normoglycemic conditions. mRNA expression profiling in diabetic mouse endothelial cells revealed significant and persistent up-regulation of Serpine1 encoding PAI-1, the hypo-fibrinolytic mediator leading to thrombotic diseases in diabetes, along with Rock2, Fn1 and Ccl2, whereas only Serpine 1 was persistently elevated in high glucose-treated mouse endothelial cells.
35	23710468	Compared to KK-a/a controls, 26-week-old KK-A (y) mice had elevated HbA1c, insulin, leptin, triglycerides, and cholesterol, and Unx further elevated these markers of metabolic dysregulation.
36	23710468	Consistent with functional and histological evidence of increased injury, fibrotic (fibronectin 1, MMP9, and TGF β 1) and inflammatory (IL-6, CD68) genes were markedly upregulated in Unx KK-A (y) mice, while podocyte markers (nephrin and podocin) were significantly decreased.
37	16973718	Here, we treated diabetic rats with TETA and evaluated its ability to ameliorate Cu(2+)-mediated LV and arterial damage by modifying the expression of molecular targets that included transforming growth factor (TGF)-beta1, Smad4, extracellular matrix (ECM) proteins, extracellular superoxide dismutase (EC-SOD), and heparan sulfate (HS).
38	16973718	LV and aortic mRNAs corresponding to TGF-beta1, Smad4, collagen types I, III, and IV, and fibronectin-1, and plasminogen activator inhibitor-1, were elevated in untreated diabetic animals and normalized after TETA treatment.
39	16973718	Candidate molecular mechanisms by which TETA could ameliorate diabetic cardiac and arteriovascular disease include the suppression of an activated TGF-beta/Smad signaling pathway that mediates increased ECM gene expression and restoration of normal EC-SOD and HS regulation.