Ignet

Gene Information

Gene symbol: INS

Gene name: insulin

HGNC ID: 6081

Related Genes

#	Gene Symbol	Number of hits
1	BCL2L1	1 hits
2	FGF2	1 hits
3	HGF	1 hits
4	ICAM1	1 hits
5	IGF1	1 hits
6	IL6	1 hits
7	PDGFA	1 hits
8	PDGFB	1 hits
9	TF	1 hits
10	TGFA	1 hits
11	TGFB1	1 hits
12	TNF	1 hits
13	VCAM1	1 hits

Related Sentences

#	PMID	Sentence
1	7129481	The system permits in vitro organotypic differentiation in a serum-free, hormone supplemented medium consisting of Dulbecco's minimal essential medium (MEM) and Ham's F12 medium supplemented with insulin, 5 microgram/ml; PGE1, 25 ng/ml; T3, 3.2 pg/ml; hydrocortisone, 5 microgram/ml; and transferrin, 5 microgram/ml.
2	10482316	Augmentation of kidney injury by basic fibroblast growth factor or platelet-derived growth factor does not induce progressive diabetic nephropathy in the Goto Kakizaki model of non-insulin-dependent diabetes.
3	10482316	Specifically, we examined whether the administration of either platelet-derived growth factor (PDGF) or basic fibroblast growth factor (bFGF) in sub-nephritogenic doses might lead to an aggravation of kidney structural changes associated with hyperglycemia, resulting in progressive kidney damage in the Goto Kakizaki (GK) rat, which is a genetic model of non-obese non-insulin-dependent diabetes mellitus (NIDDM), in which progressive kidney disease does not develop spontaneously.
4	10482316	The results demonstrate that the administration of PDGF to hyperglycemic GK rats led to acute mesangial cell proliferation and activation as assessed by 5-bromo-2'-deoxyuridine-positive nuclei and immunostaining for alpha-smooth muscle actin.
5	10482316	Augmentation of kidney injury by basic fibroblast growth factor or platelet-derived growth factor does not induce progressive diabetic nephropathy in the Goto Kakizaki model of non-insulin-dependent diabetes.
6	10482316	Specifically, we examined whether the administration of either platelet-derived growth factor (PDGF) or basic fibroblast growth factor (bFGF) in sub-nephritogenic doses might lead to an aggravation of kidney structural changes associated with hyperglycemia, resulting in progressive kidney damage in the Goto Kakizaki (GK) rat, which is a genetic model of non-obese non-insulin-dependent diabetes mellitus (NIDDM), in which progressive kidney disease does not develop spontaneously.
7	10482316	The results demonstrate that the administration of PDGF to hyperglycemic GK rats led to acute mesangial cell proliferation and activation as assessed by 5-bromo-2'-deoxyuridine-positive nuclei and immunostaining for alpha-smooth muscle actin.
8	11141501	Hepatocyte growth factor, but not insulin-like growth factor I, protects podocytes against cyclosporin A-induced apoptosis.
9	11141501	Cyclosporin A (CsA) nephropathy is associated with altered expression of apoptosis regulatory genes such as Fas-ligand and Bcl-2 family members in the glomerular, tubulointerstitial, and vascular compartments.
10	11141501	Both hepatocyte growth factor (HGF) and insulin-like growth factor (IGF-I) protect against apoptosis, and HGF specifically up-regulates Bcl-xL, a protein that regulates apoptosis.
11	11141501	We investigated whether Bcl-xL and Fas/Fas-ligand were regulated by CsA in cultured podocytes and whether CsA-induced apoptosis was prevented by HGF or IGF-I.
12	11141501	A murine podocyte cell line was treated with CsA in the presence or absence of HGF or IGF-I.
13	11141501	Apoptosis was quantitated by ELISA and by flow cytometry; Bcl-xL, Fas, and Fas-ligand were measured by Western blotting.
14	11141501	Inhibitors of MAP kinase/ERK kinase (MEK)-1 and of phosphatidylinositol 3'-kinase (PI3'-K) were used to determine the signaling pathways involved in Bcl-xL regulation.
15	11141501	HGF, but not IGF-I, prevented apoptosis and restored Bcl-xL levels.
16	11141501	The regulation of Bcl-xL by HGF was mediated by the PI3'-K but not by the MEK-1 pathway.
17	11141501	Apoptosis was prevented by pretreatment with HGF but not IGF-I.
18	11141501	Hepatocyte growth factor, but not insulin-like growth factor I, protects podocytes against cyclosporin A-induced apoptosis.
19	11141501	Cyclosporin A (CsA) nephropathy is associated with altered expression of apoptosis regulatory genes such as Fas-ligand and Bcl-2 family members in the glomerular, tubulointerstitial, and vascular compartments.
20	11141501	Both hepatocyte growth factor (HGF) and insulin-like growth factor (IGF-I) protect against apoptosis, and HGF specifically up-regulates Bcl-xL, a protein that regulates apoptosis.
21	11141501	We investigated whether Bcl-xL and Fas/Fas-ligand were regulated by CsA in cultured podocytes and whether CsA-induced apoptosis was prevented by HGF or IGF-I.
22	11141501	A murine podocyte cell line was treated with CsA in the presence or absence of HGF or IGF-I.
23	11141501	Apoptosis was quantitated by ELISA and by flow cytometry; Bcl-xL, Fas, and Fas-ligand were measured by Western blotting.
24	11141501	Inhibitors of MAP kinase/ERK kinase (MEK)-1 and of phosphatidylinositol 3'-kinase (PI3'-K) were used to determine the signaling pathways involved in Bcl-xL regulation.
25	11141501	HGF, but not IGF-I, prevented apoptosis and restored Bcl-xL levels.
26	11141501	The regulation of Bcl-xL by HGF was mediated by the PI3'-K but not by the MEK-1 pathway.
27	11141501	Apoptosis was prevented by pretreatment with HGF but not IGF-I.
28	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).
29	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.
30	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.