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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 IGF1 1 hits
5 PDGFA 1 hits
6 PDGFB 1 hits
7 TF 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 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.
4 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.
5 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.
6 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.
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 Hepatocyte growth factor, but not insulin-like growth factor I, protects podocytes against cyclosporin A-induced apoptosis.
10 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.
11 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.
12 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.
13 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.
14 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.
15 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.
16 11141501 A murine podocyte cell line was treated with CsA in the presence or absence of HGF or IGF-I.
17 11141501 A murine podocyte cell line was treated with CsA in the presence or absence of HGF or IGF-I.
18 11141501 Apoptosis was quantitated by ELISA and by flow cytometry; Bcl-xL, Fas, and Fas-ligand were measured by Western blotting.
19 11141501 Apoptosis was quantitated by ELISA and by flow cytometry; Bcl-xL, Fas, and Fas-ligand were measured by Western blotting.
20 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.
21 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.
22 11141501 HGF, but not IGF-I, prevented apoptosis and restored Bcl-xL levels.
23 11141501 HGF, but not IGF-I, prevented apoptosis and restored Bcl-xL levels.
24 11141501 The regulation of Bcl-xL by HGF was mediated by the PI3'-K but not by the MEK-1 pathway.
25 11141501 The regulation of Bcl-xL by HGF was mediated by the PI3'-K but not by the MEK-1 pathway.
26 11141501 Apoptosis was prevented by pretreatment with HGF but not IGF-I.
27 11141501 Apoptosis was prevented by pretreatment with HGF but not IGF-I.