Ignet

Gene Information

Gene symbol: EGF

Gene name: epidermal growth factor

HGNC ID: 3229

Related Genes

#	Gene Symbol	Number of hits
1	AGT	1 hits
2	AKT1	1 hits
3	AREG	1 hits
4	AURKA	1 hits
5	BTC	1 hits
6	CDKN1A	1 hits
7	CDKN1B	1 hits
8	CDKN2A	1 hits
9	COL1A1	1 hits
10	COL1AR	1 hits
11	CYSLTR2	1 hits
12	DGKA	1 hits
13	DGKB	1 hits
14	EGFR	1 hits
15	FGF2	1 hits
16	FOS	1 hits
17	GLP1R	1 hits
18	GRB2	1 hits
19	HBEGF	1 hits
20	ICAM1	1 hits
21	IDE	1 hits
22	IFNG	1 hits
23	IGF1	1 hits
24	INS	1 hits
25	INSR	1 hits
26	IRS1	1 hits
27	IRS2	1 hits
28	KSR1	1 hits
29	MAPK1	1 hits
30	MYC	1 hits
31	NAMPT	1 hits
32	NEUROG3	1 hits
33	NPPA	1 hits
34	NPR3	1 hits
35	PDGFA	1 hits
36	PIK3CA	1 hits
37	PIK3R1	1 hits
38	PLAT	1 hits
39	PRKCA	1 hits
40	PRL	1 hits
41	PTK2B	1 hits
42	PTPN1	1 hits
43	PTPN11	1 hits
44	PTPRF	1 hits
45	RAF1	1 hits
46	RPS27A	1 hits
47	RPS6KB1	1 hits
48	SGK1	1 hits
49	SHC1	1 hits
50	SLC15A2	1 hits
51	SLC9A3	1 hits
52	TGFA	1 hits
53	TGFB1	1 hits
54	TNF	1 hits
55	TRH	1 hits
56	TRHR	1 hits
57	UBASH3B	1 hits
58	UMOD	1 hits
59	VCAM1	1 hits

Related Sentences

#	PMID	Sentence
1	6380310	Addition of 1 microM insulin during the culture period led to a 30% decrease in subsequent 125I-insulin binding; the presence or absence of either epidermal growth factor or carbachol was without effect on insulin binding.
2	3530724	The receptors were highly specific for insulin, with 60% inhibition of insulin binding by an antireceptor antibody, no competition by epidermal growth factor, and an ED50 of 300 nM for proinsulin.
3	2950929	Serum EGF concentrations measured were almost the same among the control, diabetic, and insulin-treated diabetic groups.
4	2950929	These results suggest that insulin deficiency in vivo causes a decrease in hepatic EGF receptors.
5	3297960	Class II expression by thyrocytes can be induced by interferon-gamma, and is positively and negatively regulated by thyroid-stimulating hormone and epidermal growth factor, respectively.
6	2957293	Serum EGF concentrations measured were almost the same among the control, diabetic, and insulin-treated diabetic groups.
7	2957293	These results suggest that insulin deficiency in vivo causes a decrease in hepatic EGF receptors.
8	2833110	To determine if other tyrosine kinases might be altered, we have studied the epidermal growth factor (EGF) receptor kinase in wheat germ agglutinin-purified, Triton X-100-solubilized liver membranes from streptozotocin (STZ)-induced diabetic rats and the insulin-deficient BB rat.
9	2833110	A parallel decrease in EGF receptor phosphorylation was also found by immunoblotting with an anti-phosphotyrosine antibody.
10	2833110	Thus autophosphorylation of EGF receptor, like that of the insulin receptor, is decreased in insulin-deficient rat liver.
11	2458910	Dexamethasone-induced changes in insulin and epidermal growth factor (EGF) receptor number, autophosphorylation, and kinase activity were studied in intact rat hepatocytes.
12	2458910	Dexamethasone had no effect on insulin receptor number, while EGF receptor binding was slightly increased (21.3% vs. 17.2% binding/10(6) cells) after dexamethasone treatment.
13	2458910	Our data indicate that glucocorticoids modulate insulin and EGF receptor kinase activity, but the nature of their effect depends on other factors, including the dietary state of the animal.
14	3048255	Alpha lactalbumin activity can be induced to some extent in pregnant rat mammary explants by insulin and hydrocortisone alone, and to a greater extent with prolactin in addition, or with EGF in addition.
15	3048255	Physiological levels of progesterone markedly inhibit the induction in the presence of prolactin plus insulin and hydrocortisone, only weakly inhibit in the presence of insulin and hydrocortisone alone, and have no inhibitory effect in the presence of EGF plus insulin and hydrocortisone.
16	3048255	Prolactin permits some inhibition in the presence of EGF.
17	3264011	Furthermore, while both inhibit prolactin-mediated induction of alpha-lactalbumin in rabbit mammary explants, cortisol converts EGF into a stimulatory agent, but merely blocks the inhibitory effect of serum albumin.
18	2647487	Production of milk proteins can be induced in vitro by the synergistic interactions of prolactin, insulin, and glucocorticoids and is inhibited by EGF and progesterone.
19	2525915	Daily administration of insulin to the streptozotocin-induced diabetic mice increased the hepatic levels of EGF receptor messenger RNAs to almost normal levels.
20	2525915	These results indicate that EGF binding to its receptor decreases in the liver of diabetic mice, involving alterations in the level of EGF receptor messenger RNAs, and that insulin is important for the regulation of EGF receptor gene expression in the liver but not in the kidney.
21	2808704	Maximal epidermal growth factor (EGF) binding was reduced in fibroblasts from three unrelated patients with leprechaunism (Ark-1, Can-1, and Minn-1) compared with control (0.8-2.2%/mg protein vs. 5.5%/mg protein).
22	2808704	Sphingosine (40 microM), a protein kinase C inhibitor, increased EGF receptor affinity twofold in control cells and six- to nine-fold in cells of leprechaunism.
23	2164373	The EGF and insulin promoted a 202% increase over controls in collagen synthesis by day 15, while diabetic rats that received EGF or insulin alone had significantly less collagen than controls.
24	2164373	All groups that received insulin had lower collagenase activity than both controls and diabetic rats that received EGF.
25	2164373	The individual effects of insulin and EGF added synergistically for a net gain in wound collagen content after 15 days.
26	2200528	FGF responses were abolished, EGF responses were partially inhibited, whereas the response to insulin was unaffected.
27	2169527	Continuous topical application of epidermal growth factor (EGF) to granulation tissue increases the rate of collagen accumulation.
28	1702773	Likewise AFGF and EGF caused no significant change of t-PA levels.
29	1850348	We examined the effects of EGF on basal and angiotensin II (AII)-induced aldosterone synthesis in freshly isolated rat and cultured human adrenal glomerulosa cells.
30	1922015	Agents such as epidermal growth factor, insulin and platelet derived growth factor which stimulate their respective receptor-PTK activities were without effect on PTK activities of mammary carcinoma.
31	1766505	Urine EGF was 119 +/- 7.9 ng/day at day 7 in the control rats but it was significantly increased from day 2 in the diabetic rats (320 +/- 52.9 ng/day at day 2 and 298 +/- 18.4 ng/day at day 7), while in the insulin-treated rats it was significantly less than that in the diabetic rats (134 +/- 8.34 ng/day at day 2 and 220 +/- 15.2 ng/day at day 7).
32	1730782	The exact relationship between EGF-stimulated tyrosine phosphorylation, induction of the cellular proto-oncogenes c-myc and c-fos, and DNA synthesis remains uncertain.
33	1730782	They also suggest that, in MDCK cells, the EGF dependent induction of the c-fos and c-myc genes is not strictly correlated to the extent of EGF receptor autophosphorylation or EGF-stimulated DNA synthesis, and that EGF stimulation of DNA synthesis likely involves additional rate-limiting intermediate steps.
34	1532938	These data demonstrate that the reduced number of hepatocyte surface EGF receptors results from an inhibition of EGF-receptor synthesis which is not compensated by a reduced internalization rate.
35	1572403	TGF-beta at 1 ng/ml inhibited at least 50% of the effects of 20 ng/ml EGF and of 10 ng/ml IGF-I, whereas inhibition of the effect of 10 ng/ml PDGF required 10 ng/ml of TGF-beta.
36	1572403	The concentration of TGF-beta needed to inhibit 50% of the combined effect of EGF, IGF-1, and PDGF was 5 ng/ml.
37	1599438	Despite having only 30-39% sequence identity in their catalytic domains, LAR and PTPase 1B had similar relative activities between the peptide substrate and intact insulin receptors, and also displayed similar initial rates of simultaneous dephosphorylation of insulin and epidermal growth factor (EGF) receptors.
38	8380406	The insulin receptor possesses tyrosine kinase activity which is thought to mediate the biological effects of insulin upon target cells. pp120 is a liver-specific glycoprotein of apparent molecular size of 120 kDa that is phosphorylated on tyrosine residues by the receptors for insulin, insulin-like growth factor-I, and epidermal growth factor.
39	8425916	Treatment of Swiss 3T3 fibroblasts with basic fibroblast growth factor (bFGF) lead to a rapid reduction in epidermal growth factor (EGF) binding and a slower inhibition of EGF receptor autophosphorylation.
40	8253016	On day 16 the EGF concentration in milk was significantly increased in insulin-treated rats, as compared to controls [2.66 (1.40-5.08) nM vs. 1.98 (1.04-3.16) nM].
41	8134187	These results indicate that insulin deficiency in lactating rats causes a decrease in the lactational performance and in the EGF content of milk.
42	7561890	Because of its relationship to epidermal growth factor (EGF) and the heregulins, it was asked if SDGF interacts with the EGF receptor or HER2/neu.
43	7561890	SDGF binds to and causes the phosphorylation on tyrosine of the EGF receptor but not HER2/neu.
44	8662948	In contrast, ligand-stimulated EGF receptor phosphorylation in CHO/EGF-R cells was not affected by the presence of stearyl 3S-peptide-I.
45	8910437	However, Grb2 association with IRS-1 could not be detected in the basal or insulin-stimulated states, and mitogen-activated protein kinase (MAPK) activity could not be stimulated by insulin, epidermal growth factor, or platelet-derived growth factor.
46	8910437	By contrast, association of Grb2 with Shc and activation of MAPK, but not the p70 S6 kinase, could be stimulated by epidermal growth factor or platelet-derived growth factor.
47	9015760	In order to determine whether the effects of TNF-alpha might involve alterations in the expression of specific protein-tyrosine phosphatases (PTPases) that have been implicated in the regulation of growth factor receptor signalling, KRC-7 rat hepatoma cells were treated with TNF-alpha, and changes in overall tissue PTPase activity and the abundance of three major hepatic PTPases (LAR, PTP1B, and SH-PTP2) were measured in addition to effects of TNF-alpha on ligand-stimulated autophosphorylation of insulin and epidermal growth factor (EGF) receptors and insulin-stimulated insulin receptor substrate-1 (IRS-1) phosphorylation.
48	9015760	Since SH-PTP2 has been shown to interact directly with both the EGF receptor and IRS-1, increased abundance of this PTPase, may mediate the TNF-alpha effect to inhibit signalling through these proteins.
49	10683311	After an overnight incubation with EGF the TM(-) EGFR accumulated in the nucleus.
50	10683311	In mouse NR6 cells, which lack endogenous EGFR, transfected TM(-) EGFR were found in the cytoplasm, but incubation with EGF did not result in a nuclear accumulation of TM(-) EGFR.
51	11275564	FNCBD-EGF substantially stimulated cell growth after binding to collagen-coated culture plates, whereas EGF had no effect, indicating that this fusion protein acted as a collagen-associated growth factor.
52	11274179	Dominant negative mutants of these proteins block activation of Raf-1 by nocodazole, but not by epidermal growth factor (EGF).
53	11274179	Collectively, our results indicate that 1) the zinc finger exerts an inhibitory effect on Raf-1 activation, probably by preventing phosphorylation of (338)SSYY(341); 2) such inhibition is first overcome by an unknown factor binding in place of Ras-GTP to the amino-terminal regulatory region in response to nocodazole; and 3) EGF and nocodazole utilize different kinases to phosphorylate Ser(338), an event crucial for Raf activation.
54	11415460	Epidermal growth factor and alpha-thrombin stimulated total DGK activity similarly to PDGF.
55	11415460	Activation by epidermal growth factor was sensitive to R59949, again suggesting involvement of DGKalpha.
56	11420912	The excretion rate of EGF was increased at diagnosis, while that of THP was not.
57	11420912	After 20 days of treatment the excretion of EGF had normalized, while the excretion of THP was decreased.
58	11903419	EGF levels were not related to IUGR, and TGF-beta levels increased only during the first 3 months in the IUGR group.
59	11916914	Transforming growth factor (TGF)-alpha- and epidermal growth factor (EGF)-induced signal transduction was directly compared with that of glucose and insulin-like growth factor-1 (IGF-1) in INS-1 cells.
60	12138086	The ability of the growth factors epidermal growth factor (EGF), transforming growth factor alpha, and platelet-derived growth factor to exert insulin-like effects on glucose transport and lipolysis were examined in human and rat fat cells.
61	12138086	No effects were found in rat fat cells, whereas EGF (EC(50) for glucose transport approximately 0.02 nm) and transforming growth factor alpha (EC(50) approximately 0.2 nm), but not platelet-derived growth factor, mimicked the effects of insulin (EC(50) approximately 0.2 nm) on both pathways.
62	12138086	EGF increased the tyrosine phosphorylation of several proteins (the EGF receptor, insulin receptor substrate (IRS)-1, IRS-2, and Grb2-associated binder 1), whereas Shc and Gab2 were only weakly and inconsistently phosphorylated. p85, the regulatory subunit of phosphatidylinositol 3-kinase (PI 3-kinase), was also found to associate with all of these docking molecules, showing that EGF activated PI 3-kinase pools that were additional to those of insulin.
63	12138086	EGF mimics the effects of insulin on both the metabolic and mitogenic pathways but utilize in part different signaling pathways.
64	12138086	Both insulin and EGF increase the tyrosine phosphorylation and activation of IRS-1 and IRS-2, whereas EGF is also capable of activating additional PI 3-kinase pools and, thus, can augment the downstream signaling of insulin in insulin-resistant states like Type 2 diabetes.
65	12688387	The present study aimed to determine whether pharmacological treatment with gastrin and EGF can significantly stimulate beta-cell regeneration in chronic, severe insulin-dependent diabetes.
66	12663464	Hence, we investigated the stimulation of PI3K and Akt-1, -2, and -3 by insulin and epidermal growth factors (EGFs) in skeletal muscles from lean and obese insulin-resistant humans.
67	12663464	In contrast, insulin- or EGF-stimulated phosphotyrosine-associated PI3K activity was not different between lean and obese muscles.
68	12816347	Studies on receptor-mediated regulation has shown that both PepT1 and PepT2 is down-regulated by long-term exposure to epidermal growth factor (EGF) due to a decreased gene transcription.
69	15171688	In addition, TRH induced epidermal growth factor (EGF) receptor phosphorylation with a half-maximum concentration of approximately 50 nM, whereas the high affinity analogue of TRH, MeTRH, was 1 nM.
70	15171688	This suggested that the affinity of TRH ligands for the TRH receptor influences the activation of EGF receptor phosphorylation in betaTC-6 cells.
71	16954185	AGE responses also included EGF receptor (EGFR) phosphorylation in MCs or HEK293 cells, but this link was blocked in both MC-R1 and HEK293-R1 cells.
72	16514419	Inhibition of EGF and LIF signalling by pharmacological antagonists of the JAK2/STAT3 pathway, or knockdown of Ngn3 by RNA interference prevented the generation of new insulin-positive cells.
73	18053093	However, the role of EGF in regulating the major function of the pancreas, insulin secretion, has not been studied.
74	18053093	Here, we show that EGF rapidly increased insulin secretion in mouse pancreatic islets, as well as in a pancreatic beta-cell line.
75	18053093	In addition, EGF also increased plasma insulin levels and mediated glucose lowering in normal and diabetic mice.
76	18571697	Epidermal growth factor (EGF) stimulated [(35)S]sulfate incorporation and increased proteoglycan size and this was completely blocked by the EGF receptor tyrosine kinase inhibitor AG1478.
77	19896952	Furthermore, IDE exhibits a remarkable ability to preferentially degrade structurally similar peptides such as the selective degradation of insulin-like growth factor (IGF)-II and transforming growth factor-alpha (TGF-alpha) over IGF-I and epidermal growth factor, respectively.
78	20440273	Adhesion and migration of MSCs on cultured endothelial cells were ICAM1-, VCAM1- and Akt-dependent mechanism and elevated when MSCs were prestimulated with EGF compared with nonstimulated MSCs.
79	20692412	Reverse transcriptase polymerase chain reaction (RT-PCR) analysis revealed that insulin-like growth factor-1 (IGF-1), epidermal growth factor (EGF), and Exendin-4 significantly increased the expression of the transcription factor neurogenin-3, whereas the expressions of pancreatic and duodenal homeobox 1 (PDX-1), neurogenic differentiation 1 (NeuroD) were increased only among samples treated with ZnCl2 and not significantly affected by treatment with the tested growth factors.
80	21070952	This demonstrates that the PSAP motif is not rate determining in EGF receptor downregulation under normal conditions.
81	20946955	Furthermore, dephosphorylation of the scaffold protein, KSR, at a critical serine residue is also synergistically promoted by GH and EGF, suggesting that GH sensitizes these cells to EGF-induced ERK activation by augmenting the actions of KSR in facilitating MEK-ERK activation.
82	21031338	It could be shown that the applied anabolic combination significantly influenced the expression of the steroid receptor ER?, the keratinization factor CK8, the proinflammatory interleukins IL-1? and IL-1?, the growth factors FGF7, EGF, EGFR, IGF-1R, TGF? and LTF, the oncogen c-jun and other factors like actin? and ubiquitin 3.
83	11457715	The EGF effect depended on activation of its receptor tyrosine kinase but not on that of protein kinase C, mitogen-activated protein kinases, or phosphoinositide-3 kinase.
84	11457715	These studies suggest that EGF potentiates the ANP glomerular effects in diabetes by inhibition of its degradation by mesangial NPR-C via a mechanism involving AP-1.
85	15769977	Gastrin, alone or in combination with EGF, but not EGF alone, increased the expression of pancreatic and duodenal homeobox factor-1 as well as insulin and C peptide in the cytokeratin 19-positive duct cells.
86	17270172	Our results suggest that quiescence of small cells correlates with up-regulation of Cdk inhibitors p27(Kip1), p16(INK4a) and p21(CIP1), PTEN, Hep27 and Foxo1a and with down-regulation of c-Myc and the receptors for EGF, FGF2 and HGF.
87	21660636	Circulating concentrations of angiogenin, angiopoietin-1, platelet derived endothelial factor (PDGF)-AA, matrix metalloproteinase (MMP) 8 and 9, endothelial growth factor (EGF) and vascular EGF (VEGF) were also measured.
88	21814117	The application of sNAG membranes to wounds 24 hours before application of the VAC device was associated with a significant activation of wounds (expression of PDGF, TGF?, EGF), superior granulation tissue formation rich in Collagen I as well as superior wound epithelialization (8.6% � 0.3% vs. 1.8% � 1.1% of initial wound size) and wound contraction.
89	21897861	Immunoprecipitation and western blotting analysis showed that BTC treatment of MIN-6 cells induced phosphorylation of only ErbB-1 and ErbB-2 among the four EGF receptors.
90	21628885	We quantified mRNA for six adipocytokine genes: adiponectin, resistin, leptin, plasminogen activator inhibitor 1 (PAI-1), heparin-binding epidermal growth factor (EGF)-like growth factor (HB-EGF), and visfatin, in adipose tissue, in primary cultured adipocytes obtained from an obese Zucker rat, and in the preadipocyte cell line 3T3-L1.
91	12502502	We hypothesized that the GLP-1R could activate PI 3-kinase and promote beta-cell proliferation through transactivation of the epidermal growth factor (EGF) receptor (EGFR), an event possibly linked to GPCRs via activation of c-Src and the production of putative endogenous EGF-like ligands.
92	12502502	The results are consistent with a model in which GLP-1 increases PI 3-kinase activity and enhances beta-cell proliferation via transactivation of the EGFR that would require the proteolytic processing of membrane-anchored BTC or other EGF-like ligands.
93	16105029	As the epidermal growth factor (EGF) receptor is activated by both EGF and other factors implicated in diabetic nephropathy, the relationship of SGK-1 with EGFR activity was assessed. mRNA and protein expression of SGK-1 and mRNA expression of the sodium hydrogen exchanger NHE3 were measured in human PTCs exposed to 5 mmol/L (control) and 25 mmol/L (high) glucose.
94	16105029	A total of 25 mmol/L glucose and EGF (10 ng/mL) increased SGK-1 mRNA (P < 0.005 and P < 0.002, respectively) and protein (both P < 0.02) expression.
95	16105029	No EGF protein was detectable in PTCs, suggestive of phosphorylation of the EGFR by high glucose and downstream induction of SGK-1.