Ignet

Gene Information

Gene symbol: FGR

Gene name: Gardner-Rasheed feline sarcoma viral (v-fgr) oncogene homolog

HGNC ID: 3697

Synonyms: c-fgr, p55c-fgr

Related Genes

#	Gene Symbol	Number of hits
1	CCDC91	1 hits
2	CREBBP	1 hits
3	EP300	1 hits
4	ESR1	1 hits
5	GORASP2	1 hits
6	HCK	1 hits
7	IGF1	1 hits
8	LYN	1 hits
9	NCOA1	1 hits
10	NCOA2	1 hits
11	NCOA3	1 hits
12	NR0B1	1 hits
13	PAG1	1 hits
14	SRC	1 hits
15	TNFRSF1A	1 hits
16	TP53	1 hits

Related Sentences

#	PMID	Sentence
1	11160694	Soluble mediators such as interleukin-1beta, tumor necrosis factor alpha (TNF-alpha), and inducible nitric oxide synthase (iNOS) produced from activated macrophages play an important role in the destruction of pancreatic beta cells in mice infected with a low dose of the D variant of encephalomyocarditis (EMC-D) virus.
2	11160694	We examined the activation of p59/p56(Hck), p55(Fgr), and p56/p53(Lyn) in macrophages from DBA/2 mice infected with the virus.
3	11160694	We found that p59/p56(Hck) showed a marked increase in both autophosphorylation and kinase activity at 48 h after infection, whereas p55(Fgr) and p56/p53(Lyn) did not.
4	11160694	The p59/p56(Hck) activity was closely correlated with the tyrosine phosphorylation level of Vav.
5	11160694	Treatment of EMC-D virus-infected mice with the Src kinase inhibitor, PP2, resulted in the inhibition of p59/p56(Hck) activity and almost complete inhibition of the production of TNF-alpha and iNOS in macrophages and the subsequent prevention of diabetes in mice.
6	11160694	On the basis of these observations, we conclude that the Src kinase, p59/p56(Hck), plays an important role in the activation of macrophages and the subsequent production of TNF-alpha and nitric oxide, leading to the destruction of pancreatic beta cells, which results in the development of diabetes in mice infected with a low dose of EMC-D virus.
7	11160694	Soluble mediators such as interleukin-1beta, tumor necrosis factor alpha (TNF-alpha), and inducible nitric oxide synthase (iNOS) produced from activated macrophages play an important role in the destruction of pancreatic beta cells in mice infected with a low dose of the D variant of encephalomyocarditis (EMC-D) virus.
8	11160694	We examined the activation of p59/p56(Hck), p55(Fgr), and p56/p53(Lyn) in macrophages from DBA/2 mice infected with the virus.
9	11160694	We found that p59/p56(Hck) showed a marked increase in both autophosphorylation and kinase activity at 48 h after infection, whereas p55(Fgr) and p56/p53(Lyn) did not.
10	11160694	The p59/p56(Hck) activity was closely correlated with the tyrosine phosphorylation level of Vav.
11	11160694	Treatment of EMC-D virus-infected mice with the Src kinase inhibitor, PP2, resulted in the inhibition of p59/p56(Hck) activity and almost complete inhibition of the production of TNF-alpha and iNOS in macrophages and the subsequent prevention of diabetes in mice.
12	11160694	On the basis of these observations, we conclude that the Src kinase, p59/p56(Hck), plays an important role in the activation of macrophages and the subsequent production of TNF-alpha and nitric oxide, leading to the destruction of pancreatic beta cells, which results in the development of diabetes in mice infected with a low dose of EMC-D virus.
13	19000767	Thyroid hormones exert most of their physiological effects through two thyroid hormone receptor (TR) subtypes, TRalpha and TRbeta, which associate with many transcriptional coregulators to mediate activation or repression of target genes.
14	19000767	Here, we present a new methodology which employs surface plasmon resonance to investigate the interactions between TRbeta ligand binding domain (LBD) complexes and peptides derived from the nuclear receptor interaction motifs of two of its coregulators, SRC2 and DAX1.
15	19926790	We describe widely applicable, calibrated Förster resonance energy transfer methods that quantify structural and biochemical parameters for interaction of the human estrogen receptor alpha-isoform (ER alpha) with the receptor interacting domains (RIDs) of three cofactors (SRC1, SRC2, SRC3) in living cells.
16	23719562	Insulin-like growth factor 1 mRNA expression in the uterus of streptozotocin-treated diabetic mice.
17	23719562	We aimed to clarify the changes in the estrous cycle and in insulin-like growth factor 1 (IGF1) expression in the uteri of streptozotocin (STZ)-treated diabetic mice, because IGF1 is one of the main growth factors involved in estrogen-induced uterine growth.
18	23719562	Estrogen is known to stimulate Igf1 mRNA expression in the uterus, but estrogen action was abolished in the uteri of STZ-treated diabetic mice. mRNA expressions of estrogen receptor α (ERα) and steroid hormone receptor coactivators (SRC-1/Ncoa1, SRC-2/Ncoa2, SRC-3/Ncoa3 and CBP/p300/Crebbp) were reduced in the uteri of ovariectomized STZ-treated diabetic mice.
19	23719562	Igf1 expression in ovariectomized diabetic female mice was decreased, and decreased responsiveness to estrogen in the uteri of diabetic mice is probably associated with a reduction in ERα and steroid receptor coactivator mRNA expression.