Ignet

Gene Information

Gene symbol: ESR1

Gene name: estrogen receptor 1

HGNC ID: 3467

Synonyms: NR3A1, Era

Related Genes

#	Gene Symbol	Number of hits
1	ADIPOQ	1 hits
2	ADIPOR1	1 hits
3	AGRP	1 hits
4	AKT1	1 hits
5	ALB	1 hits
6	AR	1 hits
7	CAV3	1 hits
8	CREBBP	1 hits
9	CRP	1 hits
10	CTLA4	1 hits
11	CYP19A1	1 hits
12	EDN1	1 hits
13	EP300	1 hits
14	ERAL1	1 hits
15	ESR2	1 hits
16	FGF3	1 hits
17	FGR	1 hits
18	FOXC2	1 hits
19	GPER	1 hits
20	HBB	1 hits
21	HSD17B7	1 hits
22	IDDM4	1 hits
23	IDDM5	1 hits
24	IDDM8	1 hits
25	IDE	1 hits
26	IGF1	1 hits
27	INS	1 hits
28	KRT124P	1 hits
29	LEP	1 hits
30	LPAL2	1 hits
31	MLH1	1 hits
32	MT1A	1 hits
33	NCOA1	1 hits
34	NCOA2	1 hits
35	NCOA3	1 hits
36	NFKB1	1 hits
37	NMBR	1 hits
38	NOS2A	1 hits
39	NOS3	1 hits
40	NPY	1 hits
41	OPRM1	1 hits
42	PAG1	1 hits
43	PARK2	1 hits
44	PGR	1 hits
45	POMC	1 hits
46	PPARA	1 hits
47	PPARG	1 hits
48	PRKCA	1 hits
49	PTGS2	1 hits
50	RARA	1 hits
51	RXRB	1 hits
52	SHBG	1 hits
53	SLC17A5	1 hits
54	SRC	1 hits
55	STAT5B	1 hits
56	TNF	1 hits
57	TRIB3	1 hits
58	UCP2	1 hits
59	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	1608968	Here we demonstrate that both HRE binding and the transcriptional inducing activities of one member of this family, TH receptor, were markedly enhanced by heterodimerization with H-2RIIBP, a non-TH-binding member of the steroid hormone receptor superfamily.
2	2809426	The relationship between the erythrocyte sedimentation rate (ESR), glycosylated hemoglobin, and the concentrations of plasma proteins was investigated in 34 outpatients with diabetes mellitus.
3	2809426	The ESR was found to be significantly elevated, the degree of elevation correlating with the serum globulin concentration, the albumin-globulin ratio, the serum fibrinogen concentration, and the percent glycosylated hemoglobin (HbA1c).
4	3238359	The IgG-RF activity in the ELISA appears to be a good parameter for the course control of RA under gold therapy. 10 RA patients with clinical improvement of disease (declining ESR, CRP, joint index) after six months of gold therapy (= 0.6 g total gold amount) had a decline of total RF activity of 70% in median, whereas 10 patients with no clear effect on disease activity had only a decline of 20% in median.
5	8875250	It is recognized that the MHC contains multiple susceptibility loci (referred to collectively as IDDM1), including the class II antigen receptor genes, which control the major pathological feature of the disease: T-lymphocyte-mediated autoimmune destruction of the insulin-producing pancreatic beta cells.
6	8875250	However, the MHC genes, and a second locus, the insulin gene minisatellite on chromosome 11p15 (IDDM2; lambda S = 1.25), cannot account for all of the observed clustering of disease in families (lambda S = 15), and the scans suggested the presence of other susceptibility loci scattered throughout the genome.
7	8875250	There are four additional loci for which there is currently sufficient evidence from linkage and association studies to justify fine mapping experiments: IDDM4 (FGF3/11q13), IDDM5 (ESR/6q22), IDDM8 (D6S281/6q27) and IDDM12 (CTLA-4/2q33).
8	8875250	IDDM4, 5 and 8 were detected by genome scanning, and IDDM12 by a candidate gene strategy.
9	8875250	The identification of aetiological determinants requires exclusion of hitchhiking polymorphisms in regions of linkage disequilibrium, as demonstrated for the MHC and the insulin gene loci, and functional studies implicating the disease-associated variant in pathogenesis.
10	9296067	It is recognised that the MHC contains multiple susceptibility loci (referred to collectively as IDDM1), including the class II antigen receptor genes, which control the major pathological feature of the disease: T lymphocyte-mediated autoimmune destruction of the insulin-producing pancreatic beta cells.
11	9296067	However, the MHC genes, and a second locus, the insulin gene minisatellite on chromosome 11p15 (IDDM2; lambda s = 1.25), cannot account for all of the observed clustering of disease in families (lambda s = 15), and the scans suggested the presence of other susceptibility loci scattered throughout the genome.
12	9296067	There are four additional loci for which there is currently sufficient evidence from linkage and association studies to justify fine mapping experiments: IDDM4 (FGF3/11q13), IDDM5 (ESR/6q22), IDDM8 (D6S281/6q27) and IDDM12 (CTLA-4/2q33), IDDM4, 5 and 8 were detected by genome scanning, and IDDM12 by a candidate gene strategy.
13	9388356	Diabetes mellitus and inflammatory reaction such as high fervor, leukocytosis, CRP and ESR accentuation were recognized.
14	9793760	Most evidence supports IDE as the primary degradative mechanism, but other systems (PDI, lysosomes, and other enzymes) undoubtedly contribute to insulin metabolism.
15	9793760	IDE increases proteasome and steroid hormone receptor activity, and this activation is reversed by insulin.
16	9793760	This raises the possibility of a direct intracellular interaction of insulin with IDE that could modulate protein and fat metabolism.
17	9881241	Thus, it would appear that catecholoestrogens suppress islet insulin release via alpha 2-adrenergic receptors, which suggests that oestrogens may exert a dual modulatory effect on insulin secretion by enhancing release via direct interaction with the cytosolic-oestrogen receptor and inhibiting release after their local hydroxylation and the interaction of their new catechol moiety with alpha 2-adrenergic receptors.
18	10432218	Stable over-expression of estrogen receptor-alpha in ECV304 cells inhibits proliferation and levels of secreted endothelin-1 and vascular endothelial growth factor.
19	10432218	Effects of this over-expression were studied on the cell growth rate, and on the levels of secreted endothelin-1 and vascular endothelial growth factor (VEGF).
20	10432218	Our ER-over-expressing clone of ECV304 also showed an inhibition of secreted endothelin-1 and VEGF levels.
21	10432218	Moreover, the growth inhibition of this ER-over-expressing clone was reversed by the addition of endothelin-1 or VEGF to the medium.
22	10432218	In view of the growth-stimulatory effect of endothelin-1 and VEGF on vascular cells, our results indicate that estrogen receptor-alpha may bring about its growth inhibition partly by suppressing endothelin-1 and/or VEGF production in ECV304 cells.
23	10432218	Stable over-expression of estrogen receptor-alpha in ECV304 cells inhibits proliferation and levels of secreted endothelin-1 and vascular endothelial growth factor.
24	10432218	Effects of this over-expression were studied on the cell growth rate, and on the levels of secreted endothelin-1 and vascular endothelial growth factor (VEGF).
25	10432218	Our ER-over-expressing clone of ECV304 also showed an inhibition of secreted endothelin-1 and VEGF levels.
26	10432218	Moreover, the growth inhibition of this ER-over-expressing clone was reversed by the addition of endothelin-1 or VEGF to the medium.
27	10432218	In view of the growth-stimulatory effect of endothelin-1 and VEGF on vascular cells, our results indicate that estrogen receptor-alpha may bring about its growth inhibition partly by suppressing endothelin-1 and/or VEGF production in ECV304 cells.
28	10655475	We constructed a model of the inactive conformation of human retinoic acid receptor-alpha by using information derived from antagonist-bound estrogen receptor-alpha and applied a computer-based virtual screening algorithm to identify retinoic acid receptor antagonists.
29	10828087	Peroxisome proliferator-activated receptor alpha (PPARalpha) is a member of the steroid hormone receptor super family involved in the control of cellular lipid utilization.
30	10861205	Regulation of sterol regulatory-element binding protein 1 gene expression in liver: role of insulin and protein kinase B/cAkt.
31	10861205	Insulin stimulates the transcription of the sterol regulatory- element binding protein (SREBP) 1/ADD1 gene in liver.
32	10861205	Hepatocytes in primary culture were used to delineate the insulin signalling pathway for induction of SREBP1 gene expression.
33	10861205	The inhibitors of phosphoinositide 3-kinase (PI 3-kinase), wortmannin and LY 294002, abolished the insulin-dependent increase in SREBP1 mRNA, whereas the inhibitor of the mitogen- activated protein kinase cascade, PD 98059, was without effect.
34	10861205	To investigate the role of protein kinase B (PKB)/cAkt downstream of PI 3-kinase, hepatocytes were transduced with an adenovirus encoding a PKB--oestrogen receptor fusion protein.
35	10861205	The addition of OHT to transduced hepatocytes resulted in accumulation of SREBP1 mRNA, with a time-course and magnitude similar to the effect of insulin in non-transduced cells.
36	10861205	The level of SREBP1 mRNA was not increased by OHT in hepatocytes expressing a mutant form of the recombinant protein whose PKB activity was not activated by OHT.
37	10861205	Thus acute activation of PKB is sufficient to induce SREBP1 mRNA accumulation in primary hepatocytes, and might be the major signalling event by which insulin induces SREBP1 gene expression in the liver.
38	11372335	Routine blood work that includes ESR, CRP, and glucose levels, and plain radiographs and knee aspirations are obtained from our patients who have clinical suspicion of infection.
39	11453036	Regulation of estrogen receptor alpha and progesterone receptor (isoform A and B) expression in cultured human endometrial cells.
40	11453036	The effects of RU 486 together with estradiol and progesterone on estrogen receptor alpha and progesterone receptor (isoforms A and B) expression were studied in human endometrial long term cultures at the mRNA and protein level.
41	11453036	Receptor expression (estrogen receptor alpha and progesterone receptor isoform A and B) was examined at the mRNA level by RT-PCR and at the protein level by western blot analysis.
42	11453036	Regulation of estrogen receptor alpha and progesterone receptor (isoform A and B) expression in cultured human endometrial cells.
43	11453036	The effects of RU 486 together with estradiol and progesterone on estrogen receptor alpha and progesterone receptor (isoforms A and B) expression were studied in human endometrial long term cultures at the mRNA and protein level.
44	11453036	Receptor expression (estrogen receptor alpha and progesterone receptor isoform A and B) was examined at the mRNA level by RT-PCR and at the protein level by western blot analysis.
45	11453036	Regulation of estrogen receptor alpha and progesterone receptor (isoform A and B) expression in cultured human endometrial cells.
46	11453036	The effects of RU 486 together with estradiol and progesterone on estrogen receptor alpha and progesterone receptor (isoforms A and B) expression were studied in human endometrial long term cultures at the mRNA and protein level.
47	11453036	Receptor expression (estrogen receptor alpha and progesterone receptor isoform A and B) was examined at the mRNA level by RT-PCR and at the protein level by western blot analysis.
48	11453037	Differential distribution of estrogen receptor-beta and estrogen receptor-alpha in the porcine ovary.
49	11453037	It has been established that besides classical estrogen receptor-alpha (ER alpha) novel forms termed ER beta exist.
50	11453037	Differential distribution of estrogen receptor-beta and estrogen receptor-alpha in the porcine ovary.
51	11453037	It has been established that besides classical estrogen receptor-alpha (ER alpha) novel forms termed ER beta exist.
52	11529880	We previously found that the stable overexpression of oestrogen receptor-alpha in the human endothelial cell line ECV304* inhibits its growth in vitro, and that this inhibition is possibly mediated through a down-regulation of the vasoactive agents endothelin-1 and vascular endothelial growth factor.
53	11800161	The recent discovery of estrogen receptor beta as a biological partner with estrogen receptor alpha in mediating the estrogen response has come at precisely the same time as intensive research is revealing the role played by downstream coregulator proteins in linking nuclear hormone receptor activity to general transcription machinery involved in gene transcriptional activation.
54	11800161	In what is a rapidly evolving area of research, findings to date have led to a proposed model of hormonal action, in which a receptor activated by estrogen or cell-membrane-derived phosphorylation-dependent signaling pathways promotes recruitment of selected members of the multifunctional steroid receptor coactivator family and the cointegrators, p300/CBP and P/CAF.
55	11800161	On the other hand, antiestrogen-bound receptors favour the assembly of receptor-corepressor complexes containing the sequence-related corepressors N-CoR (nuclear receptor corepressor) or SMRT (silencing mediator of retinoid and thyroid hormone receptors), localizing histone deacetylase activity to the promoter and leading to transcriptional repression.
56	15111512	Potential candidate genes include ESR1, OPRM1, and NMBR.
57	15203886	All patients were on sulphonylurea treatment and their hemoglobin A(1c) (HbA(1c)) levels were above 7.5%.
58	15203886	The 2 groups did not differ in terms of treatment, frequency of hypertension, BMI, diabetes duration, age, fasting plasma glucose (FPG), HbA(1c), CRP, ESR, polymorphonuclear leukocyte (PNL) and neutrophil counts.
59	15458395	It is now known that oestrogen receptor, progesterone receptor and androgen receptor exist in adipose tissues, so their actions could be direct.
60	15458395	Leptin and lipoprotein lipase are two key proteins in adipose tissues that are regulated by transcriptional control with sex steroid hormones.
61	15458395	In the phosphoinositide cascade, diacylglycerol and inositol 1,4,5-trisphosphate are formed as second messengers ultimately causing the activation of protein kinase C.
62	16479743	In a six months follow up, patients had clinical improvement, confirmed by physical medical examination, and a statistically significant reduction in ESR and CRP mean values.
63	16646989	These changes were inversely correlated with laboratory changes, especially CRP and ESR.
64	16823992	The European League Against Rheumatism (EULAR) response criteria for PMR comprise a core set of markers for monitoring therapeutic responses in PMR, namely ESR or CRP, the visual analogue scale of patient's pain and physician's global assessment, as well as morning stiffness and the ability to elevate the upper limbs.
65	16949383	ESR1 rs3798577 was significantly associated with circulating estradiol concentrations, indicators of ovarian aging, high-density lipoprotein (HDL) cholesterol, apolipoprotein A-1, insulin sensitivity, and lumbar spine BMD.
66	16949391	SNPs from the genes encoding aromatase (CYP 19), 17beta-hydroxysteroid dehydrogenase (17HSD) type 1, and the estrogen receptors-alpha (ESR1) and -beta (ESR2) were measured.
67	16949391	Selected ESR1 and ESR2 genotypes were associated with insulin sensitivity and metabolic syndrome only in Japanese and Chinese women.
68	16949391	SNPs from the genes encoding aromatase (CYP 19), 17beta-hydroxysteroid dehydrogenase (17HSD) type 1, and the estrogen receptors-alpha (ESR1) and -beta (ESR2) were measured.
69	16949391	Selected ESR1 and ESR2 genotypes were associated with insulin sensitivity and metabolic syndrome only in Japanese and Chinese women.
70	17082313	Both the gene transfer of estrogen receptor alpha using adenovirus and treatment with the protein kinase C inhibitor bisindolylmaleimide I significantly enhanced the effects of 17beta-E2 treatment under high-glucose conditions, whereas these effects were abolished by the estrogen receptor antagonist ICI 182,780 (faslodex).
71	17175982	Body temperature, blood cell count, ESR, CRP, AST, ALT, LDH, CPK, creatine, urea, potassium, sodium, ABG, and ECG were measured on admission and in the 3-rd and 7- th day of therapy.
72	17357885	The effect of diabetes and centrally administered insulin on anterior hypothalamic estrogen receptor alpha immunoreactivity.
73	17367502	Stimulation of the PPARgamma by TZDs interferes with oestrogen receptor signalling, STAT5B and NF-kappaB signalling cascades.
74	17513703	Association of the estrogen receptor-alpha gene with the metabolic syndrome and its component traits in African-American families: the Insulin Resistance Atherosclerosis Family Study.
75	17642242	For evaluation of treatment with TNF inhibitors, RA patients should be determined for the ACR core set of measures, including tender joint count, swollen joint count, pain score, patient global assessment, physician global assessment, patient-reported functional disability, and acute phase reactants (ESR and CRP), and more practically for the 28-joint Disease Activity Score (DAS28) within the first 3-6 months, and the efficacy could be assessed using the ACR preliminary criteria and the EULAR criteria.
76	17642242	Post-marketing surveillance of INF and ETA in Japan indicated that the most serious adverse effects were bacterial pneumonia, pneumocytosis, and interstitial pneumonia, as well as tuberculosis.
77	17642242	So far no clinical predictors of response to TNF inhibitors have been identified, but genetic variation in the HLA-DRB1 and the LTA-TNF regions was shown to influence the response.
78	17714081	Aggregation responses of human platelet-rich plasma to ADP were determined in the absence or presence of 200 mg/L AGE-modified albumin (AGE-albumin), 10(-5) mol/L 17beta-oestradiol and 10(-5) mol/L ICI 182 780 (the pure oestrogen receptor antagonist). 3.
79	17714081	Intraplatelet cGMP, an index of bioactive NO, was measured by radioimmunoassay and expression of nitric oxide synthase (NOS)-3, phosphoserine-1177-NOS-3 and O-glycosylated NOS-3 was quantified by western blotting in response to these same treatments. 4.
80	17714081	Despite no effect on NOS-3 expression, AGE-albumin decreased and 17beta-oestradiol increased phosphoserine-1177-NOS-3 and 17beta-oestradiol largely prevented the decrease in phosphoserine-1177-NOS-3 induced by AGE-albumin.
81	17714081	Alone, AGE-albumin increased O-glycosylation of NOS-3 by N-acetylglucosamine, an effect largely inhibited by 17beta-oestradiol. 5.
82	17714081	In conclusion, AGE-albumin inhibits platelet NO biosynthesis through effects on serine phosphorylation and O-glycosylation of platelet NOS-3 and this may explain, at least in part, the increase in platelet aggregability induced by AGE-albumin.
83	18439911	Ablation of estrogen receptor alpha (ERalpha) prevents upregulation of POMC by leptin and insulin.
84	18439911	We investigated the role of estrogen receptor alpha (ERalpha) in the regulation of the hypothalamic POMC in females.
85	18439911	RT-PCR showed a significant attenuation of POMC expression in both ERaKOAkt and ERaKO mice, irrespective of the elevated leptin serum levels or hyperinsulinemia, while elevated serum leptin levels in AFO and B6FO mice upregulated POMC gene expression.
86	18439911	These results indicate that ERalpha plays an essential role in leptin- and insulin-stimulated upregulation of the POMC gene.
87	18439911	Ablation of estrogen receptor alpha (ERalpha) prevents upregulation of POMC by leptin and insulin.
88	18439911	We investigated the role of estrogen receptor alpha (ERalpha) in the regulation of the hypothalamic POMC in females.
89	18439911	RT-PCR showed a significant attenuation of POMC expression in both ERaKOAkt and ERaKO mice, irrespective of the elevated leptin serum levels or hyperinsulinemia, while elevated serum leptin levels in AFO and B6FO mice upregulated POMC gene expression.
90	18439911	These results indicate that ERalpha plays an essential role in leptin- and insulin-stimulated upregulation of the POMC gene.
91	18560894	Combined analysis of all subjects from both stages revealed nominal associations with 17 SNPs within genes, including suggestive associations in ESR1 and PARK2.
92	18806723	Mouse knockout models suggest a differential effect of oestrogen receptor (ER) alpha and beta on the growth plate, with ER beta possibly being more important in regulating epiphyseal fusion.
93	18806723	Future studies are required to further understand the mechanisms by which ER alpha and ER beta affect growth plate function, while longer term studies of aromatase inhibitor usage, preferably utilising animal models, are required to verify the safety of these compounds.
94	18832649	Distinct roles of estrogen receptor-alpha and beta in the modulation of vascular inducible nitric-oxide synthase in diabetes.
95	18832649	However, extracellular signal-regulated kinase 1/2 signaling was activated by DPN but not by PPT in cytokine-treated SMCs.
96	18832649	Vascular iNOS levels were decreased consistently when adding 1 nM 17beta-estradiol to aortic tissues from ER beta- but not ER alpha-knockout mice.
97	18931023	We tested the hypothesis that 17beta-estradiol (E(2)) has dual effects on the heart, increasing levels of proteins thought to have beneficial cardiovascular effects (e.g. endothelial nitric oxide (NO) synthase (eNOS)) as well as those thought to have detrimental cardiovascular effects (e.g. type 1 angiotensin II (AngII) receptor (AT(1)R)).
98	18931023	Ovariectomized Wistar rats consuming a high-sodium diet received one of four treatments (n=7 per group): group 1, placebo pellets; group 2, E(2) (0 x 5 mg/pellet, 21-day release); group 3, NOS inhibitor, N(omega)-nitro-L-arginine-methyl-ester (L-NAME; 40 mg/kg per day for 14 days) plus Ang II (0 x 225 mg/kg per day on days 11-14); group 4, E(2) plus L-NAME/Ang II.
99	18931023	E(2) increased cardiac levels of estrogen receptors ESR1 and ESR2, an ESR-associated membrane protein caveolin-3, eNOS, and phosphorylated (p)eNOS, thus, exerting potentially beneficial cardiovascular effects on NO.
100	18931023	However, E(2) also increased cardiac levels of proteins associated with cardiovascular injury and inflammation including, AT(1)R, protein kinase C delta (PRKCD), phosphorylated PRKC, and phosphorylated extracellular signal regulated kinase (pMAPK)3/1, plasminogen activator inhibitor-1 (PAI-1), osteopontin and ED-1, a monocyte/macrophage-specific protein.
101	18931023	E(2) treatment led to similar protein changes in the hearts of L-NAME/Ang II-treated rats except that the increase in peNOS was prevented, and L-NAME/Ang II and E(2) had additive effects in increasing cardiac PRKCD and PAI-1.
102	18931023	Thus, the highest levels of cardiac PAI-1 and PRKCD occurred in L-NAME/Ang II-treated rats receiving E(2).
103	19157583	Estrogen receptor alpha (ERalpha) mediates beneficial actions on endothelial nitric oxide synthase (eNOS) and cholesterol metabolism.
104	19533878	Population genetic analyses revealed that disease susceptible variants of SNPs in TRIB3, PTGS2, ADIPOR1, DGAT1, UCP2, FOXC2, and ESR1 were overrepresented in the Palau population in comparison with the Asian populations.
105	19556726	Association of polymorphism of estrogen receptor-alpha gene with circulating levels of adiponectin in postmenopausal women with type 2 diabetes.
106	19687125	Pregnancy is characterized by peripheral insulin resistance, which is developed in parallel with a plasma increase of maternal hormones; these include prolactin, placental lactogens, progesterone and oestradiol among others.
107	19687125	Classical oestrogen receptors ERalpha and ERbeta, as well as the G protein-coupled oestrogen receptor (GPER) seem to be involved in these adaptation changes.
108	19805233	Functional requirement of AgRP and NPY neurons in ovarian cycle-dependent regulation of food intake.
109	19805233	In this study, we show that changes in hypothalamic expression of agouti-related protein (Agrp) and neuropeptide Y (Npy) coincide with the cyclic changes in feeding across the estrous cycle.
110	19805233	Furthermore, E2 treatment suppresses fasting-induced c-Fos activation in AgRP and NPY neurons and blunts the refeeding response.
111	19805233	Surprisingly, although estrogen receptor alpha (ERalpha) is the key mediator of estrogen's anorexigenic effects, we find that expression of ERalpha is completely excluded from AgRP and NPY neurons in the mouse hypothalamus, suggesting that estrogen may regulate these neurons indirectly via presynaptic neurons that express ERalpha.
112	19805233	This study indicates that neurons coexpressing AgRP and NPY are functionally required for the cyclic changes in feeding across estrous cycle and that AgRP and NPY neurons are essential mediators of estrogen's anorexigenic function.
113	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.
114	19997529	We hypothesize that defects in estrogen receptor alpha (ESR1), estrogen receptor beta (ESR2) and/or the androgen receptor (AR) may also contribute to the development of lacrimal gland autoimmune sequelae in Sjögren's syndrome.
115	19997529	To begin to test this hypothesis, we examined whether mutations exist in the coding regions of ESR1, ESR2 and AR transcripts in lacrimal tissues of mouse models of Sjögren's syndrome.
116	19997529	RESULTS: Our results show that almost all ESR1, ESR2 and AR sequences in exocrine tissues of male and female autoimmune and non-autoimmune mice were identical to those of NCBI standards.
117	19997529	We hypothesize that defects in estrogen receptor alpha (ESR1), estrogen receptor beta (ESR2) and/or the androgen receptor (AR) may also contribute to the development of lacrimal gland autoimmune sequelae in Sjögren's syndrome.
118	19997529	To begin to test this hypothesis, we examined whether mutations exist in the coding regions of ESR1, ESR2 and AR transcripts in lacrimal tissues of mouse models of Sjögren's syndrome.
119	19997529	RESULTS: Our results show that almost all ESR1, ESR2 and AR sequences in exocrine tissues of male and female autoimmune and non-autoimmune mice were identical to those of NCBI standards.
120	19997529	We hypothesize that defects in estrogen receptor alpha (ESR1), estrogen receptor beta (ESR2) and/or the androgen receptor (AR) may also contribute to the development of lacrimal gland autoimmune sequelae in Sjögren's syndrome.
121	19997529	To begin to test this hypothesis, we examined whether mutations exist in the coding regions of ESR1, ESR2 and AR transcripts in lacrimal tissues of mouse models of Sjögren's syndrome.
122	19997529	RESULTS: Our results show that almost all ESR1, ESR2 and AR sequences in exocrine tissues of male and female autoimmune and non-autoimmune mice were identical to those of NCBI standards.
123	20135752	Whole blood count, CRP and ESR were determined in both groups.
124	20198931	If doubt exists, however, tests may be necessary including FBC, ESR and CRP, uric acid for suspected gout and X-rays of the affected joints especially following trauma, or pseudogout.
125	20656475	This increased risk may be explained by activation of the insulin- and insulin-like growth factor (IGF) signalling pathways and increased signalling through the oestrogen receptor.
126	22936542	Insulin stimulates the proliferation of some human breast cancer cell lines in vitro by mechanisms that use both the phosphatidylinositol-3 kinase and the mitogen-activated protein kinase/Akt signaling pathways; it is also a cell survival (anti-apoptotic) agent and enhances tumor cell migration and invasive capacity.
127	22936542	In such a system, one adipokine, leptin, has stimulatory paracrine effects on breast cancer cell proliferation and survival, while a second, adiponectin, is inhibitory.
128	22936542	Leptin, vascular endothelial growth factor, another insulin-regulated adipokine, and insulin itself also stimulate angiogenesis.
129	22936542	Insulin has complex interactions with estrogens: it induces adipose stromal cell aromatase and tumor cell sex steroid hormone receptor expression and suppresses sex hormone-binding globulin, which may enhance estrogen synthesis and bioactivity with consequent promotion of estrogen-dependent breast cancer.
130	23100221	Peroxisome proliferator-activated receptors (PPARs) are members of the steroid hormone receptor superfamily, discovered in 1990.
131	23277715	Using the PCR based RFLP method, the PvuII and XbaI polymorphisms of ESR1 and in MT1A (rs8052394 and rs11076161) gene polymorphisms were analysed.
132	23277715	This is the first Indian study to conclude that ESR1 and MT1 gene polymorphisms are not associated with increased susceptibility to type 2 diabetes in Indian women.
133	23277715	Using the PCR based RFLP method, the PvuII and XbaI polymorphisms of ESR1 and in MT1A (rs8052394 and rs11076161) gene polymorphisms were analysed.
134	23277715	This is the first Indian study to conclude that ESR1 and MT1 gene polymorphisms are not associated with increased susceptibility to type 2 diabetes in Indian women.
135	23328702	Short-term folate supplementation in physiological doses has no effect on ESR1 and MLH1 methylation in colonic mucosa of individuals with adenoma.
136	23506158	The aim of the study was to investigate if low circulating testosterone or E2 levels in combination with variants in the estrogen receptor alpha (ESR1) and estrogen receptor beta (ESR2) genes were of importance for the risk of type-2 diabetes.
137	23506158	The single nucleotide polymorphisms rs2207396 and rs1256049, in ESR1 and ESR2, respectively, were analysed by allele specific PCR in 172 elderly men from the population-based Tromsø study.
138	23506158	The aim of the study was to investigate if low circulating testosterone or E2 levels in combination with variants in the estrogen receptor alpha (ESR1) and estrogen receptor beta (ESR2) genes were of importance for the risk of type-2 diabetes.
139	23506158	The single nucleotide polymorphisms rs2207396 and rs1256049, in ESR1 and ESR2, respectively, were analysed by allele specific PCR in 172 elderly men from the population-based Tromsø study.
140	23667102	At baseline, the values of CRP, ESR, WBC, and PCT were significantly higher in patients with osteomyelitis than in those with soft-tissue infections.
141	23719562	Insulin-like growth factor 1 mRNA expression in the uterus of streptozotocin-treated diabetic mice.
142	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.
143	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.
144	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.