Ignet

Gene Information

Gene symbol: RNU1A3

Gene name: RNA, U1A3 small nuclear

HGNC ID: 10121

Related Genes

#	Gene Symbol	Number of hits
1	HSD11B1	1 hits
2	INS	1 hits
3	SPAG8	1 hits
4	USP2	1 hits

Related Sentences

#	PMID	Sentence
1	18230901	In order to determine whether elevated tissue 11beta -HSD1 contributed to obesity and metabolic disease, transgenic mice overexpressing 11beta -HSD1 in adipose tissue or liver were made.
2	18230901	Adipose-selective 11beta -HSD1 transgenic mice exhibited elevated intra-adipose and portal, but not systemic corticosterone levels, abdominal obesity, hyperglycaemia, insulin resistance, dyslipidaemia and hypertension.
3	18230901	In contrast, transgenic overexpression of 11beta -HSD1 in liver yielded an attenuated metabolic syndrome with mild insulin resistance, dyslipidaemia, hypertension and fatty liver, but not obesity or glucose intolerance.
4	18230901	Together with early data using non-selective 11beta -HSD1 inhibitors to insulin sensitise humans, this corroborated the notion that the enzyme may be a good therapeutic target in the treatment of the metabolic syndrome.
5	18230901	Further, a transgenic model of therapeutic 11beta -HSD1 inhibition, 11beta -HSD1 gene knock-out (11beta -HSD1-/-) mice, exhibited improved glucose tolerance, a 'cardioprotective' lipid profile, reduced weight gain and visceral fat accumulation with chronic high-fat feeding.
6	18230901	Recent evidence further suggests that high fat-mediated downregulation of adipose 11beta -HSD1 may be an endogenous pathway that underpins adaptive disease resistance in genetically predisposed mouse strains.
7	18230901	The efficacy of 11beta -HSD1 inhibitors has recently been extended to include increased energy expenditure and reduction of arteriosclerosis, and therefore may be of significant therapeutic value in the metabolic syndrome, with complementary effects upon liver adipose tissue, muscle, pancreas and plaque-prone vessels.
8	18230901	In order to determine whether elevated tissue 11beta -HSD1 contributed to obesity and metabolic disease, transgenic mice overexpressing 11beta -HSD1 in adipose tissue or liver were made.
9	18230901	Adipose-selective 11beta -HSD1 transgenic mice exhibited elevated intra-adipose and portal, but not systemic corticosterone levels, abdominal obesity, hyperglycaemia, insulin resistance, dyslipidaemia and hypertension.
10	18230901	In contrast, transgenic overexpression of 11beta -HSD1 in liver yielded an attenuated metabolic syndrome with mild insulin resistance, dyslipidaemia, hypertension and fatty liver, but not obesity or glucose intolerance.
11	18230901	Together with early data using non-selective 11beta -HSD1 inhibitors to insulin sensitise humans, this corroborated the notion that the enzyme may be a good therapeutic target in the treatment of the metabolic syndrome.
12	18230901	Further, a transgenic model of therapeutic 11beta -HSD1 inhibition, 11beta -HSD1 gene knock-out (11beta -HSD1-/-) mice, exhibited improved glucose tolerance, a 'cardioprotective' lipid profile, reduced weight gain and visceral fat accumulation with chronic high-fat feeding.
13	18230901	Recent evidence further suggests that high fat-mediated downregulation of adipose 11beta -HSD1 may be an endogenous pathway that underpins adaptive disease resistance in genetically predisposed mouse strains.
14	18230901	The efficacy of 11beta -HSD1 inhibitors has recently been extended to include increased energy expenditure and reduction of arteriosclerosis, and therefore may be of significant therapeutic value in the metabolic syndrome, with complementary effects upon liver adipose tissue, muscle, pancreas and plaque-prone vessels.
15	18230901	In order to determine whether elevated tissue 11beta -HSD1 contributed to obesity and metabolic disease, transgenic mice overexpressing 11beta -HSD1 in adipose tissue or liver were made.
16	18230901	Adipose-selective 11beta -HSD1 transgenic mice exhibited elevated intra-adipose and portal, but not systemic corticosterone levels, abdominal obesity, hyperglycaemia, insulin resistance, dyslipidaemia and hypertension.
17	18230901	In contrast, transgenic overexpression of 11beta -HSD1 in liver yielded an attenuated metabolic syndrome with mild insulin resistance, dyslipidaemia, hypertension and fatty liver, but not obesity or glucose intolerance.
18	18230901	Together with early data using non-selective 11beta -HSD1 inhibitors to insulin sensitise humans, this corroborated the notion that the enzyme may be a good therapeutic target in the treatment of the metabolic syndrome.
19	18230901	Further, a transgenic model of therapeutic 11beta -HSD1 inhibition, 11beta -HSD1 gene knock-out (11beta -HSD1-/-) mice, exhibited improved glucose tolerance, a 'cardioprotective' lipid profile, reduced weight gain and visceral fat accumulation with chronic high-fat feeding.
20	18230901	Recent evidence further suggests that high fat-mediated downregulation of adipose 11beta -HSD1 may be an endogenous pathway that underpins adaptive disease resistance in genetically predisposed mouse strains.
21	18230901	The efficacy of 11beta -HSD1 inhibitors has recently been extended to include increased energy expenditure and reduction of arteriosclerosis, and therefore may be of significant therapeutic value in the metabolic syndrome, with complementary effects upon liver adipose tissue, muscle, pancreas and plaque-prone vessels.
22	18230901	In order to determine whether elevated tissue 11beta -HSD1 contributed to obesity and metabolic disease, transgenic mice overexpressing 11beta -HSD1 in adipose tissue or liver were made.
23	18230901	Adipose-selective 11beta -HSD1 transgenic mice exhibited elevated intra-adipose and portal, but not systemic corticosterone levels, abdominal obesity, hyperglycaemia, insulin resistance, dyslipidaemia and hypertension.
24	18230901	In contrast, transgenic overexpression of 11beta -HSD1 in liver yielded an attenuated metabolic syndrome with mild insulin resistance, dyslipidaemia, hypertension and fatty liver, but not obesity or glucose intolerance.
25	18230901	Together with early data using non-selective 11beta -HSD1 inhibitors to insulin sensitise humans, this corroborated the notion that the enzyme may be a good therapeutic target in the treatment of the metabolic syndrome.
26	18230901	Further, a transgenic model of therapeutic 11beta -HSD1 inhibition, 11beta -HSD1 gene knock-out (11beta -HSD1-/-) mice, exhibited improved glucose tolerance, a 'cardioprotective' lipid profile, reduced weight gain and visceral fat accumulation with chronic high-fat feeding.
27	18230901	Recent evidence further suggests that high fat-mediated downregulation of adipose 11beta -HSD1 may be an endogenous pathway that underpins adaptive disease resistance in genetically predisposed mouse strains.
28	18230901	The efficacy of 11beta -HSD1 inhibitors has recently been extended to include increased energy expenditure and reduction of arteriosclerosis, and therefore may be of significant therapeutic value in the metabolic syndrome, with complementary effects upon liver adipose tissue, muscle, pancreas and plaque-prone vessels.
29	18230901	In order to determine whether elevated tissue 11beta -HSD1 contributed to obesity and metabolic disease, transgenic mice overexpressing 11beta -HSD1 in adipose tissue or liver were made.
30	18230901	Adipose-selective 11beta -HSD1 transgenic mice exhibited elevated intra-adipose and portal, but not systemic corticosterone levels, abdominal obesity, hyperglycaemia, insulin resistance, dyslipidaemia and hypertension.
31	18230901	In contrast, transgenic overexpression of 11beta -HSD1 in liver yielded an attenuated metabolic syndrome with mild insulin resistance, dyslipidaemia, hypertension and fatty liver, but not obesity or glucose intolerance.
32	18230901	Together with early data using non-selective 11beta -HSD1 inhibitors to insulin sensitise humans, this corroborated the notion that the enzyme may be a good therapeutic target in the treatment of the metabolic syndrome.
33	18230901	Further, a transgenic model of therapeutic 11beta -HSD1 inhibition, 11beta -HSD1 gene knock-out (11beta -HSD1-/-) mice, exhibited improved glucose tolerance, a 'cardioprotective' lipid profile, reduced weight gain and visceral fat accumulation with chronic high-fat feeding.
34	18230901	Recent evidence further suggests that high fat-mediated downregulation of adipose 11beta -HSD1 may be an endogenous pathway that underpins adaptive disease resistance in genetically predisposed mouse strains.
35	18230901	The efficacy of 11beta -HSD1 inhibitors has recently been extended to include increased energy expenditure and reduction of arteriosclerosis, and therefore may be of significant therapeutic value in the metabolic syndrome, with complementary effects upon liver adipose tissue, muscle, pancreas and plaque-prone vessels.
36	18230901	In order to determine whether elevated tissue 11beta -HSD1 contributed to obesity and metabolic disease, transgenic mice overexpressing 11beta -HSD1 in adipose tissue or liver were made.
37	18230901	Adipose-selective 11beta -HSD1 transgenic mice exhibited elevated intra-adipose and portal, but not systemic corticosterone levels, abdominal obesity, hyperglycaemia, insulin resistance, dyslipidaemia and hypertension.
38	18230901	In contrast, transgenic overexpression of 11beta -HSD1 in liver yielded an attenuated metabolic syndrome with mild insulin resistance, dyslipidaemia, hypertension and fatty liver, but not obesity or glucose intolerance.
39	18230901	Together with early data using non-selective 11beta -HSD1 inhibitors to insulin sensitise humans, this corroborated the notion that the enzyme may be a good therapeutic target in the treatment of the metabolic syndrome.
40	18230901	Further, a transgenic model of therapeutic 11beta -HSD1 inhibition, 11beta -HSD1 gene knock-out (11beta -HSD1-/-) mice, exhibited improved glucose tolerance, a 'cardioprotective' lipid profile, reduced weight gain and visceral fat accumulation with chronic high-fat feeding.
41	18230901	Recent evidence further suggests that high fat-mediated downregulation of adipose 11beta -HSD1 may be an endogenous pathway that underpins adaptive disease resistance in genetically predisposed mouse strains.
42	18230901	The efficacy of 11beta -HSD1 inhibitors has recently been extended to include increased energy expenditure and reduction of arteriosclerosis, and therefore may be of significant therapeutic value in the metabolic syndrome, with complementary effects upon liver adipose tissue, muscle, pancreas and plaque-prone vessels.
43	18230901	In order to determine whether elevated tissue 11beta -HSD1 contributed to obesity and metabolic disease, transgenic mice overexpressing 11beta -HSD1 in adipose tissue or liver were made.
44	18230901	Adipose-selective 11beta -HSD1 transgenic mice exhibited elevated intra-adipose and portal, but not systemic corticosterone levels, abdominal obesity, hyperglycaemia, insulin resistance, dyslipidaemia and hypertension.
45	18230901	In contrast, transgenic overexpression of 11beta -HSD1 in liver yielded an attenuated metabolic syndrome with mild insulin resistance, dyslipidaemia, hypertension and fatty liver, but not obesity or glucose intolerance.
46	18230901	Together with early data using non-selective 11beta -HSD1 inhibitors to insulin sensitise humans, this corroborated the notion that the enzyme may be a good therapeutic target in the treatment of the metabolic syndrome.
47	18230901	Further, a transgenic model of therapeutic 11beta -HSD1 inhibition, 11beta -HSD1 gene knock-out (11beta -HSD1-/-) mice, exhibited improved glucose tolerance, a 'cardioprotective' lipid profile, reduced weight gain and visceral fat accumulation with chronic high-fat feeding.
48	18230901	Recent evidence further suggests that high fat-mediated downregulation of adipose 11beta -HSD1 may be an endogenous pathway that underpins adaptive disease resistance in genetically predisposed mouse strains.
49	18230901	The efficacy of 11beta -HSD1 inhibitors has recently been extended to include increased energy expenditure and reduction of arteriosclerosis, and therefore may be of significant therapeutic value in the metabolic syndrome, with complementary effects upon liver adipose tissue, muscle, pancreas and plaque-prone vessels.
50	22447855	Ubiquitin-specific protease 2 regulates hepatic gluconeogenesis and diurnal glucose metabolism through 11β-hydroxysteroid dehydrogenase 1.
51	22447855	In this study, we identified ubiquitin-specific protease 2 (USP2) as an inducible regulator of hepatic gluconeogenesis that responds to nutritional status and clock.
52	22447855	USP2 is a target gene of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), a coactivator that integrates clock and energy metabolism, and is required for maintaining diurnal glucose homeostasis during restricted feeding.
53	22447855	At the mechanistic level, USP2 regulates hepatic glucose metabolism through its induction of 11β-hydroxysteroid dehydrogenase 1 (HSD1) and glucocorticoid signaling in the liver.
54	22447855	Pharmacological inhibition and liver-specific RNAi knockdown of HSD1 significantly impair the stimulation of hepatic gluconeogenesis by USP2.
55	22447855	Ubiquitin-specific protease 2 regulates hepatic gluconeogenesis and diurnal glucose metabolism through 11β-hydroxysteroid dehydrogenase 1.
56	22447855	In this study, we identified ubiquitin-specific protease 2 (USP2) as an inducible regulator of hepatic gluconeogenesis that responds to nutritional status and clock.
57	22447855	USP2 is a target gene of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), a coactivator that integrates clock and energy metabolism, and is required for maintaining diurnal glucose homeostasis during restricted feeding.
58	22447855	At the mechanistic level, USP2 regulates hepatic glucose metabolism through its induction of 11β-hydroxysteroid dehydrogenase 1 (HSD1) and glucocorticoid signaling in the liver.
59	22447855	Pharmacological inhibition and liver-specific RNAi knockdown of HSD1 significantly impair the stimulation of hepatic gluconeogenesis by USP2.