Ignet

Gene Information

Gene symbol: CES1

Gene name: carboxylesterase 1

HGNC ID: 1863

Synonyms: HMSE, CES2, HMSE1, SES1, CEH, CES1A1, CES1A2

Related Genes

#	Gene Symbol	Number of hits
1	AADAC	1 hits
2	ABCA4	1 hits
3	ACOT8	1 hits
4	ADIPOQ	1 hits
5	ALB	1 hits
6	ALDH1A1	1 hits
7	ANXA5	1 hits
8	FASN	1 hits
9	HBB	1 hits
10	HMGCR	1 hits
11	INS	1 hits
12	LIPC	1 hits
13	LIPE	1 hits
14	LPL	1 hits
15	ME1	1 hits
16	OGN	1 hits
17	PRDX6	1 hits
18	RPS27A	1 hits
19	SOAT1	1 hits
20	TF	1 hits
21	TNFRSF25	1 hits
22	TRPM6	1 hits
23	USP11	1 hits
24	UTS2	1 hits

Related Sentences

#	PMID	Sentence
1	126697	Also in human postheparin serum, palmitoyl-CoA hydrolase activity is shown to behave identical with hepatic triacylglycerol hydrolase activity.
2	759824	The function of the hepatic triglyceride lipase (H-TGL) is not yet clear.
3	759824	H-TGL was the lipase activity remaining after inhibition of lipoprotein lipase (LPL) by 1.0 M NaCl.
4	759824	The contributions of H-TGL and LPL to the total plasma triacylglycerol hydrolase (TGH) activity depend on the amount of heparin injected and the time of blood withdrawal after heparin injection.
5	759824	H-TGL was maximally released at higher heparin (50 U/250 g body weight) concentrations, compared to LPL which was maximally released at lower heparin (5 U/250 g body weight) concentrations.
6	759824	H-TGL and H-TGL/total TGH were 9.49 +/- 0.99 and 0.551 +/- 0.071, respectively, in rats 3 days after STZ injection, compared to H-TGL (13.46 +/- 0.69) and H-TGL/total TGH (0.739 +/- 0.052) in control nondiabetic rats.
7	759824	When diabetic rats were treated with insulin, total TGH (14.37 +/- 3.01) and H-TGL (6.77 +/- 4.12) rose to 25.16 +/- 1.02 (total TGH) and 16.49 +/- 1.13 (H-TGL), that were comparable to activities in control nondiabetic rats.
8	759824	Separation of H-TGL and LPL was performed using heparin-Sepharose affinity chromatography of postheparin plasma.
9	759824	The role of insulin in the regulation of LPL has been well documented.
10	759824	Our findings suggest that H-TGL also is under hormonal regulation by insulin in rats.
11	759824	The function of the hepatic triglyceride lipase (H-TGL) is not yet clear.
12	759824	H-TGL was the lipase activity remaining after inhibition of lipoprotein lipase (LPL) by 1.0 M NaCl.
13	759824	The contributions of H-TGL and LPL to the total plasma triacylglycerol hydrolase (TGH) activity depend on the amount of heparin injected and the time of blood withdrawal after heparin injection.
14	759824	H-TGL was maximally released at higher heparin (50 U/250 g body weight) concentrations, compared to LPL which was maximally released at lower heparin (5 U/250 g body weight) concentrations.
15	759824	H-TGL and H-TGL/total TGH were 9.49 +/- 0.99 and 0.551 +/- 0.071, respectively, in rats 3 days after STZ injection, compared to H-TGL (13.46 +/- 0.69) and H-TGL/total TGH (0.739 +/- 0.052) in control nondiabetic rats.
16	759824	When diabetic rats were treated with insulin, total TGH (14.37 +/- 3.01) and H-TGL (6.77 +/- 4.12) rose to 25.16 +/- 1.02 (total TGH) and 16.49 +/- 1.13 (H-TGL), that were comparable to activities in control nondiabetic rats.
17	759824	Separation of H-TGL and LPL was performed using heparin-Sepharose affinity chromatography of postheparin plasma.
18	759824	The role of insulin in the regulation of LPL has been well documented.
19	759824	Our findings suggest that H-TGL also is under hormonal regulation by insulin in rats.
20	759824	The function of the hepatic triglyceride lipase (H-TGL) is not yet clear.
21	759824	H-TGL was the lipase activity remaining after inhibition of lipoprotein lipase (LPL) by 1.0 M NaCl.
22	759824	The contributions of H-TGL and LPL to the total plasma triacylglycerol hydrolase (TGH) activity depend on the amount of heparin injected and the time of blood withdrawal after heparin injection.
23	759824	H-TGL was maximally released at higher heparin (50 U/250 g body weight) concentrations, compared to LPL which was maximally released at lower heparin (5 U/250 g body weight) concentrations.
24	759824	H-TGL and H-TGL/total TGH were 9.49 +/- 0.99 and 0.551 +/- 0.071, respectively, in rats 3 days after STZ injection, compared to H-TGL (13.46 +/- 0.69) and H-TGL/total TGH (0.739 +/- 0.052) in control nondiabetic rats.
25	759824	When diabetic rats were treated with insulin, total TGH (14.37 +/- 3.01) and H-TGL (6.77 +/- 4.12) rose to 25.16 +/- 1.02 (total TGH) and 16.49 +/- 1.13 (H-TGL), that were comparable to activities in control nondiabetic rats.
26	759824	Separation of H-TGL and LPL was performed using heparin-Sepharose affinity chromatography of postheparin plasma.
27	759824	The role of insulin in the regulation of LPL has been well documented.
28	759824	Our findings suggest that H-TGL also is under hormonal regulation by insulin in rats.
29	1632850	Acid cholesteryl ester hydrolase activity of mononuclear leukocytes in patients with non-insulin-dependent diabetes mellitus: studies before and after treatment of diabetes.
30	1632850	The change of acid cholesteryl ester hydrolase activity in mononuclear leukocyte following treatment of diabetes mellitus was studied in 21 patients with non-insulin-dependent diabetes mellitus (NIDDM).
31	1632850	Acid cholesteryl ester hydrolase activity of mononuclear leukocytes in patients with non-insulin-dependent diabetes mellitus: studies before and after treatment of diabetes.
32	1632850	The change of acid cholesteryl ester hydrolase activity in mononuclear leukocyte following treatment of diabetes mellitus was studied in 21 patients with non-insulin-dependent diabetes mellitus (NIDDM).
33	2382265	Acid cholesteryl ester hydrolase activity of mononuclear leukocyte in type 2 (non-insulin-dependent) diabetic patients.
34	2382265	Acid cholesteryl ester hydrolase activity of mononuclear leukocytes was measured in 52 Type 2 (non-insulin-dependent) diabetic patients.
35	2382265	Acid cholesteryl ester hydrolase activity of mononuclear leukocyte in type 2 (non-insulin-dependent) diabetic patients.
36	2382265	Acid cholesteryl ester hydrolase activity of mononuclear leukocytes was measured in 52 Type 2 (non-insulin-dependent) diabetic patients.
37	10634814	The present study, involving rats with streptozotocin (STZ)-induced diabetes, was performed to establish a PH model and to examine the relation between small intestinal acyl-coenzyme A:cholesterol acyltransferase (ACAT) activity and serum lipid levels in the postprandial state.
38	14725507	Although described initially as an intracellular adipocyte-specific triacylglycerol lipase, it is now clear that HSL (hormone-sensitive lipase) is expressed in multiple tissues and plays a number of roles in lipid metabolism, including that of a neutral cholesteryl ester hydrolase.
39	14748713	The lipases involved include arylacetamide deacetylase and/or triacylglycerol hydrolase.
40	14748713	Some, however, are returned to the cytosolic pool in a process that is stimulated by insulin and inhibited by microsomal triacylglycerol transfer protein (MTP).
41	14748713	Phospholipids also contribute to VLDL TAG in a process which involves ADP-ribosylation factor-1 (ARF-1)-mediated activation of phospholipase D.
42	15220197	Hormone-sensitive lipase has a role in lipid signaling for insulin secretion but is nonessential for the incretin action of glucagon-like peptide 1.
43	15220197	We previously reported decreased glucose-stimulated insulin secretion (GSIS) in hormone-sensitive lipase-null mice (HSL(-/-)), both in vivo and in vitro.
44	15220197	The effect of glucagon-like peptide 1 (GLP-1) on GSIS was also studied, as GLP-1 could augment GSIS via protein kinase A activation of HSL and lipolysis.
45	15220197	Neutral cholesteryl ester hydrolase activity was markedly reduced in islets from both 4- and 7-month-old male HSL(-/-) mice, whereas a marked deficiency in triglyceride lipase activity became evident only in the older mice.
46	15220197	GLP-1 also rescued GSIS in HSL(-/-) mice, indicating that signaling via HSL is not a major pathway for its incretin effect.
47	16929349	We observed a very pronounced distribution bias (P<10(-5)) of the two major DR3 CEHs, with DR3-B18 predominating in T1D and DR3-B8 in CD.
48	16940699	U-II accelerates foam cell formation by up-regulation of acyl-coenzyme A:cholesterol acyltransferase-1 in human monocyte-derived macrophages.
49	16940699	In human endothelial cells, U-II promotes cell proliferation and up-regulates type 1 collagen expression.
50	16940699	U-II also activates nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and plasminogen activator inhibitor-1 in human VSMCs, and stimulates VSMC proliferation with synergistic effects observed when combined with oxidized low-density lipoprotein, lysophosphatidylcholine, reactive oxygen species or serotonin.
51	20041776	Reductions of hepatic triglyceride and cholesterol contents in the SBE and SSE groups were related to the suppression of hepatic lipogenic enzyme activities, fatty acid synthesis (fatty acid synthase and malic enzyme), triglyceride synthesis (phosphatidate phosphohydrolase), and cholesterol synthesis (3-hydroxy-3-methylglutaryl-coenzyme A reductase) and esterification (acyl-coenzyme A:cholesterol acyltransferase).
52	20733269	Insulin suppresses HDL-mediated cholesterol efflux from macrophages through inhibition of neutral cholesteryl ester hydrolase and ATP-binding cassette transporter G1 expressions.
53	22733750	Loss of insulin-induced activation of TRPM6 magnesium channels results in impaired glucose tolerance during pregnancy.
54	22733750	Here, we show using patch clamp analysis and total internal reflection fluorescence microscopy, that insulin stimulates TRPM6 activity via a phosphoinositide 3-kinase and Rac1-mediated elevation of cell surface expression of TRPM6.
55	22733750	Interestingly, insulin failed to activate the genetic variants TRPM6(V(1393)I) and TRPM6(K(1584)E), which is likely due to the inability of the insulin signaling pathway to phosphorylate TRPM6(T(1391)) and TRPM6(S(1583)).
56	22733750	Moreover, by measuring total glycosylated hemoglobin (TGH) in 997 pregnant women as a measure of glucose control, we demonstrate that TRPM6(V(1393)I) and TRPM6(K(1584)E) are associated with higher TGH and confer a higher likelihood of developing GDM.
57	22733750	The impaired response of TRPM6(V(1393)I) and TRPM6(K(1584)E) to insulin represents a unique molecular pathway leading to GDM where the defect is located in TRPM6.
58	22796336	Compared with non-obese subjects, obese patients presented with increased carboxylesterase-1, zinc finger protein 324A, annexin A5, ubiquitin carboxyl-terminal hydrolase, α-crystallin B chain, osteoglycin, retinal dehydrogenase-1 and 14-3-3 protein γ, and decreased transferrin, complement C3, fibrinogen γ chain, albumin, α1-antitrypsin and peroxiredoxin-6, irrespective of the adipose tissue depot studied.
59	22796336	SAT and VAT differed in protein species of fibrinogen and osteoglycin, whereas adipose tissue depot and obesity interacted on the protein abundance of actin, α-actinin 1, one protein species of carboxylesterase-1, retinal dehydrogenase-1 and 14-3-3 protein γ.
60	22796336	Compared with non-obese subjects, obese patients presented with increased carboxylesterase-1, zinc finger protein 324A, annexin A5, ubiquitin carboxyl-terminal hydrolase, α-crystallin B chain, osteoglycin, retinal dehydrogenase-1 and 14-3-3 protein γ, and decreased transferrin, complement C3, fibrinogen γ chain, albumin, α1-antitrypsin and peroxiredoxin-6, irrespective of the adipose tissue depot studied.
61	22796336	SAT and VAT differed in protein species of fibrinogen and osteoglycin, whereas adipose tissue depot and obesity interacted on the protein abundance of actin, α-actinin 1, one protein species of carboxylesterase-1, retinal dehydrogenase-1 and 14-3-3 protein γ.