LXR promotes the maximal egress of monocyte-derived cells from mouse aortic plaques during atherosclerosis regression. - Wikidata - awgldk - TriplyDB

LXR promotes the maximal egress of monocyte-derived cells from mouse aortic plaques during atherosclerosis regression.

LXR promotes the maximal egress of monocyte-derived cells from mouse aortic plaques during atherosclerosis regression.

http://www.wikidata.org/entity/Q34360087

about

Antagonism of miR-33 in mice promotes reverse cholesterol transport and regression of atherosclerosis LXR-dependent and -independent effects of oxysterols on immunity and tumor growth Regulation of atherogenesis by chemokines and chemokine receptors Anti-atherogenic mechanisms of high density lipoprotein: effects on myeloid cells Regression of atherosclerosis: insights from animal and clinical studies Vitamin D deficiency induces high blood pressure and accelerates atherosclerosis in mice Divergent JAM-C Expression Accelerates Monocyte-Derived Cell Exit from Atherosclerotic Plaques Cyclodextrins as Emerging Therapeutic Tools in the Treatment of Cholesterol-Associated Vascular and Neurodegenerative Diseases Liver X receptors at the intersection of lipid metabolism and atherogenesis Regulation of Adaptive Immunity in Health and Disease by Cholesterol Metabolism Endoplasmic reticulum stress controls M2 macrophage differentiation and foam cell formation Statins promote the regression of atherosclerosis via activation of the CCR7-dependent emigration pathway in macrophages Macrophages in the pathogenesis of atherosclerosis Liver LXRα expression is crucial for whole body cholesterol homeostasis and reverse cholesterol transport in mice Mechanisms that regulate macrophage burden in atherosclerosis.Leukocyte behavior in atherosclerosis, myocardial infarction, and heart failure.Regulation and consequences of monocytosis Cyclodextrin promotes atherosclerosis regression via macrophage reprogramming.Suppressed monocyte recruitment drives macrophage removal from atherosclerotic plaques of Apoe-/- mice during disease regression Plasma cholesterol-induced lesion networks activated before regression of early, mature, and advanced atherosclerosis.High density lipoprotein stimulated migration of macrophages depends on the scavenger receptor class B, type I, PDZK1 and Akt1 and is blocked by sphingosine 1 phosphate receptor antagonists.Niacin inhibits skin dendritic cell mobilization in a GPR109A independent manner but has no impact on monocyte trafficking in atherosclerosis.The neuroimmune guidance cue netrin-1 promotes atherosclerosis by inhibiting the emigration of macrophages from plaques LXR-Mediated ABCA1 Expression and Function Are Modulated by High Glucose and PRMT2.Nanoparticles containing a liver X receptor agonist inhibit inflammation and atherosclerosis Macrophages, dendritic cells, and regression of atherosclerosis.Effector Memory T cells Are Associated With Atherosclerosis in Humans and Animal Models Vitamin D suppression of endoplasmic reticulum stress promotes an antiatherogenic monocyte/macrophage phenotype in type 2 diabetic patients.Neuroimmune guidance cue Semaphorin 3E is expressed in atherosclerotic plaques and regulates macrophage retention Cardiometabolic interventions - focus on transcriptional regulators.Inducible ApoE gene repair in hypomorphic ApoE mice deficient in the low-density lipoprotein receptor promotes atheroma stabilization with a human-like lipoprotein profile.The transcription factor NR4A3 controls CD103+ dendritic cell migration.Activation of liver X receptor attenuates lysophosphatidylcholine-induced IL-8 expression in endothelial cells via the NF-κB pathway and SUMOylation.Myeloid-specific IκB kinase β deficiency decreases atherosclerosis in low-density lipoprotein receptor-deficient mice.Netrin-1 promotes adipose tissue macrophage retention and insulin resistance in obesity.Roles of the chemokine system in development of obesity, insulin resistance, and cardiovascular disease.Hyperglycemia promotes myelopoiesis and impairs the resolution of atherosclerosis.Monocyte and macrophage dynamics during atherogenesis.Metabolism, LXR/LXR ligands, and tumor immune escape.Liver X receptors, atherosclerosis and inflammation.

P2860

Q24634165-5BA25DDC-86CE-4209-988A-677DC1C80CC0 Q26824274-883E42C2-E29E-466B-A5AA-65350999D000 Q27003124-E9A83A8E-E88A-40A9-A154-24452635C47F Q27012536-37392E83-A743-4B5B-9832-CE2C58DAFC74 Q27028112-2DEE425E-9471-486F-B755-D644D86E575D Q27318595-4D8244B9-A026-4229-850E-3B1BFA223EBC Q27333694-BD188220-ED59-4E1D-BB0F-D567D81F9E9C Q28071254-596C2D4C-4BA6-4E49-A394-671C0718B964 Q28082452-70BD9373-F7C4-4221-960E-12067481E852 Q28083961-B075B5CE-B2D9-4257-8AF3-9F46BC754626 Q28260494-70BDEA14-E625-48D8-879E-4BEEFAB2B252 Q28741815-826AA272-542F-4055-B8CC-9118C511E588 Q29617765-A8B3A01F-61C9-4259-9F98-0F77B0541EC8 Q30426995-10A106DC-D360-4D58-A1A6-E0DBCEA5E23C Q33761114-553EBB4E-370A-4B4D-A070-A6AA4B92888C Q34322056-63B78A19-739F-40A2-B315-27087C02C6A7 Q34372534-00A859A7-03F5-480E-8122-3F6593F38E58 Q34521175-5C83191A-C478-4592-B2BB-65CC904407E5 Q34876397-955DEF18-39C7-4AE9-9D9E-6EB4F7396889 Q35105781-A52A92CA-4F78-48A6-A77F-9C2483D54554 Q35238369-C6275522-3EFD-4FE9-B0EC-9BE9F1F2CCB6 Q35608570-302F54DF-1030-4830-8A29-22711982FEDF Q35685440-8ACB42D4-9E45-4CEF-9C01-9F0DB49F9B7C Q35750322-141EEF7C-164E-4E82-87AA-697FF570A031 Q35924658-B146AA42-BACA-4145-9C3A-E1DC1D2FA38F Q36193752-8C473495-CAE5-4AB3-AC94-BDAD35FF171A Q36366126-1F00FCAC-3A58-4D1D-A36D-62AF2BF8E2EC Q36385767-E25A8BC1-496C-4BB9-AEDB-7664470EF84A Q36824150-8C486FEA-8FAE-48D0-9C6A-15A98E948C7A Q37161933-9F0C069D-53B8-491F-A2CD-2E0D110069E5 Q37262945-8BB55B59-0DFD-406F-9EBA-88A020019474 Q37452166-559BF18D-705F-454C-B769-F4D443487E0A Q37466848-86EFD14F-C6D1-431C-83C9-4F5B4A7DD041 Q37691504-E748AEC8-CB37-443F-9DB6-57DA07084CBB Q37695058-3E812914-37CA-43C2-9E75-1D5B35494F53 Q37704741-1824664F-80ED-4A51-90EB-F48DFC59FEBE Q37711215-120025C3-D33B-46AE-A4B5-D03E3609C5B2 Q37890185-451A4950-AD77-4FB5-A787-BC631BC7C0F8 Q37902800-ED1929EC-A41A-47FD-8DD8-DBBF6F33363C Q37993787-E67FF0FF-506C-4411-8C3E-A70FD4EEB825

P2860

LXR promotes the maximal egress of monocyte-derived cells from mouse aortic plaques during atherosclerosis regression.

http://www.wikidata.org/entity/Q34360087

description

2010 nî lūn-bûn

@nan

2010 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի դեկտեմբերին հրատարակված գիտական հոդված

@hy

2010年の論文

@ja

2010年論文

@yue

2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

name

LXR promotes the maximal egres ...... ng atherosclerosis regression.

@ast

LXR promotes the maximal egres ...... ng atherosclerosis regression.

@en

LXR promotes the maximal egres ...... ng atherosclerosis regression.

@nl

type

label

LXR promotes the maximal egres ...... ng atherosclerosis regression.

@ast

LXR promotes the maximal egres ...... ng atherosclerosis regression.

@en

LXR promotes the maximal egres ...... ng atherosclerosis regression.

@nl

prefLabel

LXR promotes the maximal egres ...... ng atherosclerosis regression.

@ast

LXR promotes the maximal egres ...... ng atherosclerosis regression.

@en

LXR promotes the maximal egres ...... ng atherosclerosis regression.

@nl

P1433

Q34360087-6D5C83B7-D57B-47EB-A3AD-02380CDAA29B

P1476

Q34360087-0723CF5A-42AE-4824-9CDE-0B46C9421919

P2093

Q34360087-1CF29FC3-54F2-4F42-AF20-7335D76BF75E

Q34360087-4274E9E1-9409-41C4-B9E1-1837C954CC12

Q34360087-5A4986C7-A36C-44FA-A27D-F3952C034893

Q34360087-635E795E-A533-49A4-A573-D54D198C61C2

Q34360087-6F5AC080-0051-4241-97B6-CB184D38F3AB

Q34360087-864A1D6F-6345-4A0D-9A3B-66ED328AF195

Q34360087-9C6D27F3-98BB-4128-98A6-D118CE8213B5

Q34360087-B987590F-B9C3-4CEE-BF67-D64EF51BF206

Q34360087-C15F55F5-6BBD-41DF-ACD9-8BFD3DE11FE1

Q34360087-CE9878CB-A7B3-4BE3-AD34-08A773F6B5B1

P2860

Q34360087-00B50C9E-47B9-488F-B2BE-30F98F68EAF6

Q34360087-01052193-EDD9-4A94-9B7C-973E14E58284

Q34360087-0554A5AA-C53D-4AD5-AEB0-AA8A2A1CC2AA

Q34360087-07DF0069-20F6-497C-948F-56D88E884322

Q34360087-1536E29A-998A-4159-9323-95AB71FE9009

Q34360087-1DC83EBF-B61A-4328-9CC3-EF7B2B451E1F

Q34360087-20400565-9405-4143-8ED3-0EEF9BFDD179

Q34360087-22CECC2B-69A9-406B-A6F2-27EB81607489

Q34360087-24FF668B-FBE2-4194-B5A3-3959B85243EF

Q34360087-2563C4CE-E0BF-4224-A118-77F3B87275D3

P304

Q34360087-CA3E4C1F-2A98-46FE-B412-7B40136D0EE9

P31

Q34360087-BA0B3351-F5EC-49F6-9A3E-E22A429D8B72

P356

Q34360087-ECE9820A-EDB2-4A63-B866-553FDC4395CB

P407

Q34360087-40E9AB24-9A9C-4AA1-AE94-15E4A0EFD4FE

P433

Q34360087-1DA0F331-DA09-43B4-827A-7AB911C40454

P478

Q34360087-FEC700BF-DFC3-4089-9ABD-FDAC65CE8B97

P50

Q34360087-7E7E532C-A128-4B07-8A5B-7EC89D6D6049

Q34360087-BF547931-5ED5-4611-B20A-F9BCE1C64B43

Q34360087-C2F08DFD-1EE6-458B-B9C1-4FA6D5FF3EFA

Q34360087-D408B454-529D-42C8-99FD-5AF37FAED649

P577

Q34360087-C8F18C65-3E30-4A7C-A3F1-2EFF6DBB7B7D

P698

Q34360087-F4975092-990E-47D5-898C-29738183E16E

P921

Q34360087-99119C4A-2997-4B75-AC45-1D41302EB97D

Q34360087-E757A1AD-3F15-456F-B973-9AAC98A46BEA

P932

Q34360087-0D93272D-79C9-402B-9CE6-F1871CFC56C9

P356

P1433

Journal of Clinical Investigation

P1476

LXR promotes the maximal egres ...... ng atherosclerosis regression.

@en

P2093

Chaowei Wu

http://www.w3.org/2001/XMLSchema#string

Cynthia Hong

http://www.w3.org/2001/XMLSchema#string

Daniel Rubinstein

http://www.w3.org/2001/XMLSchema#string

Dusan Bogunovic

http://www.w3.org/2001/XMLSchema#string

Ines Pineda-Torra

http://www.w3.org/2001/XMLSchema#string

Jianhua Liu

http://www.w3.org/2001/XMLSchema#string

Jonathan E Feig

http://www.w3.org/2001/XMLSchema#string

Marie Sanson

http://www.w3.org/2001/XMLSchema#string

Michael Garabedian

http://www.w3.org/2001/XMLSchema#string

Michelle N Bradley

http://www.w3.org/2001/XMLSchema#string

P2860

Role of LXRs in control of lipogenesis

Human white/murine ABC8 mRNA levels are highly induced in lipid-loaded macrophages. A transcriptional role for specific oxysterols

Regulated expression of the apolipoprotein E/C-I/C-IV/C-II gene cluster in murine and human macrophages. A critical role for nuclear liver X receptors alpha and beta

Liver X receptor (LXR) regulation of the LXRalpha gene in human macrophages

Cholesterol and bile acid metabolism are impaired in mice lacking the nuclear oxysterol receptor LXR alpha

Different roles of liver X receptor alpha and beta in lipid metabolism: effects of an alpha-selective and a dual agonist in mice deficient in each subtype

Ligand activation of LXR beta reverses atherosclerosis and cellular cholesterol overload in mice lacking LXR alpha and apoE

Liver X receptor (LXR)-beta regulation in LXRalpha-deficient mice: implications for therapeutic targeting

Non-redundant roles for LXRalpha and LXRbeta in atherosclerosis susceptibility in low density lipoprotein receptor knockout mice.

CCR7 coordinates the primary immune response by establishing functional microenvironments in secondary lymphoid organs

P304

4415-4424

http://www.w3.org/2001/XMLSchema#string

P31

scholarly article

P356

10.1172/JCI38911

http://www.w3.org/2001/XMLSchema#string

P407

P433

12

http://www.w3.org/2001/XMLSchema#string

P478

120

http://www.w3.org/2001/XMLSchema#string

P50

Edward A Fisher

Emmanuel L. Gautier

Nico van Rooijen

P577

2010-12-01T00:00:00Z

http://www.w3.org/2001/XMLSchema#dateTime

P698

21041949

http://www.w3.org/2001/XMLSchema#string

P921

atherosclerosis

P932

2993578

http://www.w3.org/2001/XMLSchema#string